Cognitive Labs

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

Labels: alzheimers, helmet, infrared, led, sunderland

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

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

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

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.

Labels: alzheimers, budget, expenses, stages

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

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

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

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

Motorcycle Repair Coping with Alzheimer's Disease

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

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

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 descentthat 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

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.

Labels: alzheimers, chicago, tribune

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

Labels: alzheimers, brain, nytimes, onset

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

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

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

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."

Labels: 1984, alzheimers, brain

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.

Labels: alzheimers, gompertz, life expectancy

Melatonin, derived from getting adequate rest - may help delay or prevent Alzheimers according to this study.

Labels: alzheimers, baby, melatonin, sleep, sleep deprivation

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.

Labels: alzheimers, suntimes, thetripover

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

Flourizan, from Myriad Genetics, may offer an opportunity to turn back the tide of Alzheimer's progression.

Labels: alzheimers, myriad genetics

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

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.

Labels: alzheimers, implants, surveillance

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

A new treatment for Alzheimer's was approv