How did we develop the ability to talk and to walk on two legs, yet be the only organism that seems vulnerable to neurodegenerative diseases such as Alzheimer's? A new paper reviews several studies that show how genes can explain what makes our brains unique.
The genomics revolution has made it possible to explore another dimension of evolution - how gene expression levels changed over time. These studies show that our brain evolved differently to the rest of our body. Increases in gene levels in the adult brain in human evolution were more pronounced than in chimpanzee evolution, whereas other tissues show similar numbers of genes with increased and decreased expression levels.
Authors of the paper are: Daniel H. Geschwind, associate professor-in-residence, department of neurology, David Geffen School of Medicine at UCLA; and Todd M. Preuss, Division of Neuroscience & Center for Behavioral Neuroscience, Yerkes National Primate Research Center, Emory University.
The article appears in the Nov. online edition of the peer-reviewed journal Nature Reviews Genetics.
We all know that too much stress isn't healthy. Now, intriguing scientific evidence shows that chronic stress may accelerate aging in our immune cells.
Prof. Elissa Epel of University of California, San Francisco, may have found new evidence of how stress wears us down by making the immune cells in our bodies age prematurely.
Epel's team followed 58 mothers, 39 of whom were caring for a chronically ill child. Most of them reported higher stress levels than mothers with healthy children.
But when researchers looked at the DNA in their immune cells, they noticed a stunning finding. The telomeres, or biological clocks, in the cells of the chronically stressed women were much shorter, indicating they had aged prematurely.
"We were flabbergasted. It was something you couldn't have expected to find," Epel says.
"We found that in women with the highest stress, they were so short that the cells had aged 10 years more than in the other women. That's not a matter of normal aging but from stress."
The authors say "the exact mechanism that connect the mind and the cell are unknown." But they will now begin work to see if other types of cells are affected by stress.
The study is published in the Annals of Internal Medicine.
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Here is a useful survey of some of the leading candidates for successful development of memory enhancers, pills where researchers are striving to enhance cognitive performance, inluding some discussion of well-known natural compounds such as Gingko Biloba. Lastly, cognitive exercise is covered, having the benefit of being non-chemical in nature. As in all cases, early detection appears to be the key to effective prevention and treatment.
With new insight into the mechanisms that help keep your brain sharp, neurological researchers move closer to improving your recall with a 'memory pill'
To say that Aplysia Californicus is one of nature's least glamorous beasts would be too kind. A hermaphroditic marine snail with mottled purple skin, it keeps to itself, responding to disturbances by emitting a murky fluid that stains the water around it. Its "brain," if you can call it that, is stunningly simple, with only a few thousand oversize neurons. It is not, in short, a likely candidate for glory in the animal kingdom. But a few years from now, much of the baby-boom generation may be greatly indebted to this unprepossessing little creature. Aplysia may look homely, but to scientists hoping to develop memory-enhancing medicine, it is a thing of beauty.
Thanks to the neurological research of Nobel laureate Eric Kandel and others, Aplysia's minimal nervous system is helping scientists to make sense of how memory works on the biochemical level. The molecules of memory in sea slugs, it turns out, aren't that different from some of those in humans. They are now one of the many inspirations for drugs that may someday ward off the forgetfulness that plagues so many people as they grow older. As Americans' average age creeps upward, the search for medicines that will keep them sharp is accelerating. "We're all very, very avidly grinding up cells trying to get at the molecules," says Dr. Scott Small of Columbia University Medical Center.
No pill to improve memory, aside from alternative remedies of dubious effectiveness, is currently on the market. But several small biotech companies are launching drugs grounded in the latest research, with a few already in the early stages of clinical trials that could be finished in as little as "two years, if we're lucky," says Kandel, who is now at CUMC and the Howard Hughes Medical Institute. Some of the most promising candidates have their roots in Aplysia studies. Others take their cues from even more improbable sources like the molecular consequences of smoking, focusing on some of the same receptors that nicotine targets. (Who knew it had benefits?) "These are very exciting times for treating memory loss," says Steven Siegelbaum, a neuroscientist at CUMC and HHMI. And with trials soon to yield results, they're about to get even more exciting.
It has been a long, hard slog to reach this point. Scientists now know that the brain-relying on chemical cascades kicked off by neurotransmitters-first stores short-term information in the prefrontal cortex and then transforms selected bits into long-term memories via the hippocampus, a sea-horse-shaped region tucked deep in the folds of the temporal lobe above the ear. Even such fundamental knowledge was unthinkable some 30 years ago. The concept of memory is so complex that many midcentury researchers shied away from studying it, claiming any attempt would be an example of futile reductionism. Little progress was made before 1953, when one of medicine's more famous patients arrived on the scene. An epileptic, H.M. suffered intractable, frequent seizures until he had both of his temporal lobes removed. Now deprived of his hippocampus, H.M., like the protagonists of the movies "Memento" and "50 First Dates," was unable to form new memories of people, places or things.
The unfortunate patient's case clearly signaled that the hippocampus played a central role in memory formation. But two more decades would go by before researchers figured out why or how. "The biology of memory storage was really a black hole," says Kandel. "We knew very little about it 25 years ago." Kandel's idea-to use a deceptively simple organism to solve a complex problem-met with skepticism. No wonder, says Siegelbaum, a longtime collaborator of Kandel's: "Most people were working on very basic problems. It was sort of an audacious goal at the time."
But audacious goals often drive equally audacious science, and Kandel, working with his sea snails, was on to something. Because the snails had such large neurons, and so few of them, Kandel was able to identify the individual nerve cells responsible for specific behaviors. Those nerve cells appeared to rely on some of the same biochemical processes that power the brains of more-advanced animals. Aplysia californicus turned out to be a good model for molecular memory processes in humans. Both species rely on the neural messenger cyclic AMP, which modulates a protein called CREB that can turn genes on or off. CREB is the brain's sculptor: it forms memories by reshaping the synapses, or spaces between neurons. So changes in cyclic AMP levels-and corresponding changes in CREB levels-affect the brain's ability to remodel its synapses. Less CREB equals less memory-making ability.
The practical results of this work, as well as extensive follow-up tests in mice and rats, are several new drugs now in early development at Memory Pharmaceuticals, founded in part by Kandel in 1998. MEM1414 is the inheritor of the Aplysia findings. Cyclic AMP, the neurotransmitter that dictates CREB levels, is normally degraded in the brain by enzymes called phosphodiesterases. By inhibiting those enzymes' activity, MEM14 appears to boost CREB levels and enhance the brain's long-term memory functions; researchers hope it will enhance long-term memory in patients with age-related forgetfulness and even ward off the early stages of Alzheimer's disease, even though the two ailments are not related. There's also MEM1917, a drug similar to 1414; MEM1003, which protects neurons from damaging overloads of calcium, and MEM3454, a schizophrenia treatment that targets a receptor also known to respond to nicotine. Researchers think that some schizophrenics ease their symptoms, including loss of memory function, by self-medicating with cigarettes.
Other companies are also in the hunt. Helicon has a phosphodiesterase inhibitor of its own. Sention, cofounded by Mark Bear of the Picower Center for Learning and Memory at MIT, has gone chemically "upstream" of cyclic AMP and CREB, modulating the neurotransmitters that direct the synthesis of proteins the brain uses as the basic building blocks of memory. Its intriguing new drug, C105 (which is largely under wraps for now), is in phase II trials. Cortex Pharmaceuticals, one of the oldest memory-booster firms, is focusing elsewhere, on molecules called ampakines, which modulate "AMPA receptors" in the brain that can strengthen the synapses. The company already has one drug, CX516, through phase II trials, although it is too weak to be a practical prescription option. A revved-up version, CX717, is in the works, and several other companies are also developing their own ampakines.
Researchers are reluctant to sing the praises of any of these drugs just yet. A broad class of drugs called nootropics showed potential in the 1970s, but they were "shots in the dark," says Small, and they have since fallen out of favor with mainstream scientists. Rolipram, a drug originally intended to treat depression, works in much the same way the new phosphodiesterase inhibitors do. But its nasty side effects - patients inevitably throw up after taking it-have made it an impractical solution, and although still on the market, it is not indicated for memory boosting.
Alternative medicine has also offered remedies. Ginkgo biloba, the most well known, has been a favorite for centuries. But science has been unable to verify its effectiveness, and supplements sold over the counter are often coy about their contents; even if ginkgo does work, some pill versions may not contain enough of it to have any effect. The workable alternatives to alternative medicine, until now, have largely been limited to dozens of books containing mental gymnastics intended to keep the brain's gears well greased. There's compelling evidence for some of them, particularly crossword puzzles. Learning a new language may also be an effective memory booster. And the old saw about fish being "brain food" is also, in some respects, true-a diet heavy in omega-3 fatty acids keeps blood vessels in the brain clear of blockages, allowing the nerve cells to function to the best of their abilities. But none of these remedies can completely halt "mild cognitive impairment" in adults; they can only slow it down.
Alternative remedies and brainteasers do have one advantage-they don't raise the troubling prospect of otherwise healthy people using the drugs for a boost, like steroids for geeks. "There's a question of whether we should be in the business of making memory boosters in the first place. Once we're in a gray area we at least need to be careful," says Small. "With people who are impaired by a subtle but real change in their brain function, we might not want to sit in judgment and say, 'No, we can't help you.' But the fact that a high-school student can't do well on the SAT-is that a disease?"
Ethics questions, no matter how valid, aren't likely to keep scientists from doing the basic research that could underlie drug development. And even if that research never turns into anything in pharmaceutical form, it still holds plenty of exciting potential for those seeking to understand how memory works. Science may have made considerable progress since the '70s, but there is still much to be learned. Siegelbaum's and Kandel's labs have stumbled on to an intriguing and heretofore unknown property of ion channels, tiny protein-based structures that can transport small charged molecules across the membranes of cells. One particular type of channel is found, among other places, in the hippocampus. Lab-created mice that lack this type of channel seem to be smarter than your average mouse, especially at typical memory-based tasks like repeated mazes. The upshot: when the hippocampal channels are in use, they appear to hinder memory. It's a startling finding that could have major implications for brain science. "Why has evolution come up with this channel and put it in this region of the brain if it impairs memory?" Siegelbaum wonders. He suspects that neurotransmitters close the channels, rendering them moot, when the brain needs to remember something, but leave them open otherwise to screen out the ephemera of everyday life, the things that just aren't important enough to remember long-term. (If you remember where you were when JFK was shot, your channels were probably closed at the time. If you don't remember what you had for lunch last Wednesday, well, maybe they were closed on your lunch break.) If Siegelbaum is right, the channels offer a tantalizing possibility: what if scientists could create a drug that would close them on command, allowing for total recall? "It's a bit of a daunting task," says Siegelbaum. But whether there's a pill at the end or not, it's still great science-and that's always an audacious goal.
Well, we are on to the turkey sandwiches now, but keep these thoughts in mind for the rest of this holiday season, and as general guidelines throughout the year. All the Best to you and family throughout the season!
This may come as a surprise to you, but some of the foods most likely to enliven the holiday table are really good for you and can deliver a bundle of benefits to your heart and your brain. As a matter of fact, generally speaking, what's good for your heart is also good for your brain.
From stuffing to cranberries to red wine to hot chocolate, and even that last sip of coffee, there are many traditional dishes that boost blood flow to your most oxygen-hungry organs. These foods can preserve and even enhance mood, memory and other mental functions. Call them brain savers!
Take stuffing. Turkey’s traditional Thanksgiving partner - what makes turkey interesting at all to most people - is it is rich in antioxidants. Bread crust is packed with them, far more so than the less chewy inside of bread.
Antioxidants are premiere disease-fighters and anti-aging agents. They are compounds that scavenge free radicals of oxygen, unstable molecules given off by the body's many metabolic actions. Free radicals are thought to be responsible for making cholesterol harmful to arteries and the heart—and for impairing memory and movement with age. They are particularly drawn to the fat-rich membranes of nerve cells through which all brain activity takes place. They are implicated in immune dysfunction and in cataracts and macular degeneration of the eyes.
The body manufactures some antioxidants, although the brain needs to import those it needs from outside. Under conditions of stress, the body's ability to produce antioxidants is impaired. Fruits and vegetables are the richest source of antioxidants.
Cranberries virtually top the list of antioxidant-rich foods. Scientists recently developed a way of measuring the antioxidant content of foods, called ORAC, for Oxygen Radical Absorbance Capacity. Cranberries outpulled some highly touted antioxidant rich goodies, including strawberries, spinach, raspberries, broccoli, beets, red grapes and cherries, among 11 others.
High-ORAC food may help slow the aging process in both body and brain. Most Americans average about 1,670 ORAC units daily. Increasing fruit and vegetable intake can double antioxidant activity. One cup of blueberries—first cousin to the cranberry—alone supplies 3,200 ORAC units.
Studies in animals suggest that cranberries are particularly neuro-protective, good at protecting against chronic age-related afflictions like loss of coordination and memory. They protect brain cells from the free-radical damage that normally occurs over time, thereby preserving cognitive and motor functions.
Compared with animals fed a standard diet, aging animals given cranberries showed actual improvements in normal age-related declines in working memory, reference memory, balance and coordination. They were able to keep on learning.
The antioxidants in cranberries belong to a group of chemicals called phenols. The strongest of these, and most extensively studied, are procyanidins and anthocyanidins, which give cranberries and blueberries their deep color. They seem to be particularly adept at turning off a brain enzyme (xanthine oxidase) that actually stimulates the creation of free radicals of oxygen.
But, there are many other antioxidants in cranberries, and they are just now coming under scrutiny for their function. Researchers increasingly believe the combinations of nutrients found in food are more protective than individual nutrients taken alone.
One antioxidant compound in cranberries actually helps ward off urinary tract infections. It actually blocks some harmful bacteria from attaching to the cells lining the urinary tract.
Cranberries are so powerful in preserving brain function, researchers recently found, that by their antioxidant action they can reduce the severity of brain impairment following strokes. They protect against the brain cell damage that usually occurs in the early stages after a stroke. Exposure to a concentration of cranberry extract equivalent to about half a cup of whole cranberries resulted in a 50 percent reduction in brain cell death.
And, go ahead, finish it all off with a cup or two of coffee. Researchers have recently identified a new antioxidant in coffee that is particularly potent in preventing colon cancer.
Or, savor a cup of hot cocoa. Made with about two tablespoons of pure cocoa powder, it tops both red wine and tea in antioxidant power—two times more than red wine, two to three times more than green tea and up to five times more than black tea. Something about heating the cocoa brings out the antioxidants in it!
In addition to Paypal at cognitivelabs, our main purchase function at cognitivecare.com should be accepting non-U.S. orders now, after some downtime. Please give it a try! Thanks
Scientists have identified a new, longer species of amyloid beta-peptide that has the potential to be a new target for the treatment of Alzheimer's disease, according to research published in the Journal of Biological Chemistry, an American Society for Biochemistry and Molecular Biology journal.
Scientists have identified a new, longer species of amyloid beta-peptide that has the potential to be a new target for the treatment of Alzheimer's disease, according to research published in the Journal of Biological Chemistry, an American Society for Biochemistry and Molecular Biology journal.
One of the characteristic features of Alzheimer's disease is the deposition of amyloid beta-peptides in the brain. These amyloid beta-peptides are derived from a large amyloid precursor protein through a series of cleavage events.
Under normal conditions, cleavage first by alpha-secretase and then by gamma-secretase results in a soluble ectodomain, a short peptide called p3, and an intracellular C-terminal domain, none of which are amyloidogenic.
Alternatively, amyloid precursor protein can be processed by the enzymes beta-secretase and gamma-secretase to produce a soluble ectodomain along with the full-length amyloidogenic amyloid beta-peptide and the intracellular C-terminal domain.
Although amyloid precursor protein is found in many cells, its normal biological function is not well understood.
While the exact pathogenic role of amyloid beta-peptide in Alzheimer's disease has not yet been definitely established, accumulating evidence supports the hypothesis that amyloid beta-peptide production and deposition in the brain could be a causative event in Alzheimer's disease.
Dr Xuemin Xu of the University of Tennessee explains that the literature indicates amyloid beta-peptide itself could be toxic to synapses and the accumulation of amyloid beta-peptide could initiate a series of events contributing to cell death, including activation of cell death programs, oxidation of lipids and disruption of cell membranes, an inflammatory response, and possibly neurofibrillary tangle formation, which is a close correlate
The inventor of the monotonous "K rations" and also the Mediterranean Diet, has passed on at the age of 100. What is beneficial for the heart is good for the cognitive processes....
Ancel Keys, a University of Minnesota public health scientist who invented the K rations consumed by millions of soldiers in World War II, discovered that saturated fat was a major cause of heart disease and championed the benefits of the Mediterranean diet, died Nov. 20 at his home in Minneapolis. He was 100.
No cause of death was reported, but in recent years, Dr. Keys had several strokes and broke a hip. He was still at work earlier this year, analyzing data from his landmark epidemiological study, begun in 1958, of 12,000 middle-aged men living in Italy, the Greek islands, Yugoslavia, the Netherlands, Finland, Japan and the United States.
That "Seven Countries Study" provided evidence that a diet rich in vegetables, fruit, pasta, bread and olive oil and sparing of meat, eggs, butter and dairy products reduces the occurrence of heart disease.
"He was a giant in the field of nutrition in a variety of ways," said Walter C. Willett, chairman of the nutrition department at the Harvard School of Public Health. "His studies held up in the big picture, yes. He missed some things that are important. Smoking and obesity didn't show up. But the basic conclusion is . . . the vast majority of heart disease is preventable."
Why are we using technology more? What are the limits, and what are the effects? How do generations differ in their use of computers and mobile phones, "wired homes" and other science-fictional technologies?
We spend much time thinking through all these possibilities and the points of intersection. Once in a while we catch something that necessitates pondering and a response, as in this article in Always-On. There is so much focus on how 18 year olds use technology that we forget to consider that use depends on people, more than any particular age group.
To that article, we posted this response (you can see it at the bottom of that page if you like)has caused a lot of visitors to come over here :
The over 35 group (I am one of them, just barely) will be the surprise growth group. Everyone knows that under 25 is the future, hence all the focus on youth and products for youth.
However, increasing digital ubiquity is rapidly affecting the middle aged and aging. Why?
1. increasing bandwidth everywhere means more decentralization of work output, extension of output
2. increasing bandwidth means 'friendlier' rich applications become legion (e.g., Flash)
3. increasing bandwidth plus social networks and RSS drive knowledge diffusion and fuel demand for niche products.
broadband health, knowledge, and other personal improvement products will start to proliferate, that depend on continuous connectivity.
In health, http://www.cognitivelabs.com is just one of these...984,628 members with both bioinformatic applications and broadband consumer aps.
that last figure is dated...
got any thoughts in this area - send them to us at email@example.com and we'll share them.
advent | POSTED: 10.19.04 @12:41
If you interested, we've just posted the top referring web sites for our network... you can see it here...
The U.S. Congress has passed legislation that will make early stage memory screening the norm, and in fact, will drive awareness of the simple actions, lifestyle choices, and preventative measures people can take to detect and avert early memory loss. Many health practitioners are recommending screening as early as possible. Dr. Bill Thies of the Alzheimer's Association is spot-on with his suggestion to walk, walk, walk your way to a healthy mind. We have been involved in this process indirectly, evidenced by the many, many House.Gov hits on our secure testing website and our company website.
If you have not joined at one of our membership levels, now would be the opportune time to help support us in our work. If you have already taken the free test,please go here. If you haven't, please click on the 'free test' link in the right margin.
Thanks for your support!
>>Read more from PR Newswire>>
A Higher Body Mass Index (BMI) can be an indicator of Memory Loss and Alzheimer's, according to a new study in Neurology. Researchers in Sweden have discovered that long-term obesity in women seems to be associated with brain atrophy and onset of memory impairment at increased frequency compared with women of lower relative body mass. While the study followed women, one could come to the conclusion that excess weight, particularly for middle aged or older peoople, should be avoided.
(AP) Nov. 22, 2004 - Obesity is harmful to the brain for women, but it doesn't appear to raise the risk of dying for men who have suffered heart attacks, according to two new studies.
Swedish researchers say that women who have been obese throughout their lives are more likely to lose brain tissue in the temporal lobe compared with women of normal weight. Loss of brain tissue has been linked to cognitive decline and an increased risk for Alzheimer's disease.
Obesity is a well-known risk factor for heart disease, but a separate study surprised researchers by finding that it didn't increase the risk of death in men who had already suffered a heart attack.
The Swedish paper "is the first study to show [that] a higher body mass index is related to brain atrophy," said lead researcher Deborah Gustafson, a psychiatrist at Sahlgrenska University Hospital in Göteborg.
The only significant relationship between body mass index (BMI) and brain atrophy was found in the temporal lobe, Gustafson said. "The temporal lobe is important for a number of reasons, including hearing, speech, language, comprehension, naming, memory, and visual processing of, for example, faces," she said.
BMI is a height-to-weight ratio to determine whether someone is of healthy weight; a BMI of 25 -- a 5-foot, 7-inch person weighing 160 pounds -- or above is considered to be overweight, while a BMI of 30 -- a person of the same height weighing 190 pounds -- or higher is deemed to be obese. Increased BMI accounted for about 8 percent of all dementia, Gustafson added.
In their study, Gustafson and her colleagues collected data on 290 Swedish women born between 1908 and 1922. Each woman had four exams between 1968 and 1992. At the last exam, they underwent a CT scan to determine if they had lost any brain tissue during the 24 years of follow-up, according to the report in the Nov. 23 issue of Neurology.
The researchers found that a higher BMI was directly linked to loss of brain tissue. "BMI was related to 11 to 14 percent higher odds of temporal lobe atrophy per one unit of [increased] BMI," Gustafson said. "Women who were, on average, heavier were more likely to have temporal lobe atrophy."
However, the amount of atrophy was not related to increasing levels of BMI, Gustafson said. "In other words, those women with more severe temporal lobe atrophy did not have a higher BMI compared to women with mild atrophy," she explained.
Gustafson speculated that the connection between BMI and loss of brain tissue may be due to fat causing more oxidative stress, resulting in an increase of free radicals in the body. Another reason may be because fat leads to atherosclerosis, which can limit oxygen flow to the brain. Still another possibility may be that fat causes the release of hormones and growth factors that are harmful to brain tissue, causing brain atrophy.
According to Gustafson, it is not known whether these results apply to men, or if the effect can be modified by losing weight.
"However, maintaining a healthy body weight over the course of one's life may decrease the odds of temporal lobe atrophy and subsequent dementia," Gustafson said.
"This finding fits logically with a previous paper that showed that BMI correlates with Alzheimer's disease," said William Thies, vice president for medical and scientific affairs at the Alzheimer's Association. "People with high BMI at middle age have more Alzheimer's disease."
Moreover, these findings support the need for more public education in how to maintain a healthy brain, Thies added. "Our Maintain Your Brain program tries to get people to understand that relatively simple interventions can make a profound difference in some of the risk factors that contribute to public health," he said.
For the heart attack-obesity study, researchers collected data on 5,010 middle-aged and older men who participated in the Physicians' Health Study, according to the report in the Nov. 22 issue of the Archives of Internal Medicine.
According to the study results, men with a BMI of 28 or greater and who had had a heart attack or stroke did not have a significantly greater risk of death from cardiovascular disease compared with thinner men.
The finding was surprising, said co-author Howard D. Sesso, an assistant professor of medicine at Harvard Medical School. "One always assumes that when we deal with obesity, higher is always worse," he said.
"Our finding doesn't suggest that there are benefits to being heavier," Sesso said. "But that there was no added risk was surprising. Of course, these are men who had likely felt the impact of being obese in the first place."
Sesso believes that some of these men may have lost weight since their heart attack or stroke. In addition, treatment with medication to prevent a second heart attack or stroke may play a role in their reduced risk of death, he said.
It is not clear if the effect is the same for obese women after having a heart attack or stroke, Sesso said.
"It is not our desire to downplay the role of being heavy," Sesso explained. "We would like to replicate these findings," he said.
All around the US traditional football games were the rule yesterday. Harvard-Yale, California-Stanford (22 years after the play)| listen Ohio State-Michigan, Oregon-Oregon State, Washington-Washington State, Duke-North Carolina, Vanderbilt-Tennessee, and others. Above, California QB Aaron Rodgers hoisted aloft, holds a rose in what would could the team's first appearance in the Rose Bowl since 1959 and the days of Joe Kapp. Along the way, memories have been created for millions of fans across the U.S. Now you can take action to preserve all your memories through MemCheck, including our free trial.
Researchers at Columbia detect differences in the brains of people carrying the APOE genetic marker who showed no symptoms and were not picked up by standard paper-based tests. Our research shows MemCheck to be sensitive in these situations. So, there is one more reason to start your program today if you have already taken one of our free tests.
Using brain imaging, researchers at Columbia University Medical Center (CUMC) have found clear differences in brain function between healthy people who carry a genetic risk factor for Alzheimer's disease and those who lack the factor.
Because researchers believe that Alzheimer's disease starts changing the brain years before any symptoms appear, the disease may be most amenable to treatment in these pre-clinical stages. If so, detecting the early changes will be crucial for future therapies.
People who carry the genetic risk factor, the e4 allele of the Apolipoprotein (APOE) gene, have higher risk of developing the disease than non-carriers and usually show symptoms earlier.
"It is possible that what we're seeing in the APOE-e4 carriers are early changes in the brain caused by Alzheimer's disease," says the study's senior author, Yaakov Stern, Ph.D., of CUMC's Taub Institute and Sergievsky Center.
But he and the study's first author, Nikolaos Scarmeas, M.D., caution that more research is needed before it's known for certain if the difference is an early sign of Alzheimer's. "It's also possible that the brain differences we see are related to the APOE gene but are not necessarily directly related to incipient Alzheimer's," says Dr. Scarmeas, a neurologist in the Taub Institute, Sergievsky Center and neurology department. "Even so, the differences we've found may provide information on how the å4 allele predisposes carriers to Alzheimer's disease."
The present study appears in the Nov.-Dec. 2004 issue of the American Journal of Geriatric Psychiatry.
In the news, Google recently bought a company called Keyhole which has a cool satellite-imaging technology allowing you to fly over landscapes and perhaps, pick out the best fishing spots in the Desolation Wilderness or maybe in the more remote South Warner Range. I caught their demonstration at the VentureOne Conference in SF in April of this year. They were in the same track as my pals at GameXStream, in the search for more money. Try it out, and get your own birds eye, high-res view.
Full size picture, high pressure zone over California
The new and improved MemCheck 1.1 soon to be announced will include support for languages including Japanese, Korean, (simplified) Chinese and European Union languages. We had a cultural interface expert review our tests and deem them culturally ubiquitous, since they are based on nuances of symbol and geometric pattern recognition and recall patterns - which are patented. Bringing parts of our service to a global audience is really exciting, we have had inquiries from Honduras to Zimbabwe to Saudi Arabia, and now it will be fun to start helping people everywhere.
Understanding changes in the brain as we age or are subject to stresses seems to be critical in developing a wholistic view of cognitive processes. Perhaps, through closer study of such processes from divergent perspectives and using comparative research methods and subjects with differing conditions insight can be shed on the early stages of Alzheimer's formation. In that spirit, NASA researchers in Mountain View, CA (where we are also 'based!')are investigating the brain of the man who was the model for the character "Rain Main" in the well-known film.
SALT LAKE CITY, Utah (AP) -- NASA scientists are studying the man who was the basis for Dustin Hoffman's character in the 1988 film "Rain Man," hoping that technology used to study the effects of space travel on the brain will help explain his mental capabilities.
Last week, researchers had autistic savant Kim Peek undergo a series of tests including computerized tomography and magnetic resonance imaging, the results of which will be melded to create a three-dimensional look at his brain structure.
The researchers want to compare a series of MRI images taken in 1988 by Dr. Dan Christensen, Peek's neuropsychiatrist at the University of Utah, to see what has since changed within his brain.
Not only are Peek's brain and his abilities unique, noted Richard D. Boyle, director of the California center performing the scans, but he seems to be getting smarter in his specialty areas as he ages.
The 53-year-old Peek is called a "mega-savant" because he is a genius in about 15 different subjects, from history and literature and geography to numbers, sports, music and dates. But he also is severely limited in other ways, like not being able to find the silverware drawer at home or dressing himself.
"The goal is to measure what happens in Kim's brain when he expresses things and when he thinks about them," said his father, Fran.
Photo credit: CNN International
This story has been much in the headlines over the past few days. Our take after speaking with numerous physicians including some of our advisory board members is that probably more research needs to be done before one could make so definitive a claim. Other studies have (see Google, I have typed in the keywords for you) shown numerous positive benefits. In taking Vitamin E, as in all things in life, the best policy is one of judicious prudence, or moderation. Nevertheless, I am excerpting the story below for your perusal:
NEW ORLEANS, Louisiana (Reuters) -- Vitamin E supplements, which millions take in the hope of longer, healthier lives, may do more harm than good, researchers reported on Wednesday.
In fact, people taking high doses of vitamin E may in some cases be more likely to die earlier, although the reasons are not clear, said Dr. Edgar Miller of Johns Hopkins University in Baltimore, who led the study.
"I think people take vitamin E because they think it is going to make you live longer, but this (study) doesn't support that," Miller told reporters.
The Council for Responsible Nutrition, a trade group for supplement makers, criticized the report.
"This is an unfortunate misdirection of science in an attempt to make something out of nothing for the sake of headlines," said the group's John Hathcock.
Miller and colleagues re-analyzed 19 studies of vitamin E and health between 1993 and 2004. The trials involved more than 136,000 mostly elderly patients in North America, Europe and China.
People who took 200 international units of vitamin E a day or more died at a higher rate during the study, which lasted three years, than people who did not take supplements, they told a meeting of the American Heart Association.
"It's about a 5 percent increased risk at 45 years in the trials pooled together," Miller said.
"That doesn't sound like a lot but if you apply it to 25 percent of the (U.S.) adult population taking vitamin E, that is significant."
This piece from USA Today (which we are posting from the Alzheimer's Association's quality website) illustrates the increasing focus on maintaining and preserving the brain and our cognitive performance as we grow older. It is probably never too early to get started. Test, games and activities that engage and enable monitoring over time are important.
That climb looked difficult, didn't it? It can't be that hard to preserve your cognitive health. How about a quick workout?
Wait a minute. Is that a workout? Or is it a 80's MTV video of the GoGo's Vacation?
Nov. 15, 2004
More than half of Americans polled say they make an effort to engage in activities that help boost memory, according to a survey released today by the Alzheimer's Association. The telephone survey of 1,000 adults age 18 and older found that 52 percent said they did crossword puzzles or other activities known to keep the brain in shape.
Alzheimer's disease affects 4.5 million Americans today and is expected to explode in the near future. Age and family history are risk factors for the disease, but new research has increasingly shown that lifestyle factors may also play a role in the development of Alzheimer's, which causes memory loss and confusion.
Older adults were more likely than younger people to engage in brain-building activities: the survey found that 63 percent of people age 65 and older did so, compared with only 34 percent of people ages 18 to 44. Activities included: reading, doing crossword puzzles or playing games. The survey, conducted by Synovate's Telenation, also found that 77 percent of all those surveyed said they made an effort to eat a healthy diet, and 57 percent said they walked a mile or more.
Research suggests that a healthy diet and physical activity also may help stave off Alzheimer's, says Sam Gandy, a neurologist and spokesman for the Alzheimer's Association.
Today so far is the busiest we have yet encountered, with hundreds of people signing up and taking tests. That's because today is national memory screening day, where non-profits such as the Alzheimer's Association are focused on raising awareness about Alzheimer's. Thanks for your support. Remember to spread the word about our services. Unlike some other new sites, our tests are supported by research and protected by U.S. patents. So, come back to the original source. More updates will come. :-)
The day to day toll of memory loss changes lives in ways that are difficult to measure at first. The effects may be observed subtly through third parties before the realization comes that one is in fact in the grip of serious and, for now, incurable disease. That's why early detection through self awareness is so important. Ray Kurzweil and Terry Grossman in their new book Fantastic Voyage propose a program for detecting and defeating most ills of the body before their effects are rampant, through a philosophy of 'programming' the body with carefully assessed nutrition, coupled with moderate exercise for mind and physique, and active monitoring.
Living with Alzheimer's disease
By SALLY FRIEDMAN
Burlington County Times
MEDFORD - One day, Rosemary Kane got a call from her husband's boss. It was hardly the sort a wife would want to receive.
Her husband Dennis was making a lot of mistakes in his management job with a major company, and the boss was concerned.
The ultimate diagnosis was that at 55, Dennis Kane was in the early stages of Alzheimer's disease.
Yesterday, Rosemary Kane and her two daughters were at Lenape High School attending the daylong annual Caregiver Conference presented by the Alzheimer Association's Dela-ware Valley chapter. They were among about 175 others who have come to learn more about the disease that has changed their lives.
Cendant Mortgage was the presenting sponsor of the conference. Media sponsor was the Burlington County Times. Oth-er sponsors included Fox Re-habilitation Services, Genesis Health Care, Home Instead Se-nior Care, Kennedy Health Sys-tem, Moorestown Visiting Nurse Association/Hospice, Sa-maritan Hospice and Univer-sity of Medicine and Denistry of New Jersey-School of Osteo-pathic Medicine's Center for Aging.
"My entire life is now wrapped around my husband's needs. He is my full-time job," said Kane, an Atco resident who has given up her own job to care for her husband. Her story detailing several years of ex-haustion, sleepless nights and constant anxiety was repeated by others at yesterday's event.
"We're secondary caregivers," said Denise Geoghegan of Evesham, who, with her sister, Bridget Christy, helps with her father's care as much as she can. The sisters were instrumental in starting a support group for children of early-onset Alzheimer's patients. "The group has been a wonderful support, and our monthly meetings help us enormously, just like today's conference," said Geoghegan.
A new diagnostic method based on nanotechnology and analysis of the blood could be in the offing in the struggle against Alzheimer's, so reports the BBC. If it advances through trials, it is still probably several years away from effective deployment, but worth close monitoring.
By Paul Rincon
BBC News science reporter
A new nanotechnology-based technique could lead to a test for diagnosing the early signs of Alzheimer's disease.
The Bio-Barcode-Assay can recognise ADDL, a protein that accumulates in the brains of sufferers.
It is a million times more sensitive than conventional tests and could revolutionise disease detection.
In future, it might form the basis not only of a test for Alzheimer's but also for types of cancer, the human form of mad cow disease and HIV.
"The next exciting step would be to move to blood. If you detect it in blood, you have a huge win," said Professor Chad Mirkin. Details of the technique have been outlined at a one-day conference in London.
Doctors currently have no way of diagnosing Alzheimer's disease in their patients. The disease can only be confirmed after death, by studying brain tissue.
"Diagnosis [of Alzheimer's] is 100% accurate post-mortem. What you want is the ability to detect the marker so you can begin to think about new types of therapies," said Professor Chad Mirkin, of Northwestern University in Evanston, US.
Professor Mirkin and his research group at Northwestern developed the highly sensitive test by manipulating molecules at the nanometre scale (one billionth of a metre).
"We have done the first set of experiments that quantify the number of ADDLs in cerebrospinal fluid," Professor Mirkin said.
ADDLs are protein bundles which attack nerve synapses in the brains of people with Alzheimer's.
"Nobody is able to study this with the existing tools. A nanotechnology-enabled tool is allowing us to study these kinds of markers and link them to disease.
"The next exciting step would be to move to blood. If you detect it in blood, you have a huge win."
To perform a Bio-Barcode-Assay, researchers select antibodies on the basis of the biomarker they need to detect in a solution.
Some antibodies are fixed to magnetic particles while others are attached to spherical gold particles just 30 nanometres in diameter. Strands of DNA are fixed to the gold nanoparticle.
When antibodies bind to a target biomarker, it becomes sandwiched between a magnetic particle on one side, and a gold particle and its strands of DNA on the other.
Applying a magnetic field brings this entire "complex" out of solution. Researchers then release the DNA strands and use a DNA detection device to recognise their signature sequences.
A research assay could be available to scientists within a year, Professor Mirkin said. A clinical assay could be commercialised within two, he added.
Professor Mirkin said it could also lead to a test to diagnose breast cancer by detecting the faint presence of a protein called PSA, normally associated with prostate cancer in men.
It could also form the basis of a new test for HIV and other diseases in blood screening.
The test could be used in GPs' surgeries as well as hospitals, or even by members of the public at home.
Memory loss is truly a global problem, 4-5 Million Americans have Alzheimer's, up to 16 Million Worldwide, with almost 300 Million people potentially impacted by some degree of early memory loss. Adjusting lifestyle and other factors can help.
From the Press Trust of India:
Today, it is estimated that over 4 million Americans suffer from Alzheimer's disease. A progressive, degenerative disorder of the brain, Alzheimer's robs individuals of their memory and their mental and physical functions, leading to increasing dependence on others for care. Factors such as age and family history can contribute to the risk of developing this disease. While no cure exists yet, researchers are learning more about this disease and how to enhance the quality of life for those with Alzheimer's.
President Reagan believed in the courage and capacity of the American people to overcome any obstacle.
The National Institutes of Health plans to spend $680 million in Alzheimer's research in 2004 and an estimated $699 million in 2005, a 33 percent increase from 2001. The National Institutes of Health, along with the Department of Veterans Affairs, is testing drugs for prevention and treatment of Alzheimer's disease.
This year, the National Institute on Aging launched the Alzheimer's Disease Neuroimaging Initiative, an innovative partnership with the private sector that is using the latest technologies to observe changes in the brains of individuals who are affected by Alzheimer's. This project is researching ways to enhance early diagnosis and further the development of treatments.
In addition, the Administration on Aging is working with States to improve home and community-based services for people with dementia and their families.
Today we are upgrading the database and also going to launch a new site, veteransmemorycheck.com, where veterans can come and get a free memory check. It's the least we can do. Please help us to help veterans by supporting us, the easiest way being to subscribe to MemCheck, the best deal overall is $69.95 which, actually, works out to about 18 cents per day. Not very much, but, it will help us continue to grow and expand our services. A heartfelt thanks to those who have subscribed since Monday.
We have reached 100 new users again for the day. Also, we are upgrading cognitivelabs.com with a new online store, plus, we are readying a world service center, with new languages, just finished Francais and Korean. We are having a few DB issues concerning international orders. I heard from Celine in France about this, merci. Thanks for your support!
Here are new insights into understanding changes in learning and memory.
By analyzing the effects of altered neuronal function in mice, researchers have gained new understanding of how changes in a particular neuronal characteristic, neuronal excitability, may negatively impact learning and memory as we age. The work is reported by Geoffrey Murphy and Alcino Silva and their colleagues at the University of California, Los Angeles.
Learning and memory impairments that arise independent of overt pathology are considered to be a normal component of aging. It is estimated that about 40% of people over the age of 65 years suffer from some sort of age-related cognitive decline. The exact cause of these age-related deficits in learning and memory is not currently known, but there have been numerous studies in the past that have implicated age-related changes in two neuronal attributes: a decrease in neuronal excitability, or the ability of neurons to be stimulated to fire, and age-related deficits in synaptic plasticity, or the ability of neurons to change some types of connections to other neurons. In the new study, funded by the National Institutes of Aging, researchers have established the link among neuronal excitability, synaptic plasticity, and aging.
Studying mice that had been genetically engineered to lack a particular ion channel auxiliary subunit, the researchers showed that the mice maintained enhanced neuronal excitability into old age, and, most importantly, that these mice exhibit a reduction in the threshold for the induction of specific forms of synaptic plasticity – in other words, these mice appear to change some kinds of inter-neuronal connections more readily than do normal mice of the same age. Furthermore, the aged mutant mice out-performed their age-matched wild-type littermates in the spatial version of the Morris water maze, a laboratory test for learning and memory.
Previous data suggested that in humans, the severity of age-related cognitive decline is affected by the genetic background of the individual. This was also the case for the genetically engineered mice. By manipulating the genetic background of the mice, the investigators were able to demonstrate that in some backgrounds the engineered mutation did not significantly increase neuronal excitability and that, in these cases, the mice did not exhibit the enhanced learning effect.
The new findings indicate that interactions between neuronal excitability and synaptic plasticity play a role in learning and that manipulations of either of these two parameters could be effective in ameliorating age-related cognitive decline.
07 Nov 2004
First-Ever Genetic Study of Late-Onset Alzheimer's Disease in Hispanic Families -
Researchers at Columbia University Medical Center have found two locations in the human genome that may harbor genes that increase the risk of Alzheimer's disease. If confirmed, they will be the first genes linked to Alzheimer's disease since ApoE4 was discovered in 1993. The findings are published in the November issue of Molecular Psychiatry, a journal of the Nature Publishing Group.
"We feel confident that we may be closing in on new Alzheimer's genes," says the study's senior author, Richard Mayeux, M.D., co-director of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University Medical Center. "This is a major collection of families, and family studies really give you more confidence that the region you're looking at is significant."
Researchers think that Alzheimer's is caused by the interaction of several different genes, but so far only one gene, ApoE4, has been linked conclusively to the disease. Finding the other genes will be a huge step toward understanding how Alzheimer's begins and how it can be treated. It will also allow clinicians to predict who will develop Alzheimer's later in life and who will benefit from drugs that prevent the disease. >>Read More>>
This new finding from the University of North Carolina offers hope that those recovering from alcoholism will be able to regain cognitive function, in fact, abstinence leads to a bloom of new cell formation in the brain known as neurogenesis.
University of North Carolina at Chapel Hill scientists have reported - for the first time - a burst in new brain cell development during abstinence from chronic alcohol consumption.
The UNC findings, from research at UNC's Bowles Center for Alcohol Studies, were based on an animal model of chronic alcohol dependence, in which adult rats were given alcohol over four days in amounts that produced alcohol dependency. The study is in the Nov. 3 issue of the Journal of Neuroscience.
In 2002, Dr. Fulton T. Crews, Bowles Center director, and Bowles Center research associate Dr. Kim Nixon were the first to report that alcohol, during intoxication, has a detrimental effect on the formation of new neurons in the adult rat hippocampus. This brain region is important for learning and memory - in animals and humans - and is linked to psychiatric disorders, particularly depression.
"When used in excess, alcohol damages brain structure and function. Alcoholics have impairments in the ability to reason, plan or remember," said Crews, also professor of pharmacology and psychiatry in UNC's School of Medicine. "A variety of psychological tests show alcoholics have a difficulty in ability to understand negative consequences."
In the new study, senior co-author Crews and co-author Nixon found inhibition of neurogenesis, or brain cell development, during alcohol dependency, followed by a pronounced increase in new neuron formation in the hippocampus within four-to-five weeks of abstinence. This included a twofold burst in brain cell proliferation at day seven of abstinence.
"We looked at dividing cells after our four-day binge model of alcohol dependency and confirmed what we previously observed: When the animals were intoxicated, the measure of dividing cells decreases," said Nixon. "And after abstinence for one week, we saw a huge burst in the number of new cells being born."
Nixon said the findings were confirmed by use of several biological markers, including bromodeoxyuridine, BrdU. Animals were injected with BrdU, which labels dividing cells. BrdU inserts itself into the DNA of a cell during cell division, so that it's found only in cells that have divided during the two hours that the substance is in the animals' system.
Imaging studies report shrinkage in brain ventricles - the fluid-filled spaces within the brain - indicating that the brain is growing as the spaces shrink as alcoholics recover from alcohol dependence.
"And when they stop drinking, you can show in a period of weeks, months, years, the brain grows back, there's a return of metabolic activity, and cognitive tests show a return of function," Crews said.
The findings may have significant implications for treatment of alcoholism during recovery. The discovery of regeneration of neurons in recovery opens up new avenues of therapies aimed at regeneration of brain cells. "When animals learn, they make more neurons. When animals exercise, they make more neurons and learn faster, as well," Crews said.
"Pharmacological agents such as antidepressants and behaviors such as running, increased physical activity and learning experiences apparently help regulate the process of neurogenesis," he added. "Our research suggests they could be considered in the treatment of chronic alcohol dependency."
In their report, Nixon and Crews also said that their findings for the first time provide a neuronal regeneration mechanism that may underlie the return of normal cognitive function and brain volume associated with recovery from addiction during abstinence from alcohol.
"This is really the first biological measure of a major change in neuronal structure consistent with changes that are known to occur when individuals are able to stop drinking," said Crews.
For decades, neuroscientists believed the number of new cells, or neurons, in the adult brain was fixed early in life. Adaptive processes such as learning, memory and mood were thought tied to changes in synapses, connections between neurons.
More recently, studies have shown that the adult human brain is capable of producing new brain cells throughout life, a neurogenesis resulting in formation of hundreds of thousands of new neurons each month. "Prior to our work, everyone merely assumed that glia, the supporting cells of the brain, regenerated or that existing brain cells altered their connections," said Nixon. "We have shown a burst in new cell birth that may be part of the brain's recovery after the cessation of alcohol."
Chronic alcoholism, a disease affecting more than 8 percent of the adult U.S. population, or more than 17 million Americans, produces cognitive impairments and decreased brain volumes, both of which are partially reversed during abstinence.
Alcohol dependence also is associated with depression, which is consistent with inhibition of neurogenesis. Cessation from alcohol is associated with improved cognitive abilities, Crews said.
We're close to making a deal (OK, its a done deal) with Bio-ITWorld to offer our testing and tracking on their website and a few others they work with. BioITWorld is dedicated to a fascinating new topic: the convergence of information technology and the life sciences,on the mind of many-a-mogul. BioITWorld is published by International Data Group (IDG) the leader in tech publishing with titles such as CIO, InfoWorld, Computerworld, PC World, MacCentral, and GamePro (an awesome site) In fact, the CEO and founder of IDG has donated more than $300 Million to advance brain research at MIT through the establishment of the McGovern Institute. Like some other relationships, this one goes back more than a decade. When I was just starting out from college working for Brown, IDG Books was one of my first hits where we took out the competition, Fed Ex. As an inveterate programmer, going back to the days of GOSUB and watfiv I thought IDG Books REM was the epitome of cool REM. It still is, so we're pretty lucky.
Well, our self-propelled CAV(candy accumulation vehicle) didn't function on bumpy ground, so we swiched to using 2 scooters. By mapping out the route or loop detail(UPS), we more than doubled our take from 221 pcs. last year to 452 this year. There is no way we can eat all that, though. :-)
It turns out that trans fats may be one of the culripts in the spreading phenomenon of memory loss, having been developed around the time of World War II. Please read and consider carefully.
Foods high in trans fats may be damaging consumers' brains more than other high fat foods, leading to memory loss in old age and problems performing simple jobs, according to new animal research. Chris Mercer reports.
Experiments with middle-aged rats, roughly equivalent in age to a 60-year-old person, showed that after only eight weeks of eating high fat foods, those on a high trans fat diet could not perform simple memory tasks as well as those on a high fat diet of soybean oil.
The study was carried by scientists at the Medical University of South Carolina (MUSC), including the university’s director of the Center on Aging, Anne-Charlotte Granholm, who sees this work as another nail in the coffin for trans fats, one of the new 'evils' of food processing.
The group compared rats on a high fat diet of 12 per cent soybean oil with those on a high fat diet of 10 per cent trans fats and two per cent cholesterol. In one experiment, the rodents, all of a similar weight, had to recall the location of hidden platforms in a water-filled maze – a task the trans fat rats were around five times worse at.
A range of studies have already shown that high fat/high cholesterol diets can cause learning and memory difficulties in the brain, but the MUSC research appears to highlight trans fats as the biggest single offenders.
Granholm said that while "it is always difficult to draw comparisons between animal studies and humans," the study was nevertheless "quite alarming". She believes food companies should show greater responsibility by cutting levels of trans fats in products more quickly.
The MUSC research is another kick in the teeth for trans fats, the common name for hydrogenated fats and oils, which are already thought to significantly increase the risk of heart disease by blocking arteries and have also been linked to a higher risk of Alzheimer’s disease.
Hydrogenated fats and oils have been widely used in the food industry for the last 50 years, primarily to extend the shelf life of products because trans fats do not go rancid as quickly as unsaturated fats. The high melting point and solid nature of hydrogenated fat also helps industrial bakers to maintain structure in their breads.
A number of companies have made commitments to reduce trans fats in their products, prompted by governmental and medical concerns. In the US, Kraft foods has launched trans fat free Oreo biscuits and PepsiCo now produces trans fat free Doritos through subsidiary Frito-Lay. In Europe, United Biscuits’ unit McVities has removed trans fats from its biscuit dough, though not cream filling, and UK retailer Sainsbury now claims to use low trans fat pastry.
Some alternatives to trans fats have also begun to appear, such as Danish company Danisco’s new emulsifier/oil blends and US firm Dow Agrosciences' natural Natreon canola oil, which claim to fill the role of partially hydrogenated fat.
But MUSC study author Granholm said that trans fats should be removed even before alternatives have been perfected: "Trans fats have only been around since the Second World War and before that we obviously did fine without them."
"What will happen is that people will have to adjust their lives a little. For example, buying a loaf of bread and having it last for a month or more without freezing it may no longer be an option. In fact, most European countries live by that."
Granholm said that the next step for herself and her colleagues would be to investigate the exact process by which trans fats affect the brain, and examine further the difference between cholesterol, saturated fats and trans fats in terms of the possible detrimental effects on people. She admitted that the group's studies needed to be followed up by "careful examination of the human body" to gain greater credence.
By January 2006 all manufacturers operating in the US will have to label trans fat content on their products, according to a recent ruling by the country’s Food and Drug Administration.
In the UK, the government's Food Standards Agency has been slower to react to a threat from trans fats, warning people to consume less but concentrating its efforts on reducing salt and saturated fat levels in foods. Industry association the Food and Drink Federation said that government figures showed peoples’ trans fat intake had halved between 1985 and 2000.
Tracking and Monitoring movements of people with Alzheimer's was the focus of a recent conference in Seattle. The hope is that people (and concerned families) can maintain and extend their individual freedoms as they age by enabling third parties to remotely monitor their activities. This is also an area of interest for CAST and its sponsor Intel, a Washington D.C. association we are part of. It is even suggested that monitoring the gait of individuals as they walk can reveal cognitive decline, or at least provide a suggestion that cognitive monitoring might be necessary. In that case, Memory For Life provides the solution...
Tan Vinh, Seattle Times
By the end of the decade, Global Positioning System technology may allow Alzheimer's patients to travel alone, and house sensors that give verbal warnings to older persons may be as common as light switches.
Even the routine task of walking may tell doctors whether cognitive skills are deteriorating.
Those were among the findings presented yesterday by scientists and researchers at the "Gerontechnology Today and Tomorrow" conference at Swedish Medical Center, sponsored by the hospital and the University of Washington Institute on Aging.
With the pending new computer technology and gadgets, many older persons may avoid nursing homes and live independently or with a little assistance in the near future, many scholars said yesterday.
"There will be significant changes in five years," said Henry Kautz, UW professor of computer science and engineering. "We can't put everybody in nursing homes. There will be more and more of a trend to leave people in their own homes and [in] assisted-living homes."
Technology will play a big role in providing safety and independence for seniors, Kautz said.
Kautz is working on a cellphone with GPS reading that can guide users home if they get lost or ride the wrong bus.
A prototype called "Opportunity Knocks" has been designed and clinical tests may begin next year, said Kautz, who predicts the product will be on the market within five years.
Many researchers also think the concept of planting sensors around the home will be big. The sensors would remind seniors to check their blood pressure or to eat lunch.
At Oregon Health & Science University, researchers also are studying the use of house sensors to track seniors as they walk in their homes.
Because both cognitive thinking and walking require similar neural-network performance, said Misha Pavel, professor of biomedical engineering at Oregon Health & Science University, a slowed gait over a period of time may signal deteriorating cognitive skills.
Tracking walking speed with sensors may be a great way to catch cognitive decline in the early stages, he said.
Echoing the concerns of many in the audience, Patricia Jennings, who oversees nursing homes for the state Department of Social and Health Services, said 24-hour sensors raise privacy issues.
Eva Kahana, professor in the sociology department at Case Western Reserve University in Cleveland, said technology is fine "as long as the older person can remain in the driver's seat. I think we have to be careful about technology not being used to control other people or taking away their independence."
Pavel and his colleague, Holly Jimison, said the patient controls who gets the sensor data.
"Monitoring allows them more autonomy. Otherwise they would be in a nursing home," Jimison said