9.26.2009
What if Your Parent(s) or Grandparents have Alzheimer's?
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photo tagged 'old family photo' on the internet
A family history of the Disease is linked to greater prevalence of known genetic markers that act as signposts for Alzheimer's in some cases.
Furthermore, recent investigative research asserts that children whose parents have a history of Alzheimer's Disease are more likely to be an APOE4 allele carrier (46% vs 21%, p < 0.001) than offspring without such a parental history.
Interestingly, plasma apoE levels strongly decreased from APOE2 to APOE3 to APOE4 carrying individuals (p < 0.001), resulting in the finding that reduced plasma levels were associated with higher occurrence of Alzheimer's.
They conclude logically that lower plasma levels in middle age is linked to Alzheimer's in old age, based on a study of 400 individuals, 203 active research subjects and 197 control subjects.
Genetics potentially offers another perspective on solving the cognitive decline puzzle that aids in analysis, or triangulation, of whatever data might be available in a particular case or set of cases, micro or macro.
Labels: alzheimers, apoe, neurology, plasma
// posted by neurofuture10:33 PM permanent link
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9.22.2009
Alzheimer's Crisis Reaches a Crest
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Image: the divine wind brings a tsunami to Japan
A new report from Alzheimer's Disease International reports that there are now 35.6 million cases of Alzheimer's and will be 115 million or more by the year 2050.
At this rate, the incidence of the disease will double every twenty years, and this probably underreports the crisis since cases are normally only diagnosed when the patient is in the last stages of what has been an invisible process, possibly commencing decades before it is noticed, along with conditions such as atherosclerosis.
Early detection through screening and other indicators (genetics) and notice of any subtle changes in cognition may act like a version of early radar in the 1940's, giving observers advance notice. Doubtless today's cumbersome process will morph into a sleeker, faster, and more efficient system that will help to save brains and prolong lives.
Undiagnosed Alzheimer's is often a cause of death, since it can lead to cessation of the pulse or breathing as the brain 'forgets' how to regulate these automatic routines, with the disease actually the unlabeled cause of death, rather than the overt symptom or outward manifestation. There is hope, however, in mental, physical, and social activity - in short, staying engaged and 'plugged-in' to the vibe of life and the amazing world around us.
Labels: alzheimers, brain, diagnosis, international
// posted by neurofuture10:32 AM permanent link
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9.07.2009
Saturated Fat and Alzheimer's Causality
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From Australian Broadcasting Corp...
Researchers believe they have discovered why foods high in saturated fat increase the likelihood of developing Alzheimer's disease.
Researchers from Curtin University of Technology in Perth, found that saturated dietary fat damages the lining of blood vessels in the brains of mice, allowing a protein called amyloid to enter the brain.
The study, to be published in the British Journal of Nutrition, is one of the first to demonstrate a scientific link between diet and Alzheimer's disease.
"In the past population studies suggested that high fat diets may be a risk factor for Alzheimer's disease, but no one really understood why," says Professor Mamo, co-author of the study and National Director of the Australian Technology Network's Centre for Metabolic Fitness.
More >>
Researchers believe they have discovered why foods high in saturated fat increase the likelihood of developing Alzheimer's disease.
Researchers from Curtin University of Technology in Perth, found that saturated dietary fat damages the lining of blood vessels in the brains of mice, allowing a protein called amyloid to enter the brain.
The study, to be published in the British Journal of Nutrition, is one of the first to demonstrate a scientific link between diet and Alzheimer's disease.
"In the past population studies suggested that high fat diets may be a risk factor for Alzheimer's disease, but no one really understood why," says Professor Mamo, co-author of the study and National Director of the Australian Technology Network's Centre for Metabolic Fitness.
More >>
Labels: alzheimers, fat, saturated
// posted by neurofuture7:18 PM permanent link
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9.06.2009
Additional Alzheimer's Disease Gene Associations
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UK researchers assert that two new gene associations (in addition to APOE) may be linked to Alzheimer's....more
Labels: alzheimers, apoe, CR1, genes
// posted by neurofuture6:33 PM permanent link
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8.26.2009
Alzheimer's-Sunscreen Link?
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Researchers in Europe are examining a connection between Alzheimer's Disease and nano-sized particles that occur in sunscreen formulations. It is hypothesized that neuron links may be impacted by substances such as titanium dioxide which also occur in diesel fuels. Evidence from small animal studies implies causality, subject to future research.
"The brain itself is a very special organ. It cannot repair by replacing nerve cells – the ones you get at birth have to last all your life, which makes them peculiarly vulnerable to long-term, low-dose toxicity," said Dr. Vyvyan Howard, one of the lead scientists on the study.
Labels: alzheimers, howard, sunscreen, ulster, vyvyan
// posted by neurofuture10:48 AM permanent link
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8.04.2009
Cognitive Exercises Can Deter Dementia
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A new study of 488 subjects published today in the journal Neurology has found that brain exercises may halt the development of dementias - related to conditions such as Alzheimer's and Parkinson's Disease. The study examined a subject group over a period of 5 years.
More of the article
The body of evidence has been accumulating since late 2006's JAMA article showing increasing efficacy of cognitive exercise, particularly in the areas of speed and executive functioning - in a variety of scientific and medical journals, including our own 2008 study as well as earlier papers.
Labels: alzheimers, dementia, einstein
// posted by neurofuture8:36 AM permanent link
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6.09.2009
5 Truths that Spawned 5 Myths about Alzheimer’s and Dementia
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Dennis Fortier, President and CEO of Medical Care Corporation, contributes the following about the diagnosis and treatment of Alzheimer's:
Sometimes the truth can be very misleading. This is often the case with complex topics when an "expert" makes a narrow but accurate statement that is subsequently generalized by the lay public. This is a common phenomenon in the fields of Alzheimer’s and dementia.
Here are five examples of true statements that have been so commonly misinterpreted that they have spawned five harmful yet well-entrenched myths.
Narrow Truth: There is no cure for AD.
General Myth: Because there is no cure, nothing can be done for patients diagnosed with this disease.
Like diabetes and hypertension, we cannot yet cure Alzheimer’s disease. However, physicians can intervene and manage the symptoms with more success than most headlines would indicate. In fact, with a timely diagnosis, a physician can prescribe a treatment plan including pharmaceutical therapy, improved diet, physical exercise, mental and social activity, and certain OTC supplements. When this approach is combined with an educated caregiver, disease progression can be commonly slowed for some meaningful period of time.
Narrow Truth: The only certain method for diagnosing Alzheimer’s disease is to inspect a sample of brain tissue during autopsy.
General Myth: Alzheimer’s disease cannot be accurately diagnosed until death.
If "certain" means 100% accuracy, then there is no certain diagnostic method for many well known diseases (Lou Gehrig's disease springs immediately to mind). However, physicians following published diagnostic guidelines can get a highly accurate diagnosis of Alzheimer’s disease (90%-95), even at a fairly early stage of the disease. This diagnostic accuracy is on par with commonly accepted clinical practice.
Narrow Truth: Current treatments do not stop the progression of AD.
General Myth: Since the disease will continue to progress, there is no need to bother with treatment.
There is no doubt that reversing all memory loss would be the best treatment result and halting further memory loss would be better than ongoing decline. However, this does not mean that slowing the pace of further decline is not a worthy pursuit. We all want better treatment options in the future but until they arrive, preserving quality of life during a patient’s final years is definitely a worthwhile and attainable goal.
Narrow Truth: Cognitive decline is a part of normal aging.
General Myth: Pronounced cognitive deficits just need to be expected and tolerated
As we age, all of our organic functions tend to slow. Our ability to think, make calculations, use judgment, and store and retrieve information is not immune to this process. However, a pronounced loss of cognitive capacity severe enough to impact a person’s ability to lead an independent life is not normal. When such decline occurs, there is some underlying pathological explanation that can be identified and treated by a physician. Accepting significant loss of mental function as a normal artifact of aging is a tragedy.
Narrow Truth: It’s best not to know if you have Alzheimer’s disease
General Myth: It’s best if the problem stays undiagnosed
This final "truth" is a stretch to begin with. I can imagine that, if it were possible, an Alzheimer’s patient might enjoy life more if they could receive the highest standards of care without ever knowing they had a terrible disease. However, this does not make the case that the problem should be ignored. The published evidence in favor of managing the symptoms and prolonging a higher quality of life outweighs the presumed benefits of bliss. Additionally, patients need to know about their condition if they are to participate meaningfully in their own care and end of life decisions.
I hear and read these narrow "truths" in the media everyday. I also see first hand how the public mischaracterizes them and takes away a broader and more harmful message than is intended.
Education remains a major barrier between our current ability to care for AD patients and the higher standards that are within our immediate grasp. To address the educational gap, leading researchers distill the daily news through a non-commercial blog called "Brain Today" (it can be viewed at http://braintoday.blogspot.com).
Through this and many other educational efforts, I hope we can begin to divorce ourselves from these sound bites of misleading truth and begin to see the Alzheimer’s picture with more clarity.
Dennis Fortier
President & CEO
Medical Care Corporation
Labels: alzheimers, mccare
// posted by neurofuture11:38 AM permanent link
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5.26.2009
Vitamin D Deficiency and Alzheimer's
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A separate research study examines Vitamin D deficiency and Alzheimer's Disease. Scientists speculate that lack of adequate Vitamin D could be one of the causal factors for Alzheimer's. Another study (just published) finds an association between cognitive processing speed and administration of Vitamin D.
Labels: alzheimers, vitamind
// posted by neurofuture9:37 PM permanent link
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5.08.2009
NY Times Television Review of Alzheimers Awareness Media
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HBO is airing a wide variety of Alzheimer's Awareness programming...with an estimated 5 million people now with the disease...and millions more at risk. HBO is even leveraging new platforms such as Facebook and Youtube with channels to build community.
Labels: alz.org, alzheimers, facebook, hbo, shriver, youtube
// posted by neurofuture5:21 PM permanent link
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4.01.2009
Cognitive Decline: An Accelerating Problem
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A Brain Silenced Every 70 Seconds: It's Important to Get Involved, For Your Future and Others'
By the time you finish these first few paragraphs, Alzheimer’s disease will strike someone else. The attack on the brain will make someone lose track of the steps needed to place a phone call or remember the name of common items.
The fatal disease creeps up on someone new every 70 seconds. As the population ages, the rate will rise to every 33 seconds by mid-century, according to a study from the Alzheimer’s Association. 5.3 Million people in the U.S. have Alzheimer's (as diagnosed) and many more have not been diagnosed or have early stage impairment. This represents a 47% increase in 5 years, while the percentage growth of fatalities caused by cancers and heart disease have actually decreased during this period (WebMD).
The costs are mind-boggling. As families deal with the emotional aspects of Mom or Dad no longer recalling sons' or daughters' names, they also face giving up or cutting back on their jobs so they can care for loved ones.
About 70 percent of people with Alzheimer’s are cared for by family members, according to the Alzheimer’s Association study, titled "Alzheimer’s Disease Facts and Figures."
Costs By the numbers
Medicare costs tied to Alzheimer’s are expected to more than double the $91 billion in 2005 to $189 billion by 2015.
What's encouraging is the recognition that while age is the greatest risk factor, WebMD has recognized genetics as the 2nd risk factor, along with lifestyle.
Taking personal interest in your cognitive fitness and other aspects of your health and biometrics will help us experience life close to our full potential, whatever stage we're at presently - and on into the future. That's where the power of the Internet intervenes to make this dream possible.
By the time you finish these first few paragraphs, Alzheimer’s disease will strike someone else. The attack on the brain will make someone lose track of the steps needed to place a phone call or remember the name of common items.
The fatal disease creeps up on someone new every 70 seconds. As the population ages, the rate will rise to every 33 seconds by mid-century, according to a study from the Alzheimer’s Association. 5.3 Million people in the U.S. have Alzheimer's (as diagnosed) and many more have not been diagnosed or have early stage impairment. This represents a 47% increase in 5 years, while the percentage growth of fatalities caused by cancers and heart disease have actually decreased during this period (WebMD).
The costs are mind-boggling. As families deal with the emotional aspects of Mom or Dad no longer recalling sons' or daughters' names, they also face giving up or cutting back on their jobs so they can care for loved ones.
About 70 percent of people with Alzheimer’s are cared for by family members, according to the Alzheimer’s Association study, titled "Alzheimer’s Disease Facts and Figures."
Costs By the numbers
Medicare costs tied to Alzheimer’s are expected to more than double the $91 billion in 2005 to $189 billion by 2015.
What's encouraging is the recognition that while age is the greatest risk factor, WebMD has recognized genetics as the 2nd risk factor, along with lifestyle.
Taking personal interest in your cognitive fitness and other aspects of your health and biometrics will help us experience life close to our full potential, whatever stage we're at presently - and on into the future. That's where the power of the Internet intervenes to make this dream possible.
Labels: 70, alzheimers, seconds
// posted by neurofuture1:27 AM permanent link
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3.21.2009
86 with Alzheimers
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Yesterday I met a woman who is 86 years old. She has mild Alzheimer's Disease. She emigrated to the U.S. from Poland "60 years ago" which I guess is 1949...it may also have been before that...anyway she said it was after the War because they couldn't get away during the war. She said she can't read Polish anymore...but she still had a Polish accent. She was surprised to learn that people can compute in their own languages...she thought all keyboards were in English now.
Coming to the U.S., she eventually moved to Portola Valley and even spent some time working on mainframe computers. After selling her house she eventually moved into assisted living in Menlo Park, CA.
Despite all this, she never owned a personal computer. After spending about a half hour showing her all the great things you can do now on a ridiculously tiny laptop - search, check your email, launch free web docs, etc., with no key or EULA - she was ecstatic. And I closed the pitch by saying "Imagine, this tiny computer is 100X more powerful than the computers on the first flight to the moon, Apollo 11."
Her companion, in her late 90's (also with Alzheimer's) and in a wheelchair, wasn't sure about the moon experience and whether it was real or not...she muttered something about "the badlands" rolled her eyes and kind of chuckled but soon fell asleep.
My new friend said "Viola...she doesn't like new things" and waved her hand at her dismissively. "You know what?" she said. "Tomorrow I'm going to catch the bus, go to the store, and buy one of those. It'll be fun. I can learn new things, check the weather, maybe make free phone calls."
For her, this kind of trip seemed about as adventurous as paddling across the Mississippi river in a rubber boat.
Coming to the U.S., she eventually moved to Portola Valley and even spent some time working on mainframe computers. After selling her house she eventually moved into assisted living in Menlo Park, CA.
Despite all this, she never owned a personal computer. After spending about a half hour showing her all the great things you can do now on a ridiculously tiny laptop - search, check your email, launch free web docs, etc., with no key or EULA - she was ecstatic. And I closed the pitch by saying "Imagine, this tiny computer is 100X more powerful than the computers on the first flight to the moon, Apollo 11."
Her companion, in her late 90's (also with Alzheimer's) and in a wheelchair, wasn't sure about the moon experience and whether it was real or not...she muttered something about "the badlands" rolled her eyes and kind of chuckled but soon fell asleep.
My new friend said "Viola...she doesn't like new things" and waved her hand at her dismissively. "You know what?" she said. "Tomorrow I'm going to catch the bus, go to the store, and buy one of those. It'll be fun. I can learn new things, check the weather, maybe make free phone calls."
For her, this kind of trip seemed about as adventurous as paddling across the Mississippi river in a rubber boat.
Labels: 90s, alzheimers, portola, valley
// posted by neurofuture10:41 PM permanent link
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3.13.2009
Scans Can Detect Recording of Memories
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Positronic Emission Tomography (PET) images of brains
While believed to be a subtle biomechanical process by some neuroscientists and not prone to direct observation, new research with subjects interacting with a virtual reality environment has shown that scans can follow, record, and even predict the formulation of memories almost like an emulsion exposure process in chemical photography.
Humans create memories of locations in physical or virtual space as they move around - and it all shows up on brain scans.
Researchers tracked brain activity related to "spatial memory" as volunteers moved about inside a virtual reality setup. Their new study challenges previous scientific thinking by showing that memories are recorded in regular patterns.
"Surprisingly, just by looking at the brain data we could predict exactly where they were in the virtual reality environment," said Eleanor Maguire, a neuroscientist at the University College London in the U.K. "In other words, we could 'read' their spatial memories."
Maguire and her colleagues focused on the hippocampus, or a small part of the brain that deals with navigation, memory recall and imagining future events. Neurons known as "place cells" activate in the hippocampus and inform people of where they are as they move around.
Read more from live science
Labels: alzheimers, brain, pet
// posted by neurofuture12:49 PM permanent link
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1.31.2009
Author Pratchett Won't Stop Fighting
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When best-selling fantasy writer Sir Terry Pratchett was diagnosed with Alzheimer's Disease in December, 2007 at age 59 - he resolved to "not go down without a fight."
Pratchett invited the BBC to document the ups and downs of day to day life with the Disease, and the result is being aired in the U.K. next week.
The story is covered by Telegraph Media's Editor Anita Singh.
Labels: 59, 60, alzheimers, pratchett, singh
// posted by neurofuture8:46 PM permanent link
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12.31.2008
2008, A Glorious Year for Make Benefit of Alzheimers Condition
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In summary:
Increasing visibility into the formation of amyloid plaques, and potential cause
Increasing research into genetic determinants of cognitive dysfunctions (including our research)
Pretty clear triangulation of evidence on the hypothesis that exercise may help avert Alzheimer's from multiple studies (including one announced yesterday at Columbia)
Labels: alzheimers, benefit, glorious, kazakhstan, make
// posted by neurofuture10:50 AM permanent link
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12.12.2008
2000 Year Old Brain Found in England
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Image of brain from York, believed to be part of a ritual sacrifice
A 2,000 year old brain was discovered in York and the announcement recently hit the wires. It would be fascinating to see if the brain shows any signs of amyloid accumulation and whether or not the individual was APOEe4 positive, if it could be extracted from the DNA.
Probably not, as DNA extraction of soft tissues is notoriously fraught with difficulties, such as contamination from the modern context, and any dried blood recovered may have degraded.
Early speculation suggests that the individual, dating to around 0 or the beginning of the Common Era (C.E.), was sacrificed and placed into a peat bog, as part of a religious ceremony dating back to Druidic practice. In this era, the Britons were self-governing and independent. Other recovered bodies in the U.K. and Northern Europe have shown evidence of similar treatment.
One scholarly speculation, that lead poisoning from pipes and lead-treated ceramic vessels caused widespread dementia in the first few centuries of the common era has been shown as fallacious, since such pipes would have been used only by a small fraction of the population and, according to hydrologists, dissolved calcium carbonate (lime) deposits from the water sources and vessels would have precipitated on any exposed lead surfaces, creating a molecular barrier.
Links for background:
Peat bog burials in Northern Europe
Druidism and Sacrifice
Lead pipes + ancient dementia
Labels: 2000, alzheimers, bog, calcium, carbonate, dementia, druidsm, human, lead, lime, peat, peatbog, sacrifice, york
// posted by neurofuture4:22 PM permanent link
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12.09.2008
Herpes Simplex Type I - New Alzheimer's Risk Factor?
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Research on six patients based on post-mortem analysis has revealed that 90% had signs of Herpes Simplex virus in their brains, leading the scientists to postulate a link between herpes and Alzheimer's.
The sample size is rather small, but the potential relationship, irrespective of causality, is worth follow-up study.
Story at New Scientist
Labels: alzheimers, herpes, newscientist.com, postmortem, simplex1
// posted by neurofuture1:15 PM permanent link
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11.24.2008
Up In Smoke: Cannabis Substance May Relieve Alzheimer's Symptoms
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Deadheads in the Vanguard of Science
A legally obtainable medical formula with marijuana components may actually help Alzheimer's patients retain or enhance their memory, according to researchers at Ohio State University, led by Gary Wenk and Yannick Marchalant.
THC, or tetrahydrocannabinol, is an active ingredient which appears to ease chronic inflammation in the brain associated with the development of memory loss. Presented at the 2008 Society of Neuroscience meeting in Washington, D.C., the researchers noted that once memory impairment is evident, the treatment would not be effective.
It is still true that excessive use of marijuana can cause short-term memory loss and have other side effects. The scientists advocate the development of neural pathway agonists that mimic the effect of THC through a legal, synthetic formulation.
Labels: alzheimers, cannabis, marchalant, marijuana, neuroscience, THC, wenk
// posted by neurofuture5:14 PM permanent link
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11.06.2008
APOE positive individuals at more Cognitive risk from stress
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A new study at UCSD has found that APOE positive individuals perform poorly on cognitive tests in the presence of the stress hormone cortisol in their saliva.
The researchers analyzed a large population of 962 individuals. Research concerning the mechanisms by which chronic stress influences pathological aging and cognitive decline is important for determining interventions, either pharmacological or behavioral.
The growing evidence of significant relationships between chronic stress and cognitive changes may be particularly important in the study of Alzheimer’s disease. Recent animal studies have shown associations between chronic stress and neuropathological changes associated with Alzheimer’s disease, including synapse loss, increases in amyloid-β peptide, and tau accumulation and phosphorylation. Clearly, there are many factors that lead to the pathology and symptoms of Alzheimer’s disease, including environmental and genetic factors.
full paper
Labels: alzheimers, apoe, cognitive, cortisol, Peavy, UCSD
// posted by neurofuture9:33 AM permanent link
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10.15.2008
Cyanobacteria and Diseases of the CNS: Revisited
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You might recall this story about the possible link between Alzheimer's Disease, ALS (or Lou Gehrig's Disease), Parkinson's Disease and 2.8 billion year old cyanobacteria or blue-green algae.
The connection seems to pivot around BMAA, a powerful neurotoxin that can impact the central nervous system (CNS) and contribute to the onset of these diseases.
A related group of researchers is coming to the perspective that a protein reservoir exists within your body, first absorbing BMAA and then slowly releasing it over years and even decades, causing chronic damage to the motor neuron system.
Scientists suggest that exposure to low levels of BMAA may be mediated by most people through metabolism or excretion. However, research also suggests that a few individuals accumulate, rather than excrete BMAA, and these individuals may be at great risk for developing ALS.
The best epidemiological data indicate that a gene/environment interaction probably lies at the roots of ALS/PDC in Guam and possibly sporadic ALS elsewhere. Some experts suspect that BMAA combined with certain metal ions can cause damage to the motor neuron system in vulnerable individuals.
A recent (2008) article profiles the bloom of cyanobacteria in lakes and ponds of upstate NY and Canada, which appears to cause die-offs of fish and fowl. One theory is that run-off of unnatural phosphorous-containing fertilizers is polluting soil, waters, and other aspects of the ecosystem and causing neurological damage. While a very extended hypothesis, the increase in these kinds of diseases since the Industrial Revolution and the rise of the chemical industry (began in Germany in the latter 19th century) suggests a possible link. Alois Alzheimer did not identify the Disease bearing his name until 1907, ALS was identified in 1861 and known as Charcot's Disease in Europe, and Parkinson's in 1817. Parkinson's is sometimes linked with neurotoxins derived from pesticides, again, another product of the chemical industry.
To complicate matters in the cyanobacteria question, other scientists have isolated a compound called nostocarboline by processing cyanobacteria intensively. This substance in early animal trials appears to function as a cholinesterase inhibitor, breaking down accumulation of cholinesterase and helping the build-up of acetylcholine, which is essential for the brain's instant messaging (IM) capability. So, on the one hand, cyanobacteria is toxic to the organism, on the other, its processed byproduct may be beneficial if delivered to a discrete target. In each of these cases, compounds can interact with genes as the frame of the organism, leading either to increased or decreased risk based on observed configuration.
Labels: ALS, alzheimers, CNS, cyanobacteria, parkinsons
// posted by neurofuture12:56 AM permanent link
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9.19.2008
APOEe4 May Be Associated with Unsuccessful Aging
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A study of APOE3 and 4 gene carriers compared with APOE2 and 3 found a greater incidence of mortality in the former amongst a population in Sicily.
The researchers suggest that APOEe4 therefore, can be linked with "early, unsuccessful aging" and present Down Syndrome as a model for this declination of longevity. By studying Down Syndrome carefully, more insight can be gathered into how APOEe4 cuts short longevity. It's suggested that vascular problems play a role along with higher incidence of Alzheimer's Disease.
The researchers suggest that APOEe4 therefore, can be linked with "early, unsuccessful aging" and present Down Syndrome as a model for this declination of longevity. By studying Down Syndrome carefully, more insight can be gathered into how APOEe4 cuts short longevity. It's suggested that vascular problems play a role along with higher incidence of Alzheimer's Disease.
Labels: alzheimers, apoee4, down, DS, infraction, mycardial
// posted by neurofuture5:05 PM permanent link
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8.04.2008
Red Alert 4 Alzheimer's-Victim James Doohan's Astral Funeral
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James Doohan, "Scotty" of Star Trek fame was well-known as a character actor and also as a victim of Alzheimer's Disease.
Lesser known was his heroics on D-Day in 1944, when he landed on Juno Beach, as a member of the Royal Canadian Artillery. Crossing a mine field, he and his unit were targeted by German MG-42 machine guns. He was hit six or seven times - four bullets to the leg, the middle finger of his right hand was shot off, and a bullet struck his chest. His life was saved when it hit a silver cigarette case which had been given to him by his brother.
Both Doohan and former astronaut Gordon Cooper's ashes were destined for earth orbit aboard the aborted Space-X launch that ran into a technical glitch on Saturday, according to Boing Boing.
Labels: alzheimers, artillery, canadian, cooper, doohan, mg42, space-x
// posted by neurofuture3:11 PM permanent link
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7.28.2008
U.S. in Crisis: Do a Million Men March towards Cognitive Impairment each Year?
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Mayo Clinic Scientist Dr. Ron Peterson presented data at the International Alzheimer's Conference in Chicago that shows an astounding increase, particularly in men, in what was presented to the world media as Pre-Dementia.
Pre-Dementia, one form of which is sometimes called MCI, or Mild Cognitive Impairment, refers to decline in cognitive ability amongst younger adults that may become Alzheimer's.
Breathtakingly, up to 1 million people every year in the U.S. are new sufferers of pre-Dementia, not including the 500,000 people per annum who are diagnosed with Alzheimer's by a physician.
"We're seeing that in fact there's a much larger burgeoning problem out there" of people at risk of developing dementia, said Dr. Ronald Petersen, the Mayo scientist who led the study.
Dr. Ralph Nixon, a New York University psychiatrist and scientific adviser to the Alzheimer's Association, was blunt.
"We're facing a crisis," he said.
There are no treatments now to prevent this mental slide or reverse it once it starts.
But that may be changing. Researchers on Monday reported early, somewhat encouraging results from an experimental nose spray that seemed to improve certain memory measures in a study of mildly impaired people.
The drug, for now just called AL-108, needs testing in a longer, larger study. It is being developed by Allon Therapeutics Inc., based in Vancouver, B.C.
Doctors said it shows the potential for new types of medicines that target the protein tangles that kill nerve cells, instead of targeting the sticky brain deposits that have gotten most of the attention up to now.
The studies were reported at the International Conference on Alzheimer's Disease in Chicago.
Petersen is the scientist who defined mild cognitive impairment, or MCI, as a transition phase between healthy aging and dementia. It is more than "senior moments" like forgetting where you parked the car, but not as severe as having dementia, where you forget what a car is for.
People with it have impaired memory but not other problems like confusion, inattention or trouble putting thoughts into words.
The Alzheimer's Association says more than 5 million Americans have Alzheimer's, but no estimate for this "pre-dementia" has been available until now.
Petersen's federally funded study involved roughly 1,600 people, ages 70 through 89, living in Olmstead County, which surrounds the Mayo Clinic in Rochester, Minn. All tested normal when they were enrolled in the study, but more than 5 percent had developed mild impairment when evaluated a year later.
Men were nearly twice as likely as women to develop it. That's a surprise, because some studies have found more women with Alzheimer's than men. But there may be a simple explanation:
Even though more men may be impaired, women outlive them and therefore have more time to develop full-blown dementia.
"This is a very large and important issue for our country and for the world," said Duke University psychologist Brenda Plassman. A smaller study she published earlier this year backs up the Mayo study's findings.
The mild impairment rate is two to three times larger than many researchers had expected, Petersen said.
"It's the iceberg under the tip," agreed Dr. R. Scott Turner, incoming director of the memory disorders program at Georgetown University Medical Center. A prime goal is finding drugs to treat the mild impairment before Alzheimer's develops.
Labels: alzheimers, association, MCI, peterson, preDementia
// posted by neurofuture10:34 PM permanent link
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MRI Study Shows How Exercise Protects Brain Health
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One of the studies presented at the 2008 International Conference on Alzheimer's Disease in Chicago shows that subjects with early Alzheimer's disease who exercised frequently saw less deterioration in the areas of the brain that control memory.
MRI scans show that exercise positively affected the hippocampus region of patients' brains, an area that is important for both memory and balance. In Alzheimer's, the hippocampus is one of the first parts of the brain to suffer damage. Exercise and physical fitness have been shown to slow age-related brain cell death in healthy older adults, and earlier this month a preliminary study was published showing that exercise may help slow brain shrinkage in people with early Alzheimer's disease.
Now, researchers at the University of Kansas Medical Center in Kansas City, Kan., have used MRI and other imaging tools to analyze how exercise affects the brains of those with early Alzheimer's.
The research found that patients with early Alzheimer's had a "significant relationship" between the size of key brain areas associated with memory and fitness, unlike healthy older adults. Those patients with better fitness ratings had less brain tissue atrophy and those with worse fitness had more brain damage.
"This is the first study to get an inside look into specifically where these changes occur in the brain. We're able to locate the changes associated with fitness to the actual memory region, the hippocampus, which is a key area for Alzheimer's-related atrophy," said Robyn A. Honea, Ph.D., a lead investigator on the study. "This suggests that maintaining cardiorespiratory fitness may positively modify Alzheimer's-related brain atrophy."
Labels: 2008, alzheimers, conference, hippocampus, honea, kansas, mri
// posted by neurofuture10:34 AM permanent link
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7.18.2008
Infrared Helmet May Hold Promise for Alzheimer's and other Dementias
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A physician in the U.K. has pioneered an infrared treatment for dementia, exposing subjects to two doses of beams per day, delivered from a specially engineered helmet.
Created with with Sunderland University, 700 infrared light emitting diodes (LEDs) are used to penetrate the skull. Theorists believe that the infrared wavelengths, longer than waves in the visible spectrum, may stimulate the growth of brain cells, slowing down the decline in memory and brain function and reversing symptoms of dementia.
Clem Fennell - the head of a family engineering firm in Cincinnati, Ohio - traveled to the UK after neurologists told him nothing could stop the decline of his dementia. The family's friends had seen a report about the helmet on CBS.
"Honestly I can tell you that within ten days, the deterioration was stopped, then we started to see improvements," said Mrs. Fennell, from North Kentucky. "He started to respond to people more quickly when they talked to him."
Three weeks later, the father of two is still making gradual improvements.
His daughter, 22-year-old Maggie said: "When we go to the restaurant we usually have to order his meals for him, now he can order for himself."
"Now we are okay about letting him go to the bank or the post office but he would not have been able to do that three weeks ago.
The Alzheimer's Society of the UK had this to say:
"A treatment that reverses the effects of dementia rather than just temporarily halting its symptoms could change the lives of the hundreds of thousands of people who live with this devastating condition.
"Non-thermal near infra-red treatment for people with dementia is a potentially interesting technique. We look forward to further research to determine whether it could help improve cognition in humans. Only then can we begin to investigate whether near infra-red could benefit people with dementia."
While completely experimental, the helmet will be sold in the U.K. for the equivalent of about $20,000. More research needs to be conducted to assess the impact of the potential treatment. Referring story
Created with with Sunderland University, 700 infrared light emitting diodes (LEDs) are used to penetrate the skull. Theorists believe that the infrared wavelengths, longer than waves in the visible spectrum, may stimulate the growth of brain cells, slowing down the decline in memory and brain function and reversing symptoms of dementia.
Clem Fennell - the head of a family engineering firm in Cincinnati, Ohio - traveled to the UK after neurologists told him nothing could stop the decline of his dementia. The family's friends had seen a report about the helmet on CBS.
"Honestly I can tell you that within ten days, the deterioration was stopped, then we started to see improvements," said Mrs. Fennell, from North Kentucky. "He started to respond to people more quickly when they talked to him."
Three weeks later, the father of two is still making gradual improvements.
His daughter, 22-year-old Maggie said: "When we go to the restaurant we usually have to order his meals for him, now he can order for himself."
"Now we are okay about letting him go to the bank or the post office but he would not have been able to do that three weeks ago.
The Alzheimer's Society of the UK had this to say:
"A treatment that reverses the effects of dementia rather than just temporarily halting its symptoms could change the lives of the hundreds of thousands of people who live with this devastating condition.
"Non-thermal near infra-red treatment for people with dementia is a potentially interesting technique. We look forward to further research to determine whether it could help improve cognition in humans. Only then can we begin to investigate whether near infra-red could benefit people with dementia."
While completely experimental, the helmet will be sold in the U.K. for the equivalent of about $20,000. More research needs to be conducted to assess the impact of the potential treatment. Referring story
Labels: alzheimers, helmet, infrared, led, sunderland
// posted by neurofuture12:00 AM permanent link
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6.30.2008
How Exercise Improves Your Brain
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Scientists know that exercise is healthy for our hearts and lungs: what about our brains? If exercise improves brain function, then it also is likely beneficial for mood, cognition, and overall mental performance. Within the Cognitive Labs universe, look at Dr. Ashford, a leading Alzheimer's researcher - he runs for at least one hour every day and is in top shape.
Research studies have shown that moderately intense physical activity, and especially aerobic exercise like brisk walking and running, can lead to improvements in cognitive functions like attention, reasoning, and decision making. Experiments have compared groups of people who exercised regularly with others who did not. The improvements in brain function were most dramatic in older adults, but all ages appeared to benefit from increased physical exercise.
One recent analysis looked at the combined results of 18 different studies of the possible cognitive effects of fitness training in older adults. Although the results showed gains in all types of cognitive activity among the fitness-training groups, the greatest advances were found in the exercisers' executive functioning, which controls higher-level decision making skills like planning, scheduling, multi-tasking, and dealing with ambiguity.
We need executive functioning to be able to select appropriate social behaviors and inhibit inappropriate actions. Other types of cognitive activity include reaction time, the ability to remember or interpret visual information, and lower-level decision-making.
Surveys also show that people who are physically active throughout their lives are less likely to experience cognitive decline later in life. And those who exercise regularly are less likely to develop Alzheimer's disease.
Some clues may explain how physical activity can help the cognitive functioning of our brains. It has been shown, for example, that fitness training can improve blood flow in the brain and increase the number of capillaries carrying the blood.
Exercise also increases levels of neurochemicals that stimulate the interconnections among neurons. And exercise may increase the size of some areas of the brain or, at least, slow their rate of decrease as we age. Many of these changes are most prominent in the brain's frontal cortex, the area most important for executive functioning.
So remember, even modest increases in physical activity can be beneficial for your brain and for the important things that organ does for you. How much exercise is enough?
That depends on your age and health, but vigorous walking for 20 to 30 minutes a few days a week is a good start.
Labels: alzheimers, brain, exercise, improves, running
// posted by neurofuture11:49 AM permanent link
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6.27.2008
Controlling Enzyme Production in Brain may Slow Brain Aging
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Research in fruit flies has shown that increasing the production of a substance called neprilysin can reduce the formation of plaques and delay neuron death associated with Alzheimer's. However, a side effect is a shorter lifespan.
Scientists believe that the buildup of amyloid protein plaques within the brain is a major signpost of Alzheimer's and contributes to disease progression. In normally functioning brains, enzymes are expected to clear the plaques. However, deficiencies in the level or function of these enzymes may be a principal disease cause.
One such enzyme, called neprilysin (NEP) decreases naturally with age and this might be a cause for age-related memory decline and Alzheimer's. Enhancing NEP production might therefore be a promising therapy, and studies in mice have suggested it has potential.
Following this hypothesis, research groups led by Drs. Iijima and Iijima-Ando in Japan attempted to test it, using transgenic fruit flies expressing human NEP and amlyoid-beta protein. NEP expression successfully did reduce plaque deposits and neuron damage in the flies, but NEP also reduced the activity of important neural proteins known as CREB proteins and shortened the average lifespan of the flies (normal flies live about 60 days) by about 10 days (although NEP-flies did live longer than those only expressing amyloid protein), or about 20%.
This study sheds light on a characteristic of normal brain aging that can be possibly delayed or reversed through enzyme-related therapy,
Source: "Overexpression of Neprilysin Reduces Alzheimer's Amyloid-β 42 (Aβ42)-Induced Neuron Loss and Intraneuronal Aβ42 Deposits, but Causes a Reduction in CREB-Mediated Transcription, Age-Dependent Axon Pathology and Premature Death in DROSOPHILA."
Labels: alzheimers, ando, flies, fruit, nep, neprilysin
// posted by neurofuture11:00 PM permanent link
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6.22.2008
New Clue on Alzheimer's-Related Tau Proteins
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WASHINGTON (AP) — Researchers have uncovered a new clue to the cause of Alzheimer's disease. The brains of people with the memory-robbing form of dementia are cluttered with a plaque made up of beta-amyloid, a sticky protein. But there long has been a question whether this is a cause of the disease or a side effect. Also involved are tangles of a protein called tau; some scientists suspect this is the cause.
Now, researchers have caused Alzheimer's symptoms in rats by injecting them with one particular form of beta-amyloid. Injections with other forms of beta-amyloid did not cause illness, which may explain why some people have beta-amyloid plaque in their brains but do not show disease symptoms.
Full story on Google News
On Nature Medicine
Labels: alzheimers, amyloid, harvard, rats, selkoe, shankar, Tau
// posted by neurofuture10:59 PM permanent link
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Cost of Alzheimer's
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Here's some tips on dealing with the cost of Alzheimer's from the Wall Street Journal Online. In the earliest stages people can manage their own affairs.
However, from medication to changes in lifestyle and services, expenses quickly add up. Creating a budget, assigning individuals to manage expenses, and implementing the plan help to remove the uncertainty.
However, from medication to changes in lifestyle and services, expenses quickly add up. Creating a budget, assigning individuals to manage expenses, and implementing the plan help to remove the uncertainty.
Labels: alzheimers, budget, expenses, stages
// posted by neurofuture10:36 AM permanent link
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6.13.2008
Japanese Government Moves to Enforce Waistline Limit
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Being fat in Japan - defined as a waist size of over 33.5" for men and 35.4" for women will soon subject individuals to censure from the government and participation in an officially mandated re-education program.
The objective is to limit cases of stroke and diabetes as the population ages.
In contrast, the average male waist-size in the U.S. is a corpulent 39".
One solution is to lay off the cheese fries. However, a benefit of fuel price increases could be forcing people to get more exercise in the form of walking. However, U.S. cities and suburbs aren't designed with walking in mind, just the comfort and centrality of the freeway clover.
Being overweight is a noticeable risk factor for Alzheimer's, so it is worthwhile to keep the suggestions of the Japanese in mind. NY Times article
Labels: 33.5, alzheimers, fat, japan, metabo
// posted by neurofuture10:32 AM permanent link
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6.09.2008
115 Year Old Mind
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An autopsy was recently performed on a deceased 115 year old woman who left her body to science at age 82.
Her brain showed almost no evidence of Alzheimer's disease. The finding suggests Alzheimer's disease and other forms of dementia are not inevitable, as had been suspected.
"Our observations suggest that, in contrast to general belief, the limits of human cognitive function may extend far beyond the range that is currently enjoyed by most individuals," said lead researcher Gert Holstege, a neuroscientist at the University Medical Center Groningen, in The Netherlands.
The results are detailed in the August issue of the journal Neurobiology of Aging.
This finding underscores the need for individuals to take proactive action to manage their cognitive fitness.
Holstege is a leader in imaging and analyzing the orgasmic brain of both men and women.
Labels: alzheimers, brain, holstege, proactive
// posted by neurofuture6:35 PM permanent link
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5.06.2008
Why Ibuprofen May Help Cognitive Function
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Cognitive function may be improved, or decline averted, in early stages of Alzheimer's disease, new research suggests. Speculation is this is due to the anti-coagulant properties of the drug.
Labels: alzheimers, ibuprofen
// posted by neurofuture10:39 AM permanent link
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4.07.2008
Painting a better picture for Alzheimer's
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Art can be an effective therapy for the brain and even provide a useful outlet for people who have the disease, according to thie story.
Labels: alzheimers, paint, therapy
// posted by neurofuture1:15 PM permanent link
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4.05.2008
Zen and the Art of...
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According to Denise Grady at the NY Times, sometimes it's best to go with the flow, in terms of dealing with symptoms of the disease.
Of course, you can keep working the brain to build reserve.
In a slide show (starting with the above image) William Utermohlen’s self-portraits reveal his descent into dementia over the span of nearly four decades. A self-portrait from 1967. Click-through to see it...
Labels: alzheimers, grady, nytimes
// posted by neurofuture10:29 PM permanent link
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3.31.2008
Fat in your 40's could equal Alzheimer's
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For anybody 40 and over, take heed. (good advice for anyone over 35, too)
Belly fat is linked with increased risk of onset of Alzheimer's. Scientists led by Dr. C.W. Randolph have published in the journal Neurology, finding that beginning in the decade of the 40's, the risk escalates as hormonal changes result in imbalances in the hormonal tripod of estrogen, progesterone, and testosterone.
Dr. Randolph says estrogen dominance is the new E.D. that everyone should know about.
"Estrogen dominance is a condition that results from the shift in hormone production that occurs naturally with age." says Randolph. "This shift begins with women in their 30's and with men in their 40's. Our ovaries and testes produce three sex hormones which are estrogen, progesterone and testosterone. In a healthy person's 20s, the levels of these hormones are in optimal ratio, or equilibrium. With age, production of these hormones starts to decline. The first hormone to drop off in production is progesterone. In fact, in women, progesterone production declines 120 times more rapidly than estrogen production. The result is a hormonal imbalance within the body. The medical term for this condition is 'estrogen dominance.'"
"The bad news is that estrogen dominance predisposes the body to pack on pounds around the middle," says Genie James, M.M.Sc, co-author of From Belly Fat to Belly Flat. "Even worse, body fat produces more estrogen so an overweight person is often caught in a viscous cycle where that tire around the middle is impossible to lose. Even worse, estrogen dominant love handles predispose the body to many health risks. Unbalanced estrogen, or estrogen dominance, in the body causes cerebral edema (retention of water). The first symptom of this is foggy thinking. In addition to impaired cognitive function and Alzheimer's disease, medical studies have linked estrogen dominance and belly fat to an increased risk of breast cancer, uterine cancer, prostate cancer, heart attack and stroke."
Labels: 40s, alzheimers, fat, jacksonville
// posted by neurofuture2:51 PM permanent link
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3.16.2008
Alzheimer's or Cancer: Which Disease Would you Rather Die From?
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Excerpt From the Times Online:
What kind of person envies someone who is dying from cancer? The bestselling author Terry Pratchett, that's who. Last week, he spoke movingly about living with early-onset Alzheimer's disease, which 'strips away your living self a bit at a time.' The disease, he said, had left him with 'a sense of loss and abandonment.'
The 59-year-old fantasy author appeared at a conference for the Alzheimer's Research Trust, to which he pledged a million dollars (around £500,000). He received his diagnosis in December but revealed that he had been suffering for at least two years. He has lost the ability to touch-type, although he has not yet stopped writing.
He told the conference: "I'd like a chance to die like my father did - of cancer, at 86. Before he went to spend his last two weeks in a hospice, he was bustling around the house. He talked to us right up to the last few days, knowing who we were and who he was. Right now, I envy him."
When Pratchett appeared on the Today programme last week, he acknowledged that dementia does not have the "heroic glamour" of cancer - and that to say so would not make him popular. As he told the ART conference: "It's a shock and a shame to find out that money for [Alzheimer's] research is 3 per cent of that which goes to find cancer cures. Perhaps that is why I know three people who have survived brain tumours but no one who has beaten Alzheimer's."
It might be a controversial point of view but Pratchett is not alone in holding it. Dr. Guy Brown, a biochemist at Cambridge University, also proclaims that too much money is devoted to research into cancer and heart disease, to the detriment of studies into dementia. Brown thinks that lavishing fortunes on these conditions - that extend life span but drag out the years in which people suffer - verges on the immoral.
This is what Brown has to say about the country's 10,000 centenarians, a figure expected to rise to 250,000 by the middle of this century: "Some are in a very bad state cognitively and physically. Why are we creating these people? We are increasing life expectancy beyond what is beneficial."
It is not that being old is inherently wrong; but that the increase in longevity has not been accompanied by an increase in quality of life. There is a gap opening up between life expectancy and healthy life expectancy, and increasing numbers of us can expect to fall into the dementia-filled abyss. It is a long, painful descent that takes a decade to reach the bottom, but the relentless medical focus on postponing death means that the bottom is getting ever farther away. For example, the last decade brought a two-year increase in life span, but we can expect to spend only a quarter of it in good health. In effect, it means that modern medicine has gifted us an extra year and a half of ill-health. As Brown argues in his book, The Living End, we are not facing the consequences. "We are driving up longevity and creating more and more people with a very low quality of life," Brown points out, when we meet in his cosy office at Cambridge University. "A disproportionate amount of funding goes to cancer and heart disease, whereas stroke and dementia get much less. These are skewed priorities. We need to switch dramatically but that would mean stopping government funding for cancer and cardiovascular disease, and that would cause screams in the medical research establishment."
This realisation prompted Brown, 48, to rethink his research; he studies cell death, and shifted his focus from cardiovascular disease to dementia because he believed it would make a more positive contribution to society. To some extent, statistics are on his side. The World Health Organisation calculates that, when it comes to disability in the over-60s, dementia is responsible for about 11 per cent, cardiovascular disease for about 5 per cent, and cancer for 2.4 per cent.
Read the rest of the story
Labels: alzheimers, early_onset_alzheimers, pratchett
// posted by neurofuture5:20 PM permanent link
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2.04.2008
Alzheimer's Story Brings Writer a New Bond
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It is not as if our jobs are anonymous. Our names, after all, are conspicuously slapped above our work. We identify ourselves before we interview people, before we ask for the facts or urge others to bare their souls.
So why has my equilibrium as a reporter, a sportswriter of 25 years, been so thrown out of whack these past three weeks?
It is not the reason that seems most obvious: simply because I turned the proverbial tape recorder on myself.
Related links
*
Alzheimer's hits family hard: 'Something's not right with Mom . . . and now, Dad.'
*
Alzheimer's: Intimacy found after all is lost
*
Scientists can't get their minds around Alzheimer's
Yes, writing about my parents' decline from Alzheimer's disease, in a piece that ran Jan. 13 in the Chicago Tribune Magazine, was an emotional undertaking. But there remained a comfort level there, a familiarity with an audience I had imagined had read my coverage of the Bulls championship runs and the Bears mediocrity, who came with me to Wimbledon and the Olympics. They did not always like what I wrote, and sometimes told me so with brutal candor. But that is where it stopped.
Readers wrote. I wrote back. And we both walked away.
But baring my own soul on a topic that profoundly affects so many people involves a lot more than one story on one day, I have learned.
The sheer volume of mail was enough to set the Alzheimer's story apart from any I had ever written. But it was what people wrote that has perhaps forever changed my relationship with readers.
"The dog got a very long walk this morning," wrote Joan, who told me her mother resides in an Ohio Alzheimer's residence. "I cried ... and that was a good thing. I don't allow myself to cry enough. Your story helped me to know that it will be painful and difficult, but we will all get through the journey. Even though I cried today, I am not feeling so alone."
No longer could we walk away from each other. No longer could I hit delete and move on. How could I not get emotionally involved when a man asks me, as one did, how to tell his father that it is OK to die?
Or when another reader asked if I could persuade her siblings to forgo a feeding tube for their dying mother?
I was left with a headache and a stomachache each night as I read heartbreaking stories; brought to tears by those who told me they were brought to tears; and inspired to do more by those giving so much of themselves.
Younger people wrote of their lingering fear for the future, of dealing with their own aging parents or of perhaps developing the disease themselves. Others, in their 60s and 70s, described a dread that all but leaked through the computer and onto my lap.
There were amazing tales of love, painful honesty and aching guilt.
There was Pat, who described her father, Jim, writing love letters to her mother for the last several years of his life, something she would not discover until her mother shared them with her the night of his death.
In the letters, the family could trace the disease's progression, the early letters "beautiful and sentimental," the later ones apologetic for "all of his forgetfulness and mistakes." He asked for his wife's forgiveness and thanked her for still loving him.
"As the years passed, the letters made less sense," Pat wrote. "By the end, you could not even read them."
I thought of my own mother's letters to me during my first two years of college, a stash I found when we were cleaning out the house. They were so smart and funny and revealing, her voice all but jumping off the page. I thank God I hung on tight to them, like the handful of recipes also written in my mother's own hand -- hilariously imprecise measurements scribbled on paper by a wondrously imprecise cook -- but her voice once again back in my head.
I read the words of Alissa, who was just 23 when her mother developed Alzheimer's at 53.
"[She was] also the sweet, adorable, needlepointing, mah-jongg-playing, newspaper-reading, matzo ball-making, selfless 4-foot-11 Jewish mom who always thought for others, and never herself," the daughter wrote.
"When my mom lost all of her friends to the disease (it was too 'hard' for them to hang out with her ... and 'embarrassing' when she made mistakes)," the daughter wrote, "we joked (because that's how my family also deals with stress), that if she had breast cancer, they would all band together, wear matching T-shirts and walk for three days in her honor.
"But with Alzheimer's, people seem to run away as far as possible."
Finally, there was the man named Robert, who said he stopped reading my story after the third page, calling it "ludicrous and boring."
"My wife has the disease, and it is not the hilarious picnic that Melissa describes," he wrote.
In the past this would have annoyed me, probably angered me. I would have been tempted to whip off a sharp reply. But this time, all I could see was a man's pain. And all I could feel was sadness.
Am I left with closure, to use a word I can't stand? I don't think so. I really don't. What I am left with is a strong sense that even in a cyberspace world of infinite space and time where the story of my parents reached well beyond the audience I had imagined, there is still community. There is compassion. And there is great comfort in that.
So why has my equilibrium as a reporter, a sportswriter of 25 years, been so thrown out of whack these past three weeks?
It is not the reason that seems most obvious: simply because I turned the proverbial tape recorder on myself.
Related links
*
Alzheimer's hits family hard: 'Something's not right with Mom . . . and now, Dad.'
*
Alzheimer's: Intimacy found after all is lost
*
Scientists can't get their minds around Alzheimer's
Yes, writing about my parents' decline from Alzheimer's disease, in a piece that ran Jan. 13 in the Chicago Tribune Magazine, was an emotional undertaking. But there remained a comfort level there, a familiarity with an audience I had imagined had read my coverage of the Bulls championship runs and the Bears mediocrity, who came with me to Wimbledon and the Olympics. They did not always like what I wrote, and sometimes told me so with brutal candor. But that is where it stopped.
Readers wrote. I wrote back. And we both walked away.
But baring my own soul on a topic that profoundly affects so many people involves a lot more than one story on one day, I have learned.
The sheer volume of mail was enough to set the Alzheimer's story apart from any I had ever written. But it was what people wrote that has perhaps forever changed my relationship with readers.
"The dog got a very long walk this morning," wrote Joan, who told me her mother resides in an Ohio Alzheimer's residence. "I cried ... and that was a good thing. I don't allow myself to cry enough. Your story helped me to know that it will be painful and difficult, but we will all get through the journey. Even though I cried today, I am not feeling so alone."
No longer could we walk away from each other. No longer could I hit delete and move on. How could I not get emotionally involved when a man asks me, as one did, how to tell his father that it is OK to die?
Or when another reader asked if I could persuade her siblings to forgo a feeding tube for their dying mother?
I was left with a headache and a stomachache each night as I read heartbreaking stories; brought to tears by those who told me they were brought to tears; and inspired to do more by those giving so much of themselves.
Younger people wrote of their lingering fear for the future, of dealing with their own aging parents or of perhaps developing the disease themselves. Others, in their 60s and 70s, described a dread that all but leaked through the computer and onto my lap.
There were amazing tales of love, painful honesty and aching guilt.
There was Pat, who described her father, Jim, writing love letters to her mother for the last several years of his life, something she would not discover until her mother shared them with her the night of his death.
In the letters, the family could trace the disease's progression, the early letters "beautiful and sentimental," the later ones apologetic for "all of his forgetfulness and mistakes." He asked for his wife's forgiveness and thanked her for still loving him.
"As the years passed, the letters made less sense," Pat wrote. "By the end, you could not even read them."
I thought of my own mother's letters to me during my first two years of college, a stash I found when we were cleaning out the house. They were so smart and funny and revealing, her voice all but jumping off the page. I thank God I hung on tight to them, like the handful of recipes also written in my mother's own hand -- hilariously imprecise measurements scribbled on paper by a wondrously imprecise cook -- but her voice once again back in my head.
I read the words of Alissa, who was just 23 when her mother developed Alzheimer's at 53.
"[She was] also the sweet, adorable, needlepointing, mah-jongg-playing, newspaper-reading, matzo ball-making, selfless 4-foot-11 Jewish mom who always thought for others, and never herself," the daughter wrote.
"When my mom lost all of her friends to the disease (it was too 'hard' for them to hang out with her ... and 'embarrassing' when she made mistakes)," the daughter wrote, "we joked (because that's how my family also deals with stress), that if she had breast cancer, they would all band together, wear matching T-shirts and walk for three days in her honor.
"But with Alzheimer's, people seem to run away as far as possible."
Finally, there was the man named Robert, who said he stopped reading my story after the third page, calling it "ludicrous and boring."
"My wife has the disease, and it is not the hilarious picnic that Melissa describes," he wrote.
In the past this would have annoyed me, probably angered me. I would have been tempted to whip off a sharp reply. But this time, all I could see was a man's pain. And all I could feel was sadness.
Am I left with closure, to use a word I can't stand? I don't think so. I really don't. What I am left with is a strong sense that even in a cyberspace world of infinite space and time where the story of my parents reached well beyond the audience I had imagined, there is still community. There is compassion. And there is great comfort in that.
Labels: alzheimers, chicago, tribune
// posted by neurofuture8:13 AM permanent link
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1.03.2008
Finding Alzheimer's Early in 2008
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Scientists are beginning to realize that finding Alzheimer's earlier is the key to developing a preventative strategy.
It's possible that the destructive seeds of the disease are germinated decades before recognized onset. By then, it's almost too little, too late.
For that reason, developing a proactive approach earlier may yield dividends.
If your brain's processing speed begins to slow and the pace accelerates, that could be cause for concern.
For this self-monitoring is key. Some decline is normal with aging. Rapid decline is not. You would not want to carry 100 pounds of excess weight for 30 years and then find that your life expectancy is compromised. Well, it's the same for the brain
It's possible that the destructive seeds of the disease are germinated decades before recognized onset. By then, it's almost too little, too late.
For that reason, developing a proactive approach earlier may yield dividends.
If your brain's processing speed begins to slow and the pace accelerates, that could be cause for concern.
For this self-monitoring is key. Some decline is normal with aging. Rapid decline is not. You would not want to carry 100 pounds of excess weight for 30 years and then find that your life expectancy is compromised. Well, it's the same for the brain
Labels: alzheimers, brain, nytimes, onset
// posted by neurofuture8:56 AM permanent link
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11.28.2007
Protein Manipulation May be Key to Alzheimer's
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Bolstering disintegrating neural connections may help boost brainpower in Alzheimer's disease patients, MIT researchers and colleagues reported in the Nov. 8 issue of Neuron.
The researchers zeroed in on the enzymes that manipulate a key scaffolding protein for synapses, the connections through which brain cells communicate. Synapses are weakened and lost in neurodegenerative diseases such as Alzheimer's and Parkinson's disease.
"We identified a major underlying mechanism through which synapses are strengthened and maintained," said Morgan H. Sheng, Menicon Professor of Neuroscience at MIT's Picower Institute for Learning and Memory. "The enzymes involved could be good targets for potential drug treatments."
A protein called postsynaptic density-95 (PSD-95) is a key building block of synapses. Like the steel girders in a building, it acts as a scaffold around which other components are assembled. "The more PSD-95 molecules, the bigger and stronger the synapse," said co-author Myung Jong Kim, a Picower research scientist.
Previous research had shown that mice genetically altered to have less PSD-95 experienced learning and memory problems.
In the current study, the researchers identified for the first time the enzymes that work behind the scenes on PSD-95, adding a phosphate group to a specific amino acid in the PSD-95 protein. This process--called phosphorylation--is critical for PSD-95 to do its job in supporting synapses.
"Adding a phosphate group to a single amino acid allows PSD-95 to promote synapse size and strength," said Sheng, who also holds an appointment in MIT's Department of Brain and Cognitive Sciences and is a Howard Hughes Medical Institute investigator. "Therefore, promoting this process could help improve cognitive function."
Sheng believes manipulating PSD-95 through phosphorylation could lead to bigger and more robust synapses, which would boost brainpower in both normal and diseased brains. "It's possible that promoting PSD-95 phosphorylation could also help neuropsychiatric illnesses in which synapse function goes awry, such as schizophrenia, depression and autism," Sheng said.
reference: science daily
Labels: alzheimers, MIT, protein, sciencedaily, sheng
// posted by neurofuture8:40 PM permanent link
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11.21.2007
What is the State of the Art in Memory Monitoring?
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Cognitive Labs connected with colleagues and also met some new experts at the 60th annual meeting of the Gerontological Society of America (in S.F.), which is focused on all parts of healthy aging. Dr. Ashford presented a paper, and I was fortunate to attend a breakfast meeting on screening (or monitoring of) cognitive impairment held by Eric Hall, CEO of the Alzheimer's Foundation of America.
Among the proactively-minded, essentially, there are two schools of thought:
(a) People around age 65 should be checked for potential memory loss and
(b) People starting around age 30 should concern themselves with proactive monitoring
As you might guess, these two positions, while different are not in opposition. Scientists increasingly recognize that a number of causal factors are involved in cognitive decline and they tend to begin early - an analogy is the contributory vectors for heart disease. As you monitor your heart rate, so you should monitor your brain.
Building up cognitive reserve is the name of the game, so that as you age-slight changes in capability are counterbalanced by reinforcing cognitive reserve built up over a lifetime of education and training. Some new research involving pilots conducted by Dr. Taylor at Stanford in a forthcoming publication suggests that cognitive reserve can overcome some serious inherited challenges-such as having 2 copies of the APOEe4 gene, which is associated with increased propensity for Alzheimer's. In the genes vs. environmental stimuli debate, stimulus can overcome heritability.
Case in point, look at the website 23andme, which tells the story of a champion long-jumper who succeeded despite having genes diametrically opposed to that normally associated with star athletes, who may have 1 but more usually 2 functioning copies of the ACTN3 gene.
All agreed that there is a vast opportunity to pursue research based on access to large populations, something the Internet is extraordinarily good at, in order to begin to track, monitor, and enhance cognitive ability as a prong in the overall effort to live longer healthier lives. To that end, we look forward to working with a global collection of scientists and colleagues who can help us assess the data to find the meaningful patterns, which in turn can hone our efforts. The methodology may be cross-disciplinary - Dr. Shankle is working with a NASA planetary scientist in evaluating his information, and the irony is that the swarm of data points may hold some behavioral similarity to other patterns seen in nature, such as trace feedback from an interplanetary probe, ant colonies, or flight of geese, it was recognized during the breakfast. What algorithms are optimal for analysis? What is the best presentation? Our role is basically a technologist who is tasked to tie together these disparate links and advance the state of knowledge.
Labels: alzheimers, ashford, geron.org, nasa, shankle
// posted by neurofuture12:37 PM permanent link
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11.13.2007
Carotene may Cut Risk for Alzheimer's
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Men who take long-term supplements of beta-carotene -- an antioxidant found in carrots and other vegetables -- may enjoy less cognitive decline, according to a US study published Monday.
The study led by Francine Grodstein, of Brigham and Women's Hospital and Harvard Medical School, could have implications for the prevention of Alzheimer's and other debilitating mental conditions.
Beta-carotene, which gives carrots their orange color, is broken down by the liver to become a form of vitamin A and is also helpful against damage caused by free radicals. Other sources include spinach, sweet potatoes and coriander.
Labels: alzheimers, beta-carotene, men
// posted by neurofuture11:08 AM permanent link
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9.19.2007
Alzheimer's Diagnosis Stuck in 1984
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1984 was an amazing year. First, it was the year in which George Orwell's dystopia was set, dominated by "newspeak" a language that reduced the ability of the average citizen to question authority with aphorisms such as 'plusgood' and 'doubleplusgood' as discourse was reduced to totalitarian simplicity.
Secondly, there was a revolt against 1984 with the release of the MacIntosh, and the celebrated destruction of IBM's new newspeak, personified by its boring corporate PC clones and rows of droning, grey-suited organization men, by the hammer throwing jogger. Researchers in the British medical journal Lancet are calling for a similar revolt in the treatment of Alzheimer's Disease. It's time to change the way doctors diagnose Alzheimer's disease, says an international panel of experts.
Despite more than two decades of scientific advances in understanding Alzheimer's disease, doctors are still stuck in 1984. That's when a U.S. National Institutes of Health working group came up with the clinical criteria for a formal diagnosis of Alzheimer's disease.
It's time for radical change, argue Bruno Dubois, MD, of Salpêtrière Hospital, Paris, and 18 other leading Alzheimer's experts.
The old criteria "have now fallen behind the unprecedented growth of scientific knowledge," Dubois and colleagues write in the August issue of The Lancet Neurology.
That's true, says Norman Foster, MD, director of the Center for Alzheimer's Care, Imaging, and Research at the University of Utah, Salt Lake City. Foster's editorial accompanies the paper by Dubois and colleagues.
"We now are seeing the potential to disrupt the basic development of Alzheimer's disease with medications," Foster said. "So we want early diagnosis and early intervention. The current criteria get in the way of this."
High-Tech Alzheimer's Diagnosis
People are said to have probable Alzheimer's disease if they have two clinical signs: a memory disorder and impairment of at least one other mental function. For an Alzheimer's diagnosis, both these problems must interfere with social function or the activities of daily living.
That was a big breakthrough 25 years ago. Since then, doctors have learned that several other conditions cause the same impairments. Yet with an emphasis on earlier treatment, there's pressure on doctors to diagnose Alzheimer's disease as early as possible.
"We are caught between a rock and a hard place as clinicians," Foster says. "We cannot distinguish accurately when mild cognitive impairment represents Alzheimer's disease, when it represents some other significant illness, or when it is just a passing problem."
Dubois and colleagues propose using a new formula. To get an Alzheimer's diagnosis, a person would first have to suffer memory loss that gets worse over a six-month period. That person would also have to have at least one physical "biomarker" of Alzheimer's disease:
* An MRI scan showing shrinking of a particular part of the brain
* Abnormal proteins -- beta-amyloid or tau tangles -- in the cerebrospinal fluid
* A PET scan showing patterns of brain activity linked to Alzheimer's disease
* A genetic mutation linked to Alzheimer's disease
These are expensive, high-tech tests. All have yet to be "validated" -- that is, proven to detect Alzheimer's disease within specified limits.
Foster says the most promising of these high-tech Alzheimer's tests is already in use: genetic testing for an Alzheimer's gene. However, only a small percentage of Alzheimer's patients carry the genetic mutations known to cause Alzheimer's disease.
The next most promising of these tests, Foster says, is a PET scan for deposits of amyloid protein in the brain. Today, those deposits very likely mean Alzheimer's if a person already has symptoms. It's still unclear what these deposits mean for people who do not have symptoms.
Finally, Foster says that looking for amyloid or tau proteins in the cerebrospinal fluid holds great promise. But it's not yet clear how often these proteins predict Alzheimer's disease.
Dubois and colleagues call for intensive research aimed at validating the new criteria. Foster strongly agrees.
"Diagnosis is the foundation of effective treatment for Alzheimer's disease," he says. "When physicians and families just accept terms like 'senility' or 'dementia,' they give up the opportunity for more effective, targeted therapy."
Secondly, there was a revolt against 1984 with the release of the MacIntosh, and the celebrated destruction of IBM's new newspeak, personified by its boring corporate PC clones and rows of droning, grey-suited organization men, by the hammer throwing jogger. Researchers in the British medical journal Lancet are calling for a similar revolt in the treatment of Alzheimer's Disease. It's time to change the way doctors diagnose Alzheimer's disease, says an international panel of experts.
Despite more than two decades of scientific advances in understanding Alzheimer's disease, doctors are still stuck in 1984. That's when a U.S. National Institutes of Health working group came up with the clinical criteria for a formal diagnosis of Alzheimer's disease.
It's time for radical change, argue Bruno Dubois, MD, of Salpêtrière Hospital, Paris, and 18 other leading Alzheimer's experts.
The old criteria "have now fallen behind the unprecedented growth of scientific knowledge," Dubois and colleagues write in the August issue of The Lancet Neurology.
That's true, says Norman Foster, MD, director of the Center for Alzheimer's Care, Imaging, and Research at the University of Utah, Salt Lake City. Foster's editorial accompanies the paper by Dubois and colleagues.
"We now are seeing the potential to disrupt the basic development of Alzheimer's disease with medications," Foster said. "So we want early diagnosis and early intervention. The current criteria get in the way of this."
High-Tech Alzheimer's Diagnosis
People are said to have probable Alzheimer's disease if they have two clinical signs: a memory disorder and impairment of at least one other mental function. For an Alzheimer's diagnosis, both these problems must interfere with social function or the activities of daily living.
That was a big breakthrough 25 years ago. Since then, doctors have learned that several other conditions cause the same impairments. Yet with an emphasis on earlier treatment, there's pressure on doctors to diagnose Alzheimer's disease as early as possible.
"We are caught between a rock and a hard place as clinicians," Foster says. "We cannot distinguish accurately when mild cognitive impairment represents Alzheimer's disease, when it represents some other significant illness, or when it is just a passing problem."
Dubois and colleagues propose using a new formula. To get an Alzheimer's diagnosis, a person would first have to suffer memory loss that gets worse over a six-month period. That person would also have to have at least one physical "biomarker" of Alzheimer's disease:
* An MRI scan showing shrinking of a particular part of the brain
* Abnormal proteins -- beta-amyloid or tau tangles -- in the cerebrospinal fluid
* A PET scan showing patterns of brain activity linked to Alzheimer's disease
* A genetic mutation linked to Alzheimer's disease
These are expensive, high-tech tests. All have yet to be "validated" -- that is, proven to detect Alzheimer's disease within specified limits.
Foster says the most promising of these high-tech Alzheimer's tests is already in use: genetic testing for an Alzheimer's gene. However, only a small percentage of Alzheimer's patients carry the genetic mutations known to cause Alzheimer's disease.
The next most promising of these tests, Foster says, is a PET scan for deposits of amyloid protein in the brain. Today, those deposits very likely mean Alzheimer's if a person already has symptoms. It's still unclear what these deposits mean for people who do not have symptoms.
Finally, Foster says that looking for amyloid or tau proteins in the cerebrospinal fluid holds great promise. But it's not yet clear how often these proteins predict Alzheimer's disease.
Dubois and colleagues call for intensive research aimed at validating the new criteria. Foster strongly agrees.
"Diagnosis is the foundation of effective treatment for Alzheimer's disease," he says. "When physicians and families just accept terms like 'senility' or 'dementia,' they give up the opportunity for more effective, targeted therapy."
Labels: 1984, alzheimers, brain
// posted by neurofuture12:53 PM permanent link
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9.12.2007
Life Expectancy in U.S. Accelerates
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The official statistics have been calculated, by the National Center of Health Statistics and the good news is that life expectancy has reached another all time high: 77.9 years for the average person in 2005 the U.S, an incease of .1 year over 2004.
This Gompertz function has been used for the last 180 years or so to plot lifespan and risk (it's also used by insurance carriers and actuaries).
Interestingly, while death rate from stroke and heart disease declined, deaths from cancer increased by just less than 0.8%
There was a significant 5.0% increase in deaths from Alzheimer's Disease year-to-year; however Alzheimer's Disease is sometimes not listed as a cause of mortality in favor of a condition that it promotes such as pneumonia, understating its impact.
The problem with Alzheimer's is that it will eventually become the world's leading cause of mortality, as gains in treating other illnesses continue to advance.
This Gompertz function has been used for the last 180 years or so to plot lifespan and risk (it's also used by insurance carriers and actuaries).
Interestingly, while death rate from stroke and heart disease declined, deaths from cancer increased by just less than 0.8%
There was a significant 5.0% increase in deaths from Alzheimer's Disease year-to-year; however Alzheimer's Disease is sometimes not listed as a cause of mortality in favor of a condition that it promotes such as pneumonia, understating its impact.
The problem with Alzheimer's is that it will eventually become the world's leading cause of mortality, as gains in treating other illnesses continue to advance.
Labels: alzheimers, gompertz, life expectancy
// posted by neurofuture8:17 AM permanent link
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9.06.2007
Sleeping like a Baby may Prevent Alzheimer's
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Melatonin, derived from getting adequate rest - may help delay or prevent Alzheimers according to this study.
Labels: alzheimers, baby, melatonin, sleep, sleep deprivation
// posted by neurofuture11:00 PM permanent link
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8.28.2007
Alzheimers Will Not Slow You Down
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Who says Alzheimer's slows you down? Case in point is Don Hayen, a 73-year old retired physician who blogs and even knows how to install an Internet 'widget' better than people on Facebook.
He was just interviewed by the Chicago Sun Times and is becoming an Internet celebrity of self-actualization.
As he says he was diagnosed with early-stage Alzheimer's, not early onset Alzheimer's, which can affect anyone around 45 or so, sometimes in the 30's.
He was just interviewed by the Chicago Sun Times and is becoming an Internet celebrity of self-actualization.
As he says he was diagnosed with early-stage Alzheimer's, not early onset Alzheimer's, which can affect anyone around 45 or so, sometimes in the 30's.
Labels: alzheimers, suntimes, thetripover
// posted by neurofuture2:28 PM permanent link
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Statins Offer Hope
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Statin drugs, commonly used to lower cholesterol, may offer potential in delaying the onset of Alzheimer's according to a study mentioned here.
Labels: alzheimers, globeandmail, science, statins
// posted by neurofuture11:23 AM permanent link
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8.07.2007
Myriad Genetics- Alzheimer's
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Flourizan, from Myriad Genetics, may offer an opportunity to turn back the tide of Alzheimer's progression.
Labels: alzheimers, myriad genetics
// posted by neurofuture8:42 AM permanent link
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8.04.2007
Flavenoids in Apples May Prevent Alzheimer's
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A new study asserts that an antioxidant in apples may prevent cognitive decline. The substance quercetin contains even more antioxidants than Vitamin C and resides primarily in the skin of fresh apples.
Labels: alzheimers, apples, flavenoids, skin of apples
// posted by neurofuture10:07 PM permanent link
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7.21.2007
Chip Implants for Alzheimer's Patients? It May Happen
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Workers in a few cases have been 'tagged' with implants to follow their movements. The same technology could be used to monitor Alzheimer's patients and perhaps, young children.
A couple of years ago I jokingly told a friend about kidtrack - a sim-card powered GPS service you could get for your mobile phone - this was a product idea, nothing more; today an analagous service offering from one of the major carriers has been rolled out.
Certainly there are ethical and legal issues surrounding such technologies meant to keep us 'safe' but with a perhaps, 1984-style surveillance component.
A couple of years ago I jokingly told a friend about kidtrack - a sim-card powered GPS service you could get for your mobile phone - this was a product idea, nothing more; today an analagous service offering from one of the major carriers has been rolled out.
Certainly there are ethical and legal issues surrounding such technologies meant to keep us 'safe' but with a perhaps, 1984-style surveillance component.
Labels: alzheimers, implants, surveillance
// posted by neurofuture10:02 PM permanent link
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7.17.2007
UCLA researchers Isolate Anti-Alzheimer's Compound in Curry
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Researchers such as Greg Cole (UCLA/VA) previously have studied the antioxidant properties of curry - attributing it to curcumin. But new research reveals the exact compound...
bisdemethoxycurcumin, an ingredient in curcumin that may help the immune system clear the amyloid beta that forms the plaques found in Alzheimer's disease. Curcumin is a natural substance found in tumeric root, frequently used in Indian curries. Using blood samples of Alzheimer's patients, researchers found that bisdemethoxycurcumin boosted immune cells called macrophages to clear amyloid beta.
Labels: alzheimers, bisdemethoxycurcumin, cole, curcumin, curry, ucla
// posted by neurofuture9:12 PM permanent link
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7.09.2007
New Alzheimer's Treatment
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A new treatment for Alzheimer's was approved - Exelon delivered via patch instead of a pill. The rationale is less nausea and more direct access to the bloodstream.
Labels: alzheimers, novartis exelon
// posted by neurofuture8:58 AM permanent link
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6.10.2007
Alzheimer's Cases to Quadruple by the Year 2050
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WASHINGTON - More than 26 million people worldwide have Alzheimer's Disease, and a new forecast says the number will quadruple by 2050. At that rate, one in 85 people will have the brain-destroying disease in 40 years, researchers from Johns Hopkins University conclude. The new estimates, being presented Sunday at an Alzheimer's Association conference in Washington, are not very different from previous projections of the looming global dementia epidemic with the graying of the world's population.
But they serve as a sobering reminder of the toll to come if scientists cannot find better ways to battle Alzheimer's and protect aging brains.
"If we can make even modest advances in preventing Alzheimer's disease, or delay its progression, we could have a huge global public health impact," said Johns Hopkins public health specialist Ron Brookmeyer, who led the new study.
The biggest jump is projected for densely populated Asia, home of almost half of today's Alzheimer's cases, 12.6 million. By 2050, Asia will have 62.8 million of the world's 106 million Alzheimer's patients, the study projects.
A recent U.S. study estimated that this nation's Alzheimer's toll will reach 16 million by 2050, compared with more than 5 million today. The new estimate is significantly lower, suggesting only 3.1 million North American cases today and 8.8 million by 2050.
Among the estimates for other regions are:
_Africa, 1.3 million today and 6.3 million in 2050.
_Europe, 7.2 million and 16.5 million.
_Latin America and the Caribbean, 2 million and 10.8 million.
_Oceania, 200,00 and 800,000.
Labels: alzheimers
// posted by neurofuture8:49 AM permanent link
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6.03.2007
Air Supply Affects Alzheimer's
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The latest science news on the brain and Alzheimer's is the connection between air supply, and lack thereof and memory loss. To make sure you have enough, we've provided this video, which hopefully you have forgotten, if indeed - you ever saw it :
But on a more serious note, see this piece from the Scotsman (UK)
But on a more serious note, see this piece from the Scotsman (UK)
AN INCIDENT of reduced oxygen to the brain caused by a stroke, heart attack, or even heavy snoring could make people more vulnerable to Alzheimer's disease, according to scientists. It can leave the patient more open to the gradual build-up of toxic chemicals which can cause Alzheimer's, a team at Leeds University said. This means a stroke victim may still be more at risk of developing Alzheimer's decades after they have made a full recovery.
Professor Chris Peers, of the school of medicine, who led the research, said: "Our research is looking into what happens when oxygen levels in the brain are reduced by a number of factors, from long-term conditions like emphysema and angina, to sudden incidents such as a heart attack, stroke or head trauma.
"Even though the patient may outwardly recover, the hidden cell damage may be irreversible.
"It could even be an issue for people who snore heavily. It can be anything that stops the heart and lungs working together."
Professor Susanne Sorensen, head of research at the Alzheimer's Society, said: "This is exciting because rather than focusing on neurons they looked at processes in the brain, which up until now have not been resesarched in much detail.... read more of the articleLabels: air supply, alzheimers, brain, leeds, neurons
// posted by neurofuture10:12 PM permanent link
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5.10.2007
The Mechanics of Aging
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Jacob Israel Avedon, photo by Richard Avedon
Why does aging occur? This question was recently asked in a descriptive piece in the New Yorker.
Aging really can be defined as molecular change (see article) mitigated by time. Others, for example, longevity researcher Aubrey DeGrey, posit a free-radical theory of human decline.
In something of a counterpoint, according to Dr. Ashford, a Stanford/VA scientist, "The problem is a species adaptation to an ecological niche with evolution occurring at all system levels of the organism including the social interactions between members of the species during the adaptation."
"Evolution and adaptation is ever continuing and may lead to a longer life for the organisms of the species, but it takes a long time. I think free-radicals are just part of life, carefully adapted into the living process, and you can’t just treat this molecular mechanism or any other one and expect to live forever. Look what happened to Roy Walford, the starvation for aging man, who ended up dying of leukemia at a younger age than his normal life-expectancy."
Labels: aging, alzheimers, free_radical
// posted by neurofuture8:52 AM permanent link
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5.02.2007
Heart Attack Rate Cut in Half
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A new study conducted in 14 different countries over six years has found a 50% decline in the rate of heart attacks in patients who are hospitalized, compared to the rate of heart attacks experienced in in the year 1995. The advance is attributed to newer procedures such as angioplasty, more effective blood-thinning medications, and where possible, earlier intervention.
As efforts to treat cardiovascualar risk become more effective, along with cancer treatments, Alzheimer's moves into a more threatening position. Not only is the incidence of Alzheimer's increasing, as populations age, it impacts a greater percentage of people - as the risk factors for Alzheimer's include age, genetics, and lifestyle.
Labels: alzheimers, heart
// posted by neurofuture7:43 AM permanent link
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4.30.2007
Mental Stimulation and a Memory Pill said to Reverse Alzheimers'
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WASHINGTON (Reuters) - Mental stimulation and drug treatment may help people with brain ailments such as Alzheimer's disease regain seemingly lost memories, according to research published on Sunday.
Scientists used two methods to reverse memory loss in mice with a condition like Alzheimer's -- placing them in sort of a rodent Disneyland to stimulate their brains, and also using a type of drug that encourages growth of brain nerve cells.
Neuroscientist Li-Huei Tsai of the Howard Hughes Medical Institute and the Massachusetts Institute of Technology said such methods might yield similar benefits in people with Alzheimer's disease or other types of dementia that rob them of their memory and ability to learn.
"We show, I believe, the first evidence that even if the brain suffered some very severe neurodegeneration and the individual exhibits very severe learning impairment and memory loss, there is still the possibility to improve learning ability and recover to a certain extent lost long-term memories," Tsai said in a telephone interview.
Tsai said if apparently lost long-term memories could be retrieved, this suggested the memories had not been actually erased from the brain.
Instead, she and colleagues reported in the journal Nature, the memories probably remained in storage but could not be accessed or retrieved due to the brain damage.
The researchers used genetically engineered elderly mice in which they were able to activate a protein that triggered brain pathology very much like that of people with Alzheimer's, with atrophy and loss of nerve cells.
save brains. get
the code
MOUSE FUNHOUSE
Previous research has shown that regular mental stimulation such as reading or playing a musical instrument may reduce one's risk for Alzheimer's. And a stimulating environment also has been shown to improve learning in mice.
In one part of their study, the researchers took mice out of their usual bland cages and placed them in a sort of mouse playground loaded with an ever-changing assortment of colorful toys, treadmills and other mice.
The researchers previously had used a "fear-conditioning" test -- placing mice in a chamber and delivering a mild electric shock to their feet -- to establish an enduring memory.
Mice with Alzheimer's-like brain damage put in the stimulating environment could remember that shock test far better than similar animals kept in standard cages. The playground mice also were better at learning new things than those kept in standard cages.
After exploring the biological mechanism behind the improvement in mice placed in the enriched environment, the researchers tested on the mice a class of drugs called histone deacetylase, or HDAC, inhibitors.
Memory and learning improved in the mice, similar to improvements caused by environmental stimulation, the researchers said. They said this indicated such drugs represent a potential way to treat people with conditions like Alzheimer's.
Tsai said most current treatments for Alzheimer's were intended to affect the disease's early stages before profound memory loss occurred, but this research showed that even after major brain damage had occurred it was still possible to improve learning and memory
Labels: alzheimers, mental_sharpness, reversal, stimuli
// posted by neurofuture7:56 PM permanent link
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4.23.2007
Alzheimer's Forum on Neuroplasticity
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The Alzheimer's Research Forum is probably the top resource on real-time developments in the field. If you are interested in the topic of neuroplasticity, here is an interesting thread on the evolution of the concept, as discussed by researchers.
Labels: alzheimers, neuroplasticity
// posted by neurofuture11:15 PM permanent link
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4.13.2007
Get Our Newsletter
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Take a test, get our newsletters and shortcuts...people seem to appreciate them, around the world.
"Thank you Michael for sending me the links. i am a clinical Psychologist currently doing Ph.D. at IIT Kanpur. These links are quite handy to me, as iam planning to work with alzheimer's patients"
--Shweta
"Thank you Michael for sending me the links. i am a clinical Psychologist currently doing Ph.D. at IIT Kanpur. These links are quite handy to me, as iam planning to work with alzheimer's patients"
--Shweta
Labels: alzheimers, IIT, Kanpur, memory-test
// posted by neurofuture8:22 AM permanent link
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4.05.2007
Mutant Genes May be Key to Expanding Memory
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McGill University researchers have discovered that a mutant gene improves the long-term memory of laboratory mice, a discovery they hope will one day lead to a better quality of life for Alzheimer’s patients and others suffering from memory impairment.
"We now have an excellent target for the development of new drugs that would be capable of doing the same thing that we did, which could be of great benefit to an aging population with memory loss," said Dr. Mauro Costa-Mattioli, a post-doctoral fellow in the laboratory of Dr. Nahum Sonenberg, James McGill Professor of Translational Control Mechanisms in the Department of Biochemistry and a Howard Hughes Medical Institute International Scholar at McGill.
Using a mutant gene that regulates the switch from short to long-term memory in mice, Dr. Costa-Mattioli and his colleagues were able to manipulate biochemical reactions in the animals’ brains to control their memory and cognitive behaviour – both extending and reducing long-term memory functions. Their findings appear in the April 6 issue of the journal Cell.
To study spatial memory, the researchers used such tests as the Morris water maze, in which a mouse is placed in a pool of water containing a hidden platform located just below the surface. Visual cues are placed around the pool and over a number of trials, researchers analyze how quickly the mice remember how to locate the hidden platform using these cues. In this and other tests, the researchers found that the mice with the altered gene exhibited enhanced learning and memory.
Drs. Mauro Costa-Mattioli and Sonenberg conducted the research in collaboration with Dr. Jean-Claude Lacaille of Université de Montréal, Dr. Kobi Rosenblum of the University of Haifa and Dr. Randal Kaufman of the University of Michigan, as well as a team of colleagues from McGill, consisting of Drs. Jerry Pelletier, Wayne Sossin, Claudio Cuello, Kresimir Krnjevic and Karim Nader, a McGill psychology professor best known for his discovery that the impact of traumatic memories can be lessened with drug treatment.
"Our next step is to look at many different compounds to start searching for a drug that can be designed to improve long-term memory in humans," said Dr. Sonenberg.
Labels: alzheimers, McGill, memory, mice
// posted by neurofuture8:08 PM permanent link
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3.27.2007
Mamas and Papas Beginnings (2)
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More on the beginning of the Mamas and the Papas, early to mid 1960's...Just click to watch and listen
Labels: 60s, alzheimers, brain, mamasandpapas
// posted by neurofuture10:15 PM permanent link
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3.24.2007
Beatles: Help
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Here's the Fab Four piece. You'll know the song
Labels: alzheimers, Beatles, brain
// posted by neurofuture8:52 PM permanent link
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Microsoft Gets into the Memory Business
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We Can Remember it for you Wholesale...Pictures jog Your Memory. This is the premise of Memory TV and also our new test variations....good thing we've filed the patents
Scientists have found that Alzheimer's sufferers who were given a "human black box", have shown significant improvements in long-term memory.
The 'human black box' called 'SenseCam' is a square black camera 3in square and half an inch think, and is worn around the neck. It has a series of sensors that trigger a fish-eye lens to take pictures in response to changes such as motion and light variation, gestures or heat from a person in front of the camera.
The research was conducted by Microsoft.
As part of the study it was found that a patient, who without the camera, had virtually no recall of events five days after they happen, was able to recall details of trips several months after viewing images taken by the device to trigger her own memories, the Telegraph reported.
The device takes up to 2,000 pictures per day, which are downloaded to a home computer, and can be viewed as a speeded up slideshow or one by one. Microsoft is still testing prototypes.
The researchers claim that the miniature camera can enrich the lives of people with dementia and other memory problems.
SenseCam can also be used for tourism or as a personal digital diary. Combined with other sensors such as a heart rate monitor, it could have other medical applications.
The findings were revealed at the British Psychological Society conference in New York.
Scientists have found that Alzheimer's sufferers who were given a "human black box", have shown significant improvements in long-term memory.
The 'human black box' called 'SenseCam' is a square black camera 3in square and half an inch think, and is worn around the neck. It has a series of sensors that trigger a fish-eye lens to take pictures in response to changes such as motion and light variation, gestures or heat from a person in front of the camera.
The research was conducted by Microsoft.
As part of the study it was found that a patient, who without the camera, had virtually no recall of events five days after they happen, was able to recall details of trips several months after viewing images taken by the device to trigger her own memories, the Telegraph reported.
The device takes up to 2,000 pictures per day, which are downloaded to a home computer, and can be viewed as a speeded up slideshow or one by one. Microsoft is still testing prototypes.
The researchers claim that the miniature camera can enrich the lives of people with dementia and other memory problems.
SenseCam can also be used for tourism or as a personal digital diary. Combined with other sensors such as a heart rate monitor, it could have other medical applications.
The findings were revealed at the British Psychological Society conference in New York.
Labels: alzheimers, microsoft, remember, wholesale
// posted by neurofuture5:16 PM permanent link
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3.22.2007
Good Things Come in Threes
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What does that mean? There is an allusion to "3" in this piece. Just click the arrow on the box below to get started. Another view of the 1960's, and providing you an introduction to the stories we've been running over the past few days...and there's more, so stay tuned.
Labels: alzheimers, alzheimers exercise brain canada, mamasandpapas
// posted by neurofuture9:18 PM permanent link
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SuperComputer Holds Keys to Alzheimer's???
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A "supercomputer" is being harnessed by U.S. scientists to help pinpoint the causes of neurological disease like Parkinson's and Alzheimer's.
The massive machine has already been used by scientists at the University of California at San Diego to map out a model of how a protein called alpha-synuclein damages cells by creating structures on human membranes that resemble rings or pores.
This is the same type of damage found in the brain cells of patients with Parkinson's and Alzheimer's diseases, the researchers said.
"This is one of the first studies to use supercomputers to model how alpha-synuclein complexes damage the cells, and how that could be blocked," said Eliezer Masliah, professor of neurosciences and pathology at U.C. San Diego. "We believe that these ring- or pore-like structures might be deleterious to the cells, and we have a unique opportunity to better understand how alpha-synuclein is involved in the pathogenesis of Parkinson's disease, and how to reverse this process."
The supercomputer's modeling approach might also unlock keys to other diseases, like rheumatoid arthritis, the researchers noted.
The study is published in this week's Federation of European Biochemical Societies Journal.
The massive machine has already been used by scientists at the University of California at San Diego to map out a model of how a protein called alpha-synuclein damages cells by creating structures on human membranes that resemble rings or pores.
This is the same type of damage found in the brain cells of patients with Parkinson's and Alzheimer's diseases, the researchers said.
"This is one of the first studies to use supercomputers to model how alpha-synuclein complexes damage the cells, and how that could be blocked," said Eliezer Masliah, professor of neurosciences and pathology at U.C. San Diego. "We believe that these ring- or pore-like structures might be deleterious to the cells, and we have a unique opportunity to better understand how alpha-synuclein is involved in the pathogenesis of Parkinson's disease, and how to reverse this process."
The supercomputer's modeling approach might also unlock keys to other diseases, like rheumatoid arthritis, the researchers noted.
The study is published in this week's Federation of European Biochemical Societies Journal.
Labels: alzheimers, computation
// posted by neurofuture9:14 PM permanent link
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2.12.2007
Scientists: Vasectomies Linked to Alzheimer's
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Northwestern University researchers have discovered men with an unusual form of dementia have a higher rate of vasectomy than men the same age who are cognitively normal.
The dementia is Primary Progressive Aphasia ( PPA ), a neurological disease in which people have trouble recalling and understanding words. In PPA, people lose the ability to express themselves and understand speech. It differs from typical Alzheimer's disease in which a person's memory becomes impaired.
Sandra Weintraub, principal investigator and professor of psychiatry and behavioral sciences and of neurology at Northwestern's Feinberg School of Medicine, began investigating a possible link between the surgery and PPA when one of her male patients connected the onset of his language problem at age 43 to the period after his vasectomy.
At a twice-yearly Chicago support group for PPA patients Weintraub sees from around the country, the male patient rushed into the room and asked the men sitting there, "OK, guys, how many of you have PPA?" Nine hands went up.
"How many of you had a vasectomy?" he demanded next. Eight hands shot up.
Weintraub and her team of researchers surveyed 47 men with PPA who were being treated at Northwestern's Cognitive Neurology and Alzheimer's Disease Center and 57 men with no cognitive impairment who were community volunteers. They ranged from 55 to 80 years old.
Of the non-impaired men, 16 percent had undergone a vasectomy. In contrast, 40 percent of the men with PPA had had the surgery.
"That's a huge difference," said Weintraub, director of neuropsychology in the Cognitive Neurology and Alzheimer's Disease Center. "It doesn't mean having a vasectomy will give you this disease, but it may be a risk factor to increase your chance of getting it."
In addition, the men who had undergone a vasectomy developed PPA at a younger age ( 58 years ) than men with PPA who hadn't had one ( 62 years. )
While PPA robs people of their ability to speak and understand language, an unusual twist of the disease is patients are still able to maintain their hobbies and perform other complicated tasks for a number of years before other symptoms develop. Some people garden, build cabinets and even navigate a city subway system. By contrast, Alzheimer's patients lose interest in their hobbies, family life and may become idle. As PPA progresses over a number of years, however, patients eventually lose their ability to function independently.
Preliminary evidence from the study also seemed to connect another form of dementia to a vasectomy. In a smaller group of 30 men with a dementia called frontotemporal dementia ( FTD, ) 37 percent had undergone a vasectomy. The earliest symptoms of FTD are personality changes, lack of judgment and bizarre behavior. As in PPA, FTD usually starts at an earlier age, in the 40s and 50s.
One of Weintraub's patients with FTD was eating lunch in a restaurant with his family and excused himself to go to the bathroom. When he hadn't returned after 10 minutes, his sons went to investigate. They found him doing pushups on the bathroom floor. Other FTD patients begin shoplifting, compulsively gambling, misspending large amounts of money or become sexually demanding.
The most common form of dementia caused by brain deterioration in individuals over age 65 is Alzheimer's disease. Weintraub did not find an increased rate of vasectomy in patients with Alzheimer's.
Many patients with FTD and PPA share a common brain disease that is completely different from Alzheimer's. Whether a patient will get the behavioral or language problems depends on where the disease causes the most destruction in the brain. In FTD, most of the damage is in the frontal lobes; in PPA, it's in the language centers of the left hemisphere of the brain.
Weintraub theorizes a vasectomy may raise the risk of PPA ( and possibly FTD ) because the surgery breeches the protective barrier between the blood and the testes, called the blood-testis barrier.
Certain organs � including the testes and the brain � exist in what is the equivalent of a gated community in the body. Tiny tubes within the testes ( in which sperm are produced ) are protected by a physical barrier of Sertoli cells. The tight connections between these cells prevent blood-borne infections and poisonous molecules from entering the semen.
After a vasectomy, however, the protective barrier is broken and semen mixes into the blood. The immune system recognizes the sperm as invading foreign agents and produces anti-sperm antibodies in 60 to 70 percent of men.
Weintraub said these antibodies might cross the blood-brain-barrier and cause damage resulting in dementia. "There are other neurological models of disease which you can use as a parallel," Weintraub said. Certain malignant tumors produce antibodies that reach the brain and cause an illness similar to encephalitis, she noted.
The next step in Weintraub's research will be to launch a national study to see if her results will be confirmed in a larger population.
"I don't want to scare anyone away from getting a vasectomy," Weintraub stressed. "It's obviously a major birth control alternative. This is just a correlational observation," she said of the dementia connection. "We need to do more research to find out."
Labels: alzheimers, brain, vasectomy
// posted by neurofuture11:54 AM permanent link
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2.11.2007
Former NFL Player Diagnosed with Early Alzheimer's like Condition at age 34
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Former NFL player Ted Johnson of the New England Patriots has been diagnosed with the likely early stages of Alzheimer's Disease at age 34. Johnson's condition appears to result from repetitive concussions suffered while a player. Concussions have a cumulative degrading effect on cognitive ability. Scientists are just now realizing how tremendously damaging the effect of this kind of injury can be.
Labels: alzheimers, johnson, patriots
// posted by neurofuture5:34 PM permanent link
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2.09.2007
3 Cups of Coffee Per Day: Key to Fighting Alzheimers
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Having three cups of coffee a day can significantly reduce the chance of developing Alzheimer's disease, say researchers.
A ten-year study of 600 elderly men found those getting a regular caffeine fix experienced a much smaller decline in their mental abilities than non coffee-drinkers.
The results support earlier studies that show coffee has a protective effect on the brain.
Researchers believe caffeine may trigger a chain reaction in the brain that prevents the damage of Alzheimer's.
In a report on their findings, published in the European Journal of Clinical Nutrition, they raised the possibility that doctors may one day recommend coffee to the elderly.
"Drinking three cups a day was associated with the smallest cognitive decline," they said."
Labels: alzheimers, coffee, cups
// posted by neurofuture8:11 PM permanent link
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2.05.2007
Alzheimer's expert dies in plane crash
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Pioneering Alzheimer's researcher Dr. Leon Thal perishes in small plane crash in the mountains east of San Diego. Dr. Thal organized large, national studies of Alzheimer's Disease and orchestrated efforts in California to research the promising areas, such as the large study of the substance Huperzine A which is ongoing now...
Labels: alzheimers, huperzine, nih, thal
// posted by neurofuture8:41 AM permanent link
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2.02.2007
brain.com - test mecca
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Roughly 1,000 people per day are signing up on brain.com - now a cognitivelabs.com property - and this is giving a shot in the arm to our registration efforts - now closing in on the 2 million mark - (just under 100,000 away)
This is basically people just going to the site and registering...it is now ranked 4th on yahoo and 5th on google when you enter the word "brain". You can help us reach #1 by placing those quality, organic links.
brain.com is a little easier to remember than cognitivelabs.com, though the latter has built a quality brand in its own right.
This is basically people just going to the site and registering...it is now ranked 4th on yahoo and 5th on google when you enter the word "brain". You can help us reach #1 by placing those quality, organic links.
brain.com is a little easier to remember than cognitivelabs.com, though the latter has built a quality brand in its own right.
Labels: alzheimers, brain, brain.com, cognitivelabs.com, Google, yahoo
// posted by neurofuture1:36 PM permanent link
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2.01.2007
Take Action to Help your Brain
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Do you want to read more about tests and games for your brain? Then go over to the blog section at healthcentral and read about what you can do right now from Jacqueline Marcell.
Healthcentral is a new concept in health content, as is evident on their site(s). Investors include Allen & Company (like CAA in days yore, too cool to have a website), Sequoia Capital, Polaris Ventures, and the Carlyle Group. Sequoia 'invented' pong according to their site, among other things.
Healthcentral is a new concept in health content, as is evident on their site(s). Investors include Allen & Company (like CAA in days yore, too cool to have a website), Sequoia Capital, Polaris Ventures, and the Carlyle Group. Sequoia 'invented' pong according to their site, among other things.
Labels: alzheimers, games, healthcentral, marcell, tests
// posted by neurofuture4:38 PM permanent link
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1.27.2007
Simple Prevention-Brain Exercise - Yahoo! Health
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Yahoo! Health has a feature on simple tips to prevent a weakening memory and Alzheimer's - from "mind games" to diet and exercise...
Labels: alzheimers, health, simple, tips, yahoo, yahoo_image
// posted by neurofuture10:58 AM permanent link
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1.23.2007
Learning Slows Alzheimer's: UC Irvine Study
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Exercising your mind does pay off - for the first time, scientists have shown that learning slows the build-up in the brain of protein plaques and tangles that are the signature of Alzheimer's disease.
Although the study was conducted in mice, it does reinforce the idea that, in humans, maintaining an active mind may help delay or even prevent Alzheimer's disease.
"This has shown for the first time that using your brain can protect you physically," said Kim Green, co-lead author of the study and a postdoctoral researcher at the University of California, Irvine. "We show that when you do this, it causes changes in the brain, and these changes are protective."
"It's an interesting study, and part of what it does is advance the notion that mental exercise has a protective effect against Alzheimer's," said Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City.
According to the Alzheimer's Association, about 4.5 million Americans have the brain-robbing disorder, a number that has more than doubled since 1980. Many more suffer from cognitive impairment, which could be a harbinger of Alzheimer's.
Many experts believe that Alzheimer's is caused by a steady accumulation of amyloid plaque proteins in the brain.
Previous studies had shown that "mental exercise" could delay the onset of the disease, but the proof came only in the form of memory and other cognitive testing measures.
The study involved hundreds of "transgenic" mice -- mice that had been genetically altered to develop human Alzheimer's disease.
Mice in a "learning" group were allowed to swim in a tank of water until they discovered a submerged platform on which to stand. This training took place four times a day for one week at two, six, nine, 12, 15 and 18 months of age. The other group of mice swam in the tank just once before their learning and memory skills were tested and their brains examined.
Mice up to 1 year old in the learning group developed 60 percent less of the proteins that form plaques and tangles compared to mice in the non-learning group, the researchers found.
"The sort of learning we gave the animals was fairly mild, yet it still had a big effect," Green said.
However, by 15 months of age, the learning mice had declined and were now physically and cognitively identical to the non-learning mice.
Text Continues Below
Can these findings be extrapolated to humans?
"We do find a lot of similarities, but clinical data also backs up what we've shown in this study," Green said.
"I think it's reasonable to extrapolate," Kennedy added. "The recommendation certainly is to keep your mind active."
"Think of the brain as a computer," Kennedy continued. "Alzheimer's degrades the hardware, and education enhances the software. The brain is also a muscle, and conditioning may protect it."
Green and his colleagues hope to use the information to one day develop a drug for the disease.
"We want to identify exactly how learning influences pathology and identify a novel drug target," he said.
The study is appearing in the Jan. 24 issue of the Journal of Neuroscience.
Although the study was conducted in mice, it does reinforce the idea that, in humans, maintaining an active mind may help delay or even prevent Alzheimer's disease.
"This has shown for the first time that using your brain can protect you physically," said Kim Green, co-lead author of the study and a postdoctoral researcher at the University of California, Irvine. "We show that when you do this, it causes changes in the brain, and these changes are protective."
"It's an interesting study, and part of what it does is advance the notion that mental exercise has a protective effect against Alzheimer's," said Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City.
According to the Alzheimer's Association, about 4.5 million Americans have the brain-robbing disorder, a number that has more than doubled since 1980. Many more suffer from cognitive impairment, which could be a harbinger of Alzheimer's.
Many experts believe that Alzheimer's is caused by a steady accumulation of amyloid plaque proteins in the brain.
Previous studies had shown that "mental exercise" could delay the onset of the disease, but the proof came only in the form of memory and other cognitive testing measures.
The study involved hundreds of "transgenic" mice -- mice that had been genetically altered to develop human Alzheimer's disease.
Mice in a "learning" group were allowed to swim in a tank of water until they discovered a submerged platform on which to stand. This training took place four times a day for one week at two, six, nine, 12, 15 and 18 months of age. The other group of mice swam in the tank just once before their learning and memory skills were tested and their brains examined.
Mice up to 1 year old in the learning group developed 60 percent less of the proteins that form plaques and tangles compared to mice in the non-learning group, the researchers found.
"The sort of learning we gave the animals was fairly mild, yet it still had a big effect," Green said.
However, by 15 months of age, the learning mice had declined and were now physically and cognitively identical to the non-learning mice.
Text Continues Below
Can these findings be extrapolated to humans?
"We do find a lot of similarities, but clinical data also backs up what we've shown in this study," Green said.
"I think it's reasonable to extrapolate," Kennedy added. "The recommendation certainly is to keep your mind active."
"Think of the brain as a computer," Kennedy continued. "Alzheimer's degrades the hardware, and education enhances the software. The brain is also a muscle, and conditioning may protect it."
Green and his colleagues hope to use the information to one day develop a drug for the disease.
"We want to identify exactly how learning influences pathology and identify a novel drug target," he said.
The study is appearing in the Jan. 24 issue of the Journal of Neuroscience.
Labels: alzheimers, brain, learning, neuroscience, uc-irvine
// posted by neurofuture5:31 PM permanent link
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1.21.2007
How to Really Boost Your Brain
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Nerve Conduction Velocity is one of the accurate objective measures of mental performance. The less time it takes to perform a specified task within a controlled system, the more efficient the system is. Through targeted exercise, it is possible to enhance the speed at which cognitive tasks are performed. As the individual engages in a variety of tasks with measurable performance, particularly with reversals and unexpected stimuli, the brain becomes more effective and better able to process complex information. Improvement and regular practice can lead to a sustained level of performance and prevention of cognitive decline.
Boost your brain
Boost your brain
Labels: alzheimers, boost, brain, nerves, stimuli
// posted by neurofuture11:33 AM permanent link
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1.18.2007
Common Anesthetic linked to Alzheimer's
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The commonly used anesthetic isoflurane can lead to the death of brain cells and the production of amyloid-beta plaque, a hallmark of Alzheimer's disease, Harvard researchers report.
Their study appears in the January issue of the Journal of Gerontology, which is devoted to the problems of dementia and delirium. In the United States, delirium accounts for $7 billion per year in hospital expenses and more than $100 billion a year when rehabilitation, institutionalization and long-term care are added to the equation.
The Harvard study raises questions about the safety of isoflurane, which has been used for years for all ages of patients.
"Many people, especially the elderly, who have anesthesia suffer from postoperative cognitive dysfunction, scrambling and delirium that can last six hours or two weeks or months," said lead researcher Rudolph Tanzi, a professor of neurology at the Genetics and Aging Research Unit of the Massachusetts General Institute for Neurodegenerative Disease.
"To me, a big dose of isoflurane mimics a stroke or a bang to the head, and you don't want that as a risk factor for Alzheimer's disease at any age," Tanzi said.
In experiments with cells that had an amyloid-beta protein, Tanzi's team exposed them to isoflurane for six hours.
The researchers found that isoflurane caused these cells to die. "It also caused the cell to overproduce the toxic molecule responsible for the pathology of Alzheimer's disease, particularly amyloid-beta," Tanzi said.
This is a warning, Tanzi said. "Isoflurane may be one reason why the elderly are more prone to cognitive dysfunction following anesthesia," he said.
"Any trauma to the brain induces cell death. Isoflurane now joins that list of insults to the brain that can cause cell death and excessive production of this key molecule in Alzheimer's pathology," Tanzi. "This does increase the risk for Alzheimer's disease."
Tanzi believes that isoflurane should be avoided, when possible. "We don't have enough data yet to ban isoflurane," he said. "But I'm convinced enough that I won't let my mother have it. I would advise any family or friends to stay away from isoflurane," he said. "There is a lot of speculation here, and a lot of work needs to be done, but at this point I wouldn't take a chance."
Despite the findings, one expert doesn't agree that isoflurane is dangerous.
"Most of the studies that have been done have been done in isolated cell types," said Dr. Piyush Patel, a professor of anesthesiology at the University of California, San Diego. "Not only that, but the cells they are using are not normal cells."
Patel believes, however, that the findings are provocative enough that there needs to be further research on the issue. "Studies need to be done in cells that are closer to normal cells, and then in animals," he said.
Moreover, it isn't clear that this same effect would be seen in humans, Patel said. "Isoflurane has had a long history of safety in all aged patients, all the way from premature babies to octogenarians. There is absolutely no evidence right now in human beings that that drug is harmful," he said. "To extrapolate these findings to humans would be irresponsible."
Their study appears in the January issue of the Journal of Gerontology, which is devoted to the problems of dementia and delirium. In the United States, delirium accounts for $7 billion per year in hospital expenses and more than $100 billion a year when rehabilitation, institutionalization and long-term care are added to the equation.
The Harvard study raises questions about the safety of isoflurane, which has been used for years for all ages of patients.
"Many people, especially the elderly, who have anesthesia suffer from postoperative cognitive dysfunction, scrambling and delirium that can last six hours or two weeks or months," said lead researcher Rudolph Tanzi, a professor of neurology at the Genetics and Aging Research Unit of the Massachusetts General Institute for Neurodegenerative Disease.
"To me, a big dose of isoflurane mimics a stroke or a bang to the head, and you don't want that as a risk factor for Alzheimer's disease at any age," Tanzi said.
In experiments with cells that had an amyloid-beta protein, Tanzi's team exposed them to isoflurane for six hours.
The researchers found that isoflurane caused these cells to die. "It also caused the cell to overproduce the toxic molecule responsible for the pathology of Alzheimer's disease, particularly amyloid-beta," Tanzi said.
This is a warning, Tanzi said. "Isoflurane may be one reason why the elderly are more prone to cognitive dysfunction following anesthesia," he said.
"Any trauma to the brain induces cell death. Isoflurane now joins that list of insults to the brain that can cause cell death and excessive production of this key molecule in Alzheimer's pathology," Tanzi. "This does increase the risk for Alzheimer's disease."
Tanzi believes that isoflurane should be avoided, when possible. "We don't have enough data yet to ban isoflurane," he said. "But I'm convinced enough that I won't let my mother have it. I would advise any family or friends to stay away from isoflurane," he said. "There is a lot of speculation here, and a lot of work needs to be done, but at this point I wouldn't take a chance."
Despite the findings, one expert doesn't agree that isoflurane is dangerous.
"Most of the studies that have been done have been done in isolated cell types," said Dr. Piyush Patel, a professor of anesthesiology at the University of California, San Diego. "Not only that, but the cells they are using are not normal cells."
Patel believes, however, that the findings are provocative enough that there needs to be further research on the issue. "Studies need to be done in cells that are closer to normal cells, and then in animals," he said.
Moreover, it isn't clear that this same effect would be seen in humans, Patel said. "Isoflurane has had a long history of safety in all aged patients, all the way from premature babies to octogenarians. There is absolutely no evidence right now in human beings that that drug is harmful," he said. "To extrapolate these findings to humans would be irresponsible."
Labels: alzheimers, brain
// posted by neurofuture10:56 AM permanent link
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1.14.2007
SORL gene tagged as Causal Factor for Alzheimer's
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...Scientists said on Sunday they have pinpointed a new gene linked to
Alzheimer's disease, the incurable brain disorder that is the top cause of dementia in the elderly.
Abnormalities in a gene called SORL1 increased the risk for the disease, and this finding could help scientists develop new treatments, the researchers reported in the journal Nature Genetics.
The researchers looked at DNA samples from 6,000 people from four ethnic groups: Caribbean-Hispanics, North Europeans, black Americans and Israeli-Arabs. They found certain variations of SORL1 more often in people with late-onset Alzheimer's disease than in healthy people.
The late-onset form, affecting people age 65 and up, represents about 90 percent of Alzheimer's cases. The rarer early-onset form affects people from about age 30 to 65.
Only one other gene, called ApoE4, has been identified as a risk factor for late-onset Alzheimer's. It was identified in 1993.
Several genes are linked with early Alzheimer's, and study of both types might lead to better understanding of how the disease begins and how to tackle it.
Many scientists think Alzheimer's begins with the buildup in the brain of a gooey material called amyloid that clumps together to form plaques. That material stems from a protein called amyloid precursor protein, or APP.
SORL1 controls the distribution of APP inside nerve cells of the brain. When working normally, the gene prevents APP from being degraded into a toxic byproduct called amyloid beta peptide. When SORL1 is deficient, it allows more of the bad amyloid beta peptide to accumulate, fostering amyloid plaques.
Alzheimer's is a complex disease that gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Scientists have struggled to understand the biology of the disease and its genetic and environmental causes.
'PIECE OF THE PUZZLE'
"It's another clue to the way in which this disease comes about, another piece of the puzzle," Dr. Peter St. George-Hyslop, director of the Center for Research in Neurodegenerative Diseases at the University of Toronto and one of the key researchers, said in a telephone interview.
"Every time you get a piece of the puzzle and you can relate it to something else in the puzzle, you're that much closer to knowing what the picture on the puzzle is," he added.
St. George-Hyslop said it is premature to say what percentage of cases of late-onset Alzheimer's disease can be attributed to SORL1. ApoE4, which also may be involved in the production of amyloid plaques, has been linked to about 20 percent of late-onset Alzheimer's cases.
"This appears to be the fifth Alzheimer's disease gene, and there are likely to be other important genetic variants that need to be identified before the entire picture is complete," Dr. Richard Mayeux of Columbia University Medical Center in New York, also involved in the research, said in a statement.
The disease first affects parts of the brain controlling memory and thinking, but as it advances it kills cells elsewhere in the brain. Eventually, if the patient has no other serious illness, the loss of brain function will prove fatal.
Researchers from Boston University and the Mayo Clinic College of Medicine in Jacksonville, Florida, also took part in the five-year study.
Alzheimer's disease, the incurable brain disorder that is the top cause of dementia in the elderly.
Abnormalities in a gene called SORL1 increased the risk for the disease, and this finding could help scientists develop new treatments, the researchers reported in the journal Nature Genetics.
The researchers looked at DNA samples from 6,000 people from four ethnic groups: Caribbean-Hispanics, North Europeans, black Americans and Israeli-Arabs. They found certain variations of SORL1 more often in people with late-onset Alzheimer's disease than in healthy people.
The late-onset form, affecting people age 65 and up, represents about 90 percent of Alzheimer's cases. The rarer early-onset form affects people from about age 30 to 65.
Only one other gene, called ApoE4, has been identified as a risk factor for late-onset Alzheimer's. It was identified in 1993.
Several genes are linked with early Alzheimer's, and study of both types might lead to better understanding of how the disease begins and how to tackle it.
Many scientists think Alzheimer's begins with the buildup in the brain of a gooey material called amyloid that clumps together to form plaques. That material stems from a protein called amyloid precursor protein, or APP.
SORL1 controls the distribution of APP inside nerve cells of the brain. When working normally, the gene prevents APP from being degraded into a toxic byproduct called amyloid beta peptide. When SORL1 is deficient, it allows more of the bad amyloid beta peptide to accumulate, fostering amyloid plaques.
Alzheimer's is a complex disease that gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. Scientists have struggled to understand the biology of the disease and its genetic and environmental causes.
'PIECE OF THE PUZZLE'
"It's another clue to the way in which this disease comes about, another piece of the puzzle," Dr. Peter St. George-Hyslop, director of the Center for Research in Neurodegenerative Diseases at the University of Toronto and one of the key researchers, said in a telephone interview.
"Every time you get a piece of the puzzle and you can relate it to something else in the puzzle, you're that much closer to knowing what the picture on the puzzle is," he added.
St. George-Hyslop said it is premature to say what percentage of cases of late-onset Alzheimer's disease can be attributed to SORL1. ApoE4, which also may be involved in the production of amyloid plaques, has been linked to about 20 percent of late-onset Alzheimer's cases.
"This appears to be the fifth Alzheimer's disease gene, and there are likely to be other important genetic variants that need to be identified before the entire picture is complete," Dr. Richard Mayeux of Columbia University Medical Center in New York, also involved in the research, said in a statement.
The disease first affects parts of the brain controlling memory and thinking, but as it advances it kills cells elsewhere in the brain. Eventually, if the patient has no other serious illness, the loss of brain function will prove fatal.
Researchers from Boston University and the Mayo Clinic College of Medicine in Jacksonville, Florida, also took part in the five-year study.
Labels: alzheimers, apoe, gene, sorl
// posted by neurofuture11:12 AM permanent link
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12.27.2006
CETP W Gene may protect against Alzheimer's
>
A new study at the Albert Einstein College of Medicine has linked a gene that helps people live longer to increased mental ability and delayed onset of Alzheimer's Disease.
The study is published in the current issue of Neurology and was conducted by researchers at the Albert Einstein College of Medicine of Yeshiva University in the Bronx, New York, and forms part of the Longevity Genes Project.
Dr Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine, and his team looked at 158 people who were aged 95 and over and descended from Ashkenazi Jews who originally came from Eastern Europe. They asked this group, and another group of people of the same age who were not of Ashkenazi descent to complete cognitive tests of mental ability.
The scientists found that those who completed the test successfully (by correctly answering 25 of thirty questions) were two to three times more likely to possess the W variant of the CETP gene than those who did not.
In a later study the researchers examined a group of 124 people also of Ashkenazi descent, aged between 75 and 85. In this study they found that the ones who did not develop dementia on follow up were five times more likely to have the CETP W gene than those who did not.
The researchers chose to look at Ashkenazi people because they came from a small number of ancestors, making it easier to detect the differences in the genetic make up of the individuals due to the more uniform nature of their genetic patterns compared to the public at large.
This research comes on top of earlier studies, also by Dr. Barzilai and his team where they first showed that CETP W helps people live longer and also pass this gene onto their descendants. This study suggested that CETP W changes the size of good (HDL) and bad (LDL) cholesterol molecules in the blood - which helps people live longer because the smaller ones get stuck in the blood vessels more easily, leading to clots.
The centenarians in that study were three times more likely to have the CETP W variant and also had the larger HDL and LDL cholesterol molecules in their blood.
This latest study suggests that the cholesterol changing properties of CETP W may be protecting mental function by preventing the build up of cholesterol in the brain's blood vessels, thus reducing strokes and heart attacks, or by some other means that is yet to be discovered.
“Without good brain function, living to age 100 is not an attractive proposition,” says Dr. Barzilai in a press release. “We’ve shown that the same gene variant that helps people live to exceptional ages has the added benefit of helping them think clearly for most of their long lives."
In the population at large, the chances of living to 100 is one in 10,000. The Ashkenazi population has a strong family history of longevity. Dr Barzilai pointed out that the odds of living much longer are much increased if you already have a centenarian in your family, and it is not necessarily lifestyle related. Many of the long living Ashkenazis are not vegetarian or athletic, and some of them have smoked for 90 years.
Cholesterol is an essential molecule for building cells. High levels of oxidized LDL cholesterol is thought to thicken artery walls (atherosclerosis) and increases risk of heart diseases. HDL cholesterol and the larger HDL in particular is thought to help remove cholesterol from thickened artery walls and high levels of HDL are linked to lower incidence of atherosclerosis and may even help to reverse the condition.
The study is published in the current issue of Neurology and was conducted by researchers at the Albert Einstein College of Medicine of Yeshiva University in the Bronx, New York, and forms part of the Longevity Genes Project.
Dr Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine, and his team looked at 158 people who were aged 95 and over and descended from Ashkenazi Jews who originally came from Eastern Europe. They asked this group, and another group of people of the same age who were not of Ashkenazi descent to complete cognitive tests of mental ability.
The scientists found that those who completed the test successfully (by correctly answering 25 of thirty questions) were two to three times more likely to possess the W variant of the CETP gene than those who did not.
In a later study the researchers examined a group of 124 people also of Ashkenazi descent, aged between 75 and 85. In this study they found that the ones who did not develop dementia on follow up were five times more likely to have the CETP W gene than those who did not.
The researchers chose to look at Ashkenazi people because they came from a small number of ancestors, making it easier to detect the differences in the genetic make up of the individuals due to the more uniform nature of their genetic patterns compared to the public at large.
This research comes on top of earlier studies, also by Dr. Barzilai and his team where they first showed that CETP W helps people live longer and also pass this gene onto their descendants. This study suggested that CETP W changes the size of good (HDL) and bad (LDL) cholesterol molecules in the blood - which helps people live longer because the smaller ones get stuck in the blood vessels more easily, leading to clots.
The centenarians in that study were three times more likely to have the CETP W variant and also had the larger HDL and LDL cholesterol molecules in their blood.
This latest study suggests that the cholesterol changing properties of CETP W may be protecting mental function by preventing the build up of cholesterol in the brain's blood vessels, thus reducing strokes and heart attacks, or by some other means that is yet to be discovered.
“Without good brain function, living to age 100 is not an attractive proposition,” says Dr. Barzilai in a press release. “We’ve shown that the same gene variant that helps people live to exceptional ages has the added benefit of helping them think clearly for most of their long lives."
In the population at large, the chances of living to 100 is one in 10,000. The Ashkenazi population has a strong family history of longevity. Dr Barzilai pointed out that the odds of living much longer are much increased if you already have a centenarian in your family, and it is not necessarily lifestyle related. Many of the long living Ashkenazis are not vegetarian or athletic, and some of them have smoked for 90 years.
Cholesterol is an essential molecule for building cells. High levels of oxidized LDL cholesterol is thought to thicken artery walls (atherosclerosis) and increases risk of heart diseases. HDL cholesterol and the larger HDL in particular is thought to help remove cholesterol from thickened artery walls and high levels of HDL are linked to lower incidence of atherosclerosis and may even help to reverse the condition.
Labels: alzheimers, brain, CETP W, gene
// posted by neurofuture12:32 PM permanent link
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New Levels of Intensity for Your Brain
>
With the Coming of the New Year, you'll now be able to test and train your brain a little bit, or a lot.
There are several completely new exercises and, in addition, on every test there is an intensity adjuster. Start low, at 5 or 10 repetitions - and increase to 30 or 40 repetitions as you get more proficient.
This might remind you of a routine at the gym.
As you increase your ability to concentrate and focus, you'll begin to change your brain for the better. As the experts have said, regular workouts for an extended period of time are the key. But even if you can only spend a few minutes a day, with the lower rep settings you can exercise your brain in just a few minutes - with a variety of exercises that focus on different memory and attention capacities - a much more concentrated form of exercise than suggestions to "read" or do "crossworld puzzles," and 2X to 3X more effective, in less time according to a recent JAMA article, with benefits measureable many years into the future.
While they may be fun, crosswords don't have a time element. Time-definite exercise trains your brain to be quicker through enhancement of "neural conduction velocity" which is the scientific term used for "brain speed."
These changes can make your brain act younger by stimulating neural connections and if you are young, increase the potential to learn, store, and recall information. The variety and depth insures that you get a balanced exercise.
Labels: alzheimers, brain, brainage, brainspeed, learning, neural, nintendo, velocity, youth
// posted by neurofuture8:11 AM permanent link
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12.20.2006
Scientists: Speed of Processing Exercises Stave Off Mental Decline at Any Age - JAMA
>
If you know about Cognitive Labs tests, your already using the leading provider of speed-of-processing exercises, now shown to be far more effective than any other memory improvement strategy.
Short Mental Workouts May Slow Decline of Aging Minds, Study Finds
By Shankar Vedantam
Washington Post Staff Writer
Wednesday, December 20, 2006
Ten sessions of exercises to boost reasoning skills, memory and mental processing speed staved off mental decline in middle-aged and elderly people in the
first definitive study to show that honing intellectual skills can bolster the mind in the same way that physical exercise protects and strengthens the body.
The researchers also showed that the benefits of the brain exercises extended well beyond the specific skills the volunteers learned. Older adults who did
the basic exercises followed by later sessions were three times as fast as those who got only the initial sessions when it came to activities of daily living, such as reacting to a road sign, looking up a number in a telephone book or checking the ingredients on a medicine bottle -- abilities that can spell the difference between living independently and needing help.
Experts said the federally funded study is a call to action for anyone who has ever worried about developing Alzheimer's, dementia and similar disorders. Americans spend billions of dollars each year on their physical well-being, but there are no comparable efforts to keep people mentally agile and strong.
If anything, the study suggests, there is a bigger payoff to mental exercise, because the brief training sessions seemed to confer enormous benefits as many
as five years later. That would be as if someone went to the gym Monday through Friday for the first two weeks of the new year, did no exercise for five
years, and still saw significant physical benefits in 2012.
The researchers divided the volunteers into four groups, including a control group that received no training. A second group was trained in reasoning skills
-- being asked to spot the pattern in the sequence "a, c, e, g, i," for example -- every other letter of the alphabet. A third group was taught memory
skills, which involved remembering word lists and using visualizations and associations as memory aids. A fourth group was given exercises to speed up mental
processing -- being asked to identify an object flashed briefly on a computer screen while fighting off distractions.
Each of the groups being trained had 10 sessions, each lasting an hour to 75 minutes, and each session presented progressively more challenging problems.
Compared with the control group, those who got memory training did 75 percent better on memory tasks five years later, those who got the reasoning training
did 40 percent better on reasoning tasks, and those who got the speed training did 300 percent better than the control group.
Researchers noted that mental skills can sometimes compensate for physical disabilities: Knowing how to figure out directions and find a new route on a map,
for example, could allow someone to retain mobility even after their night vision deteriorates to the point where driving on certain roads becomes difficult.
The study tracked 2,802 healthy adults from diverse backgrounds who were, on average, 73 years old. Although it did not examine the effects of mental
exercise on people who had begun to show signs of Alzheimer's or other brain disorders, previous studies have pointed toward the conclusion that anyone can
benefit.
"People think education is for people who are already educated," said Michael Marsiske, one of the researchers. "This kind of training works no matter where
you are in society."
"If you think you have come to a time in your life when new learning is impossible and there are no benefits of continuing mental activity, the study shows
that for a large number of people that this is not true," added Marsiske, a clinical and health psychologist at the University of Florida at Gainesville.
The participants in the study ranged from age 65 to their early 90s, but Marsiske said the findings apply to people in their 50s or even younger. Mental
skills acquired earlier in life persist well into old age, he said.
"I don't like to play my son's video games, but I keep telling myself to challenge myself," said Marsiske, 41. "What I personally take away from the study
is, if you challenge yourself to do some new learning, something that isn't easy at the start, it can have dividends."
The study did not indicate that mental training can hold off all cognitive decline permanently. Rather, as is the case with physical exercise, strengthening
the mind appeared to slow decline.
Sherry L. Willis, the lead author of the study and a Pennsylvania State University professor of human development, said those who had the training also
reported greater confidence in their ability to solve everyday problems, and this was especially true of the group that got the reasoning training. In
performing daily functions, people who got the speed training along with a handful of follow-up sessions significantly outperformed those who did not get
such training.
The results, being published today in the Journal of the American Medical Association, are heartening, but Willis and Marsiske cautioned that the biggest
challenge lies ahead, in getting people to apply the findings to their lives. Whether it is encouraging people to eat right or to exercise, they said, the
hardest part is not getting them to start doing the right things but getting them to keep doing the right things.
"It's just like physical exercise -- when we are approaching the new year we will buy a pass for the gym and go fervently in January and then slack off,"
Willis said. "Mental exercise is the same way. It has to be consistent, and it has to be challenging. Just like you have to keep increasing the weights at
the gym to make it challenging, you have to do the same with mental activity."
To reap the benefits, Willis said, people need to get outside their comfort zones. For someone who likes to solve crossword puzzles, it is important to make
sure the puzzles get harder with time -- or to start playing chess. Someone who hates to play games, she said, should find something else that stretches the
mind. Mental activities do not have to involve expensive toys; everyday life can offer a variety of mental challenges. Finding a friend who can join in a new
activity can be a powerful motivator, she added.
Sally Shumaker, a professor of public health science at Wake Forest University in North Carolina who wrote an editorial accompanying the study, said it
pointed the way to a future in which mental training is made widely available.
"I can imagine a situation in which facilities are available in community centers and libraries and aging centers, where people can play some games that are
specifically designed to improve cognitive ability," she said. "People are fearful of cognitive decline, and the idea that a small and simple intervention
can have an impact is pretty compelling."
© 2006 The Washington Post Company
Short Mental Workouts May Slow Decline of Aging Minds, Study Finds
By Shankar Vedantam
Washington Post Staff Writer
Wednesday, December 20, 2006
Ten sessions of exercises to boost reasoning skills, memory and mental processing speed staved off mental decline in middle-aged and elderly people in the
first definitive study to show that honing intellectual skills can bolster the mind in the same way that physical exercise protects and strengthens the body.
The researchers also showed that the benefits of the brain exercises extended well beyond the specific skills the volunteers learned. Older adults who did
the basic exercises followed by later sessions were three times as fast as those who got only the initial sessions when it came to activities of daily living, such as reacting to a road sign, looking up a number in a telephone book or checking the ingredients on a medicine bottle -- abilities that can spell the difference between living independently and needing help.
Experts said the federally funded study is a call to action for anyone who has ever worried about developing Alzheimer's, dementia and similar disorders. Americans spend billions of dollars each year on their physical well-being, but there are no comparable efforts to keep people mentally agile and strong.
If anything, the study suggests, there is a bigger payoff to mental exercise, because the brief training sessions seemed to confer enormous benefits as many
as five years later. That would be as if someone went to the gym Monday through Friday for the first two weeks of the new year, did no exercise for five
years, and still saw significant physical benefits in 2012.
The researchers divided the volunteers into four groups, including a control group that received no training. A second group was trained in reasoning skills
-- being asked to spot the pattern in the sequence "a, c, e, g, i," for example -- every other letter of the alphabet. A third group was taught memory
skills, which involved remembering word lists and using visualizations and associations as memory aids. A fourth group was given exercises to speed up mental
processing -- being asked to identify an object flashed briefly on a computer screen while fighting off distractions.
Each of the groups being trained had 10 sessions, each lasting an hour to 75 minutes, and each session presented progressively more challenging problems.
Compared with the control group, those who got memory training did 75 percent better on memory tasks five years later, those who got the reasoning training
did 40 percent better on reasoning tasks, and those who got the speed training did 300 percent better than the control group.
Researchers noted that mental skills can sometimes compensate for physical disabilities: Knowing how to figure out directions and find a new route on a map,
for example, could allow someone to retain mobility even after their night vision deteriorates to the point where driving on certain roads becomes difficult.
The study tracked 2,802 healthy adults from diverse backgrounds who were, on average, 73 years old. Although it did not examine the effects of mental
exercise on people who had begun to show signs of Alzheimer's or other brain disorders, previous studies have pointed toward the conclusion that anyone can
benefit.
"People think education is for people who are already educated," said Michael Marsiske, one of the researchers. "This kind of training works no matter where
you are in society."
"If you think you have come to a time in your life when new learning is impossible and there are no benefits of continuing mental activity, the study shows
that for a large number of people that this is not true," added Marsiske, a clinical and health psychologist at the University of Florida at Gainesville.
The participants in the study ranged from age 65 to their early 90s, but Marsiske said the findings apply to people in their 50s or even younger. Mental
skills acquired earlier in life persist well into old age, he said.
"I don't like to play my son's video games, but I keep telling myself to challenge myself," said Marsiske, 41. "What I personally take away from the study
is, if you challenge yourself to do some new learning, something that isn't easy at the start, it can have dividends."
The study did not indicate that mental training can hold off all cognitive decline permanently. Rather, as is the case with physical exercise, strengthening
the mind appeared to slow decline.
Sherry L. Willis, the lead author of the study and a Pennsylvania State University professor of human development, said those who had the training also
reported greater confidence in their ability to solve everyday problems, and this was especially true of the group that got the reasoning training. In
performing daily functions, people who got the speed training along with a handful of follow-up sessions significantly outperformed those who did not get
such training.
The results, being published today in the Journal of the American Medical Association, are heartening, but Willis and Marsiske cautioned that the biggest
challenge lies ahead, in getting people to apply the findings to their lives. Whether it is encouraging people to eat right or to exercise, they said, the
hardest part is not getting them to start doing the right things but getting them to keep doing the right things.
"It's just like physical exercise -- when we are approaching the new year we will buy a pass for the gym and go fervently in January and then slack off,"
Willis said. "Mental exercise is the same way. It has to be consistent, and it has to be challenging. Just like you have to keep increasing the weights at
the gym to make it challenging, you have to do the same with mental activity."
To reap the benefits, Willis said, people need to get outside their comfort zones. For someone who likes to solve crossword puzzles, it is important to make
sure the puzzles get harder with time -- or to start playing chess. Someone who hates to play games, she said, should find something else that stretches the
mind. Mental activities do not have to involve expensive toys; everyday life can offer a variety of mental challenges. Finding a friend who can join in a new
activity can be a powerful motivator, she added.
Sally Shumaker, a professor of public health science at Wake Forest University in North Carolina who wrote an editorial accompanying the study, said it
pointed the way to a future in which mental training is made widely available.
"I can imagine a situation in which facilities are available in community centers and libraries and aging centers, where people can play some games that are
specifically designed to improve cognitive ability," she said. "People are fearful of cognitive decline, and the idea that a small and simple intervention
can have an impact is pretty compelling."
© 2006 The Washington Post Company
Labels: alzheimers, brain, brain_games, brainspeed, cognitive_labs, jama, wapo
// posted by neurofuture8:13 PM permanent link
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12.13.2006
Laugh to Light Up Your Brain
>
Tip Seven in our recent series on suggestions for staying mentally sharp was to laugh more and be lighthearted. After all, you have one life, you might as well enjoy it and look on the bright side. And now, British scientists are reporting that just the sound of laughter can make you smile and laugh.
"It seems that it's absolutely true that 'laugh and the whole world laughs with you,'" Sophie Scott, PhD, says in a news release. Scott is a professor at University College London's Institute of Cognitive Neuroscience.
Scott's team says when people hear the sound of laughter, their brain areas that control smiling and laughing become active.
The researchers played the sounds of laughter through headphones to 20 healthy people with good hearing (average age: 32).
While listening to laughter, participants got brain scans using functional magnetic resonance imaging (fMRI).
The brain scans showed activity in brain areas that control facial muscles used in smiling and laughing.
In short, the sound of laughter spurred the brain to get ready to laugh and smile.
Participants' brain scans showed similar activity upon hearing tapes of people cheering, but not after hearing cries of fear or disgust.
The findings may explain how the brain mirrors other people's positive emotions.
"We usually encounter positive emotions, such as laughter or cheering, in group situations, whether watching a comedy program with family or a football game with friends," Scott says.
"This response in the brain, automatically priming us to smile or laugh, provides a way of mirroring the behavior of others, something which helps us to interact socially," she says.
"It could play an important role in building strong bonds between individuals in a group," Scott adds.
The study is due for publication in today's Journal of Neuroscience
Labels: alzheimers, exercise, laughter, mri
// posted by neurofuture8:43 PM permanent link
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12.04.2006
So You Want to Improve Your Brain? 7 Tips
>
So you want to improve your brain? After spending a long time listening to people knowledgeable on this topic, asking questions, and reviewing all of the most recent literature (try Google scholar to speed-read primary sources) here are some of the takeaways.
1. Drink plenty of water. 8-12 servings of water per day keep the brain and its protective tissues hydrated.
2. Exercise, improving your breathing and bloodflow. An action as simple as walking pumps blood into your upper body and head more efficiently than when you are at rest.
3. Maintain a 'Mediterranean' diet with whole grains, legumes, and olive oils
4. Use spices such as cumin, curcumin, and corriander (ingredients in curry) that have a known antioxidant effect, as well as dark berries such as blueberries.
5. Stay engaged with education, work that requires intellectual focus and concentration and socialization
6. Exercise your brain with demanding tasks or games that require a "shift" in attention and quick reaction, that can be increased in intensity, forcing your brain to adapt and rely on different neuronal arrays. Taking up programming or learning languages is an excellent way to supplement this.
7. Stimulate and unleash your right-brain by learning a new instrument, drawing, painting, or writing (blogging, even)
repeat
These simple tips, combined with regular laughter and joy, can help you stay focused and sharp for your whole life.
Labels: alzheimers, brain, brain_games, curcumin, tips
// posted by neurofuture11:14 AM permanent link
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12.03.2006
Chemotherapy Shrinks brain and Impacts cognitive ability
>
Researchers have linked chemotherapy with short-term structural changes in cognitive areas of the brain, according to a new study. Published in the January 1, 2007 issue of CANCER, a peer-reviewed journal of the American Cancer Society, the study reveals that within 12 months of receiving adjuvant chemotherapy, significant regions of the brain associated with memory, analysis and other cognitive functions were significantly smaller in breast cancer patients who received chemotherapy than those who did not. Within four years after treatment, however, there were no differences in these same regions of the brain.
While the development of chemotherapy has had substantial and beneficial impact on cancer survival rates, it is also linked to significant short- and long-term adverse effects. Gastrointestinal complaints, immunosuppression, and painful mucositis, for example, are the immediate risks of the treatment.
Patients receiving chemotherapy have also long complained of problems with memory, problem-solving and other cognitive abilities. Although chemotherapy was thought not to affect brain cells due to the blood-brain barrier, recent clinical studies have confirmed declines in cognitive functions in patients receiving chemotherapy. Animal studies have shown physical changes in the brain and in neurons caused by chemotherapy drugs. In human studies, however, the little data that is available is only available through imaging and is not consistent in the long-term. In addition, lack of controls in studies makes it difficult discern cancer- versus drug-effects.
Led by Masatoshi Inagaki, M.D., Ph.D., of the Breast Cancer Survivors' Brain MRI Database Group in Japan, researchers used MRI to take high-resolution images and measure volumes in specific areas of the brain of breast cancer patients who received chemotherapy and those who did not one-year after surgery and three-years after surgery. In addition, they compared brains of cancer survivors one-year after surgery and three-years after surgery with healthy subjects.
They found that at one-year, patients treated with chemotherapy had smaller volumes in cognitively sensitive areas, such as the prefrontal, parahippocampal and cingulate gyri, and precuneus regions. However, at three-years post-surgery there was no volume differences. That there were no differences between cancer patients and healthy controls at any time point demonstrates that there is no observable cancer-effect in cognitive deficits.
Labels: alzheimers, brain, cancer, chemotherapy, cognitive
// posted by neurofuture3:16 PM permanent link
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11.25.2006
Read This Before You Sign up for that Space Flight!
>
--Even though astronauts have toured the universe for decades, scientists are just now beginning to understand how space's low gravity environment can affect the brain. New biological studies show that outer space, at least temporarily, impacts brain mechanisms involved in a variety of functions, including movement and navigation. The research may lead to the development of strategies that protect humans from the consequences of space travel as well as help those with related, earth-based ailments. In addition, the insights on the brain's ability to adapt to aspects of the space assault may help scientists find ways to initiate these adaptations in order to treat a variety of brain disorders.
If technology and science advance at a break-neck pace, recreational trips to outer space in this millennium are a good bet. But before you place a deposit on that moon-travel special, consider how the unusual change in environment, particularly the warp in gravity, could tinker with your brain.
On Earth, gravity's invisible downward force draws us toward the center of the planet and holds us on the surface. This pull, however, barely registers in space.
An increasing amount of biological evidence is now indicating that space's skimpy gravity impacts the brain in a variety of ways. The discoveries are leading to:
An understanding of the importance of gravity on biological systems.
New insight into the brain's ability to adapt to even the strangest situations.
Clues on ways to ward off side effects of space flight as well as some related Earth-based ailments.
For years, researchers have seen signs that space affects the brain. For example, space travelers often experience stints of disorientation and weird visual illusions. They may feel upside down when they are right side up. Travelers also face space motion sickness, marked by dizziness and nausea, and brief disturbances in balance and movement, which occur both in space and upon return to Earth.
In the past few years, scientists decided to take a closer look. A slew of new biological studies now are confirming and starting to explain how space flight influences the brain.
Several experiments have uncovered changes that appear to underlie the movement and balance-related disturbances observed in astronants. One study found that, following 24 hours of space flight, rats had alterations in the cell organization of the cerebellum brain area. This region is critical for learning movements, coordination and balance. As a next step, the researchers are trying to determine if the changes are permanent, even after return to Earth, or whether the reworking of cell communication networks is temporary. Based on those results scientists may be able to find ways to speed up useful cell network adaptations in astronauts, as well as to slow down or prevent destructive adaptations. They also may be able to readjust brains that malfunction from various disorders experienced on Earth.
Other biological studies indicate that space also alters the brain's movement system by changing muscle activity. Unlike Earth, muscles in space don't have to push against a gravity force to maintain upright posture. Research shows that upon re-entry to Earth's environment the alterations trigger shortened steps and tremors. Currently, scientists are developing robotic devices that will train the astronauts' movement systems to better adapt to space flight. These devices may also help people with other types of movement problems that also possibly arise from diminished muscle use.
Other new biological evidence of space's impact relates to astronauts' feelings of disorientation. One study indicates that cells, dubbed place cells, located in the hippocampus brain area are involved. It's thought that place cell activity aids navigation by providing a sort of mental map of the enviornment. Scientists found, however, that the cell activity goes out of whack in rats during the early days of space flight when they try to complete a three-dimensional maze. Further insights may help researchers find ways to prevent disorientation in astronauts and tackle hippocampus-related disorders on Earth.
Early biological findings also hint that space may influence the overall activity of cells throughout the brain. A preliminary analysis of mice embryos collected in space uncovered alterations in some essentials of cell function, such as basic metabolic processes and internal movements of the cell nucleus. Researchers hope to determine if the changes also occur in adults and if they affect overall abilities.
These and other insights are launching the understanding of the brain into a new orbit, so hold on to your seat.
Specific brain areas that undergo changes when exposed to space flight include the cerebellum and hippocampus, according to new studies. The cerebellum, tucked away in the back of the brain, is important for coordination and balance. Deep in the brain, the seahorse-shaped hippocampus is critical for certain memory functions including those for navigation.
If technology and science advance at a break-neck pace, recreational trips to outer space in this millennium are a good bet. But before you place a deposit on that moon-travel special, consider how the unusual change in environment, particularly the warp in gravity, could tinker with your brain.
On Earth, gravity's invisible downward force draws us toward the center of the planet and holds us on the surface. This pull, however, barely registers in space.
An increasing amount of biological evidence is now indicating that space's skimpy gravity impacts the brain in a variety of ways. The discoveries are leading to:
An understanding of the importance of gravity on biological systems.
New insight into the brain's ability to adapt to even the strangest situations.
Clues on ways to ward off side effects of space flight as well as some related Earth-based ailments.
For years, researchers have seen signs that space affects the brain. For example, space travelers often experience stints of disorientation and weird visual illusions. They may feel upside down when they are right side up. Travelers also face space motion sickness, marked by dizziness and nausea, and brief disturbances in balance and movement, which occur both in space and upon return to Earth.
In the past few years, scientists decided to take a closer look. A slew of new biological studies now are confirming and starting to explain how space flight influences the brain.
Several experiments have uncovered changes that appear to underlie the movement and balance-related disturbances observed in astronants. One study found that, following 24 hours of space flight, rats had alterations in the cell organization of the cerebellum brain area. This region is critical for learning movements, coordination and balance. As a next step, the researchers are trying to determine if the changes are permanent, even after return to Earth, or whether the reworking of cell communication networks is temporary. Based on those results scientists may be able to find ways to speed up useful cell network adaptations in astronauts, as well as to slow down or prevent destructive adaptations. They also may be able to readjust brains that malfunction from various disorders experienced on Earth.
Other biological studies indicate that space also alters the brain's movement system by changing muscle activity. Unlike Earth, muscles in space don't have to push against a gravity force to maintain upright posture. Research shows that upon re-entry to Earth's environment the alterations trigger shortened steps and tremors. Currently, scientists are developing robotic devices that will train the astronauts' movement systems to better adapt to space flight. These devices may also help people with other types of movement problems that also possibly arise from diminished muscle use.
Other new biological evidence of space's impact relates to astronauts' feelings of disorientation. One study indicates that cells, dubbed place cells, located in the hippocampus brain area are involved. It's thought that place cell activity aids navigation by providing a sort of mental map of the enviornment. Scientists found, however, that the cell activity goes out of whack in rats during the early days of space flight when they try to complete a three-dimensional maze. Further insights may help researchers find ways to prevent disorientation in astronauts and tackle hippocampus-related disorders on Earth.
Early biological findings also hint that space may influence the overall activity of cells throughout the brain. A preliminary analysis of mice embryos collected in space uncovered alterations in some essentials of cell function, such as basic metabolic processes and internal movements of the cell nucleus. Researchers hope to determine if the changes also occur in adults and if they affect overall abilities.
These and other insights are launching the understanding of the brain into a new orbit, so hold on to your seat.
Specific brain areas that undergo changes when exposed to space flight include the cerebellum and hippocampus, according to new studies. The cerebellum, tucked away in the back of the brain, is important for coordination and balance. Deep in the brain, the seahorse-shaped hippocampus is critical for certain memory functions including those for navigation.
Labels: 2001, AI, algorithmic, alzheimers, brain, galactic, hal, neurons, rocket, space_odyssey, spaceflight, virgin, xprize
// posted by neurofuture4:15 PM permanent link
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11.21.2006
BACE gene leads to insight on Alzheimer's
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Canadian scientists have found a specific gene which they believe may hold the key to the degenerative brain disorder Alzheimer's disease.
Lead researcher Weihong Song, a professor of psychiatry who holds a Canada Research Chair in Alzheimer's disease at the University of British Columbia in Vancouver, says the results of their study with mice found that lower oxygen levels (hypoxia) increased the activity of a specific gene.
The gene called BACE 1, encodes a protein that converts the precursor amyloid molecule to the more dangerous beta-amyloid form.
Professor Song says if blood to the brain is less oxygenated it may mean a build-up of the protein plaques that are so closely tied to Alzheimer's disease
In mice, hypoxia was found to increase amyloid plaque formation and memory loss.
The fact that lowered brain-oxygen levels, caused by reduced blood flow, increases the risk of Alzheimer's disease has been observed by other scientists along with greater propensity for stroke. It would seem that exercise would be the most effective preventative.
The study is published in the current issue of the Proceedings of the National Academy of Sciences.
Lead researcher Weihong Song, a professor of psychiatry who holds a Canada Research Chair in Alzheimer's disease at the University of British Columbia in Vancouver, says the results of their study with mice found that lower oxygen levels (hypoxia) increased the activity of a specific gene.
The gene called BACE 1, encodes a protein that converts the precursor amyloid molecule to the more dangerous beta-amyloid form.
Professor Song says if blood to the brain is less oxygenated it may mean a build-up of the protein plaques that are so closely tied to Alzheimer's disease
In mice, hypoxia was found to increase amyloid plaque formation and memory loss.
The fact that lowered brain-oxygen levels, caused by reduced blood flow, increases the risk of Alzheimer's disease has been observed by other scientists along with greater propensity for stroke. It would seem that exercise would be the most effective preventative.
The study is published in the current issue of the Proceedings of the National Academy of Sciences.
Labels: alzheimers, brain, canada, oxygen, vancouver
// posted by neurofuture10:45 PM permanent link
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5.31.2006
MemoryTV News Blast on Memorypix
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Memorytv (Memory TV) take favorite images and enjoy a memory game, scientifically-validated. Here's the current list of exercises.
Labels: alzheimers, brain, cognitive_labs, memory_test, memorytv
// posted by neurofuture3:00 PM permanent link
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