Links for Keyword: Alzheimers

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Antioxidant pills don’t help against Alzheimer’s disease: What does?

By Deborah Kotz, Globe Staff Another disappointing clinical trial found that over-the-counter dietary supplements work no better than placebos at halting the detrimental effects of Alzheimer’s disease. This time, the supplements tested were antioxidants -- vitamin E, vitamin C, the omega-3 fatty acid ALA, and coenzyme Q. The same research group determined in a study published 18 months ago that fish oil supplements didn’t stop the progresson of Alzheimer’s either. The current study, published Monday in the Archives of Neurology, was small but well designed, randomly assigning two different combinations of daily antioxidants or placebos to some 60 patients with mild to moderate Alzheimer’s disease for nearly four months. At the end of the study, samples of spinal fluid collected from the patients at the beginning and end of the study showed no change in levels of markers associated with Alzheimer’s, including amyloid proteins that form telltale plaques in the brain. What’s troubling, though, is that the group that received a combination of vitamins E, C, and the fatty acid ALA had a greater amount of cognitive decline compared with the group given placebos or the one given coenzyme Q. “That was a really surprising finding,” said Dr. Gad Marshall, associate medical director of clinical trials at Brigham and Women’s Hospital’s Center for Alzheimer Research & Treatment, who wasn’t involved in the study. “I would have expected these supplements to have had a neutral effect on symptoms.” © 2012 NY Times Co.

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 16555 - Posted: 03.22.2012

Exercising an Aging Brain

By DENISE GRADY MORE and more retired people are heading back to the nearest classroom — as students and, in some cases, teachers — and they are finding out that school can be lovelier the second time around. Some may be thinking of second careers, but most just want to keep their minds stimulated, learn something new or catch up with a subject they were always curious about but never had time for. For many, at least part of the motivation is based on widespread reports that exercising the brain may preserve it, forestalling mental decline and maybe even Alzheimer’s disease and other types of dementia. Is there any truth to it? And if there is, what type of learning is best suited to the older brain? Many studies do find that being mentally active is associated with a lower risk of Alzheimer’s disease. But the standard caveat applies: association does not prove cause and effect, and there is always the chance that the mentally active people who never got Alzheimer’s simply had healthier brains to begin with. Even, so, researchers say, there is no harm in telling people to try to stay engaged. “When you and I are having this conversation, you’re taking notes, thinking, remembering pieces of it, trying to relate it to other things,” said Arthur Toga, a professor of neurology and director of the laboratory of neuroimaging at the University of California, Los Angeles. “You’re changing the circuitry in your brain. That is because you have changed something in your brain to retain that memory.” © 2012 The New York Times Company

Alzheimer's patients 'should stay on drugs for longer'

By Jane Dreaper Health correspondent, BBC News Thousands of patients with advanced Alzheimer's disease could benefit from drugs, research suggests. A study in the the New England Journal of Medicine found that patients who stayed on the dementia drug Aricept had a slower decline in their memory. The drug tends not to be prescribed once sufferers progress beyond moderate symptoms. Medicines regulator NICE said its guidelines supported continuing treatment where there were benefits. The patent for the medicine Aricept, which is used to treat Alzheimer's disease, expired recently. Much cheaper versions under the generic name donepezil are already available for about £12 a month. The researchers say their new evidence could lead to twice as many Alzheimer's sufferers worldwide being given medication. The trial involved 295 Alzheimer's patients in England and Scotland who had been taking Aricept. One set were given placebo tablets while another set stayed on Aricept. A third set were given another drug, Ebixa, or memantine, which is usually prescribed only in the later stages of Alzheimer's. BBC © 2012

Alzheimer's around the world, through a personal lens

Andrew Purcell, online producer “If you’ve known one person with Alzheimer’s disease… you’ve known one person with Alzheimer’s disease,” asserts sociologist Cathy Greenblat. Greenblat, professor emerita of sociology at Rutgers University, New Jersey, has spent years taking photographs of people with Alzheimer’s and their families around the world, visiting homes, memory clinics and residential centres on three continents. This week, she launched her second photographic compendium illustrating the diversity of Alzheimer’s, Love, Loss and Laughter: Seeing Alzheimer’s differently, alongside an accompanying global exhibition tour. According to Greenblat, the different ways Alzheimer’s disease manifests itself is key to people with the condition being helped to live full and rich lives. This diversity comes across in her photographs, some of which emphasise the importance of art and music in helping Alzheimer’s patients stay active and mentally stimulated. Greenblat argues that art therapy can be useful for those with both early and advanced stages of Alzheimer’s disease. She says that music in particular can be a great tool for improving concentration, bonding and releasing pent-up emotions: “Because music is processed in many areas of the brain, people with Alzheimer’s disease are often able to engage meaningfully with live music even when they have severe cognitive impairment.” She also says that the term “art” should be interpreted as broadly as possible to include things like creative storytelling and visits to cultural venues. For example, an art therapy session may include a visit to the local art gallery or natural history museum, followed by discussion and interpretation of what the group has seen. © Copyright Reed Business Information Ltd.

Reversing Alzheimer’s gene ‘blockade’ can restore memory, other cognitive functions

Anne Trafton, MIT News Office MIT neuroscientists have shown that an enzyme overproduced in the brains of Alzheimer’s patients creates a blockade that shuts off genes necessary to form new memories. Furthermore, by inhibiting that enzyme in mice, the researchers were able to reverse Alzheimer’s symptoms. The finding suggests that drugs targeting the enzyme, known as HDAC2, could be a promising new approach to treating the disease, which affects 5.4 million Americans. The number of Alzheimer’s victims worldwide is expected to double every 20 years, and President Barack Obama recently set a target date of 2025 to find an effective treatment. Li-Huei Tsai, leader of the research team, says that HDAC2 inhibitors could help achieve that goal, though it would likely take at least 10 years to develop and test such drugs. “I would really strongly advocate for an active program to develop agents that can contain HDAC2 activity,” says Tsai, director of the Picower Institute for Learning and Memory at MIT. “The disease is so devastating and affects so many people, so I would encourage more people to think about this.” Tsai and her colleagues report the findings in the Feb. 29 online edition of Nature. Lead author of the paper is Johannes Gräff, a postdoc at the Picower Institute.

How Exercise Jogs the Brain

By Stephani Sutherland The lifelong mental benefits of exercising have long been known, from improving learning in kids to staving off dementia in seniors. Yet how working up a sweat leads to better cognition is much less clear. A study in the Journal of Applied Physiology reveals that the key may lie in the body’s power supply. Just as a booming metropolis might build new power plants to meet a rising need for electricity, our muscles respond to the demands of exercise by producing new mitochondria, the tiny structures inside cells that supply the body with energy. J. Mark Davis, a physiologist at the University of South Carolina, and his colleagues wondered if brain cells might do the same thing. While studying mice, they found that quantities of a signaling molecule, dubbed by researchers “a master regulator” of mitochondria production, increased in the brain after half an hour a day of treadmill running. The mice’s brain cells also had more mitochondrial DNA—distinct from the regular cellular DNA found in the nucleus—providing “gold standard” evidence of more mitochondria. It appears that the brain “adapts and changes by bringing more of these powerhouses” online, Davis says. The increased energy supply allows the brain to work faster and more efficiently. The finding could help scientists understand how exercise staves off age- and disease-related declines in brain function, because neurons naturally lose mitochondria as we age, Davis explains. Although past research has shown that exercise encourages the growth of new neurons in certain regions, the widespread expansion of the energy supply could underlie the benefits of exercise to more general brain functions such as mood regulation and dementia prevention. “The evidence is accumulating rapidly that exercise keeps the brain younger,” Davis says. © 2012 Scientific American

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 16453 - Posted: 03.01.2012

Nutrition: Brainpower Tied to Omega-3 Levels

By NICHOLAS BAKALAR Low blood levels of omega-3 fatty acids are associated with smaller brain volume and poorer performance on tests of mental acuity, even in people without apparent dementia, according to a new study. In the analysis, published online Monday in the journal Neurology, scientists examined 1,575 dementia-free men and women whose average age was 67. The researchers analyzed the fatty acids of the subjects’ red blood cells, a more reliable measurement than a plasma blood test or an estimate based on diet. They used an M.R.I. scan to measure brain volume and white matter hyperintensities, a radiological finding indicative of vascular damage. People in the lowest one-quarter for omega-3 levels had significantly lower total cerebral brain volume than those in the highest one-quarter, even after adjusting for age, body mass index, smoking and other factors. They also performed significantly worse on tests of visual memory, executive function and abstract memory than those in the highest one-quarter. There was no significant association with white matter hyperintensity volume. “We feel that omega-3’s reduce vascular pathology and thus reduce the rate of brain aging,” said Dr. Zaldy S. Tan, the lead author and associate professor of medicine at the University of California, Los Angeles. Few in the study were taking omega-3 supplements, Dr. Tan said. The main reason that some had higher blood levels of omega-3’s was that they ate more fatty fish. © 2012 The New York Times Company

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of Internal States
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 16450 - Posted: 02.28.2012

Life, With Dementia

By PAM BELLUCK SAN LUIS OBISPO, Calif. — Secel Montgomery Sr. stabbed a woman in the stomach, chest and throat so fiercely that he lost count of the wounds he inflicted. In the nearly 25 years he has been serving a life sentence, he has gotten into fights, threatened a prison official and been caught with marijuana. Despite that, he has recently been entrusted with an extraordinary responsibility. He and other convicted killers at the California Men’s Colony help care for prisoners with Alzheimer’s disease and other types of dementia, assisting ailing inmates with the most intimate tasks: showering, shaving, applying deodorant, even changing adult diapers. Their growing roster of patients includes Joaquin Cruz, a convicted killer who is now so addled that he thinks he sees his brother in the water of a toilet, and Walter Gregory, whose short-term memory is ebbing even as he vividly recalls his crime: stabbing and mutilating his girlfriend with a switchblade. “I cut her eyes out, too,” Mr. Gregory declared recently. Dementia in prison is an underreported but fast-growing phenomenon, one that many prisons are desperately unprepared to handle. It is an unforeseen consequence of get-tough-on-crime policies — long sentences that have created a large population of aging prisoners. About 10 percent of the 1.6 million inmates in America’s prisons are serving life sentences; another 11 percent are serving over 20 years. © 2012 The New York Times Company

Dementia death risk doubles on some antipsychotics

Dementia is estimated to affect about 500,000 Canadians and up to five million people in the U.S.Dementia is estimated to affect about 500,000 Canadians and up to five million people in the U.S. (Associated Press) An analysis of tens of thousands of people in nursing homes in the U.S. suggests that residents who take certain antipsychotic drugs for dementia are at about double the risk of dying compared to residents not taking those specific medications. All the residents in the study, published Friday in the British Medical Journal (BMJ), were over age 65. The Harvard Medical School study, the largest ever undertaken among U.S. nursing home residents, focused on 75,445 nursing-home residents from 45 states from 2001 to 2005. Their risks of death were looked at during a six-month period. Facts about dementia in Canada What is it? An umbrella term for a variety of brain disorders. Symptoms include loss of memory, judgment and reasoning, and changes in mood and behaviour. Prevalence: In 2010, more than 500,000 Canadians were living with dementia. Of these, about 71,000 were under age 65. One in 11 Canadians over 65 have the condition. Who is most at risk? Women account for 72 per cent of all Alzheimer's cases, and 62 per cent of all dementia cases. © CBC 2012

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 16431 - Posted: 02.25.2012

Alzheimer's Drug May Impair Memory

By Rachael Rettner VANCOUVER – A class of drugs being investigated to treat Alzheimer's disease may actually have the opposite effect of the original intent — they may impair memory, a new study in animals suggests. The drugs, known as BACE1 inhibitors, are designed to prevent the formation of the protein plaques in the brain that are a hallmark of Alzheimer's disease. However, the new study suggests these drugs interfere with the brain's wiring, potentially affecting the formation of new memories. While the drugs aren't approved by the Food and Drug Administration, several companies are pursuing their development, and some have been tested in human trials. The new findings are not a red light for BACE1 inhibitor development, study researcher Robert Vassar, a professor of cell and molecular biology at Northwestern University Feinberg School of Medicine, said here today at the American Association for the Advancement of Science's annual meeting. But researchers should proceed with caution, Vassar said. "It's something the drug makers need to keep their eyes out for," Vassar told MyHealthNewsDaily. The enzyme BACE1 is involved in forming amyloid beta proteins, which aggregate to form plaques. The drugs are based on the idea that blocking the enzyme could slow the disease, or help with symptoms. © 2012 Yahoo! Inc.

Father, son develop drug to fight brain diseases

Erin Allday It began over a glass of good red wine. Paul Muchowski thought he'd found a molecular compound that could slow down the damage done in the brains of people with neurodegenerative diseases. But he didn't know how to get his hands on the compound, which was made by a major pharmaceutical and wouldn't be loaned out without a lot of cost and hassle. So one night, after a family dinner at his parents' home in Sunnyvale, he asked his dad for help. "Paul says, 'Do you think you could make this compound?' And I said any competent chemist could do it," said Joseph Muchowski, now 75, who had decades of experience making drugs and is far beyond "competent" in chemistry. "I made him just under 50 grams in a week," Muchowski said, "and that's how the relationship started." The relationship is a rare one in science: a father and son, one a highly credentialed chemist, the other an up-and-coming biologist, working together on a new drug that, if it works, could be among the first to treat terrible brain diseases such as Alzheimer's and Huntington's. The pair are working at the Gladstone Institutes, an independent research group affiliated with UCSF. Paul Muchowski, 40, is a full-time investigator at Gladstone. His father, now retired from the Swiss drug maker Roche, splits his time between a lab at Gladstone and his current home just east of Vancouver in British Columbia. © 2012 Hearst Communications Inc.

Finding Joy in Alzheimer’s

By ROBERT LELEUX Seven years ago, when my grandmother JoAnn was first diagnosed with Alzheimer’s, the news sent me into a tailspin of fear and sadness. In my splintered Southern family, JoAnn had been more than my grandmother. The Auntie Mame of my Texas childhood, she taught me that happiness requires a great deal of thumbing one’s nose at convention. When I was 4, during an afternoon trip to the art museum, she told me to run my fingers along the brushstrokes of a particularly stunning Van Gogh: “They may kick us out of here, darlin,’ ” she drawled into my impressionable little ear, “but you’ll never not have touched that painting.” It was a life-affirming, if inappropriate, lesson. Without JoAnn’s outrageous example, I’m not sure I’d have had the courage to move to Manhattan, to come out of the closet, or ironically, to accompany her through the final years of her life. Little did I know that even after she was diagnosed with Alzheimer’s, my grandmother had only begun to educate me. “The wonderful thing about Alzheimer’s,” she once quipped after her diagnosis, “is that you always live in the moment.” This was a zinger intended to conceal her frustration at having forgotten the punch line to one of her signature anecdotes. But it was, nevertheless, quite true. Through the haze of our grief, my grandfather Alfred and I began noticing that, along with her memories, JoAnn’s grudges, hurt feelings, worries and regrets were disappearing. In fact, within a year, she seemed happier than ever, more present and at peace. © 2012 The New York Times Company

Slow walking 'predicts dementia'

The speed someone walks may predict the likelihood of developing dementia later in life, according to researchers in the US. They also told a conference that grip strength in middle-age was linked to the chance of a stroke. The scientists said more studies were needed to understand what was happening. Experts said the findings raised important questions, but more research was needed. Suggestions of a link between slow walking speed and poor health have been made before. A study, published in the British Medical Journal in 2009, said there was a "strong association" between slow walking speed and death from heart attacks and other heart problems. A Journal of the American Medical Association study suggested a link between walking faster over the age of 65 and a longer life. Dr Erica Camargo, who conducted the latest study at the Boston Medical Centre, said: "While frailty and lower physical performance in elderly people have been associated with an increased risk of dementia, we weren't sure until now how it impacted people of middle age." Brain scans, walking speed and grip strength were recorded for 2,410 people who were, on average, 62 years old. BBC © 2012

Group mental activities help people with dementia, review shows

Kerry Grens Reuters NEW YORK (Reuters Health) - A series of group activities designed to stimulate thought, conversation and memory appears to improve the mental functioning of people with mild or moderate dementia, according to a new review of the evidence. "This is good news for the industry," said Robert Winningham, a professor at the University of Western Oregon, who was not involved in this study. "This is showing the people who work in memory care communities and nursing homes and assisted living facilities that they can improve cognitive function, and they need to be providing these kinds of interventions." Cognitive stimulation, as the therapy is called, involves structured activities in a group setting, usually one or more times a week for at least a month. The sessions might include a discussion of current events, a sort of show-and-tell with objects, baking, drawing or other activities that get the participants to engage their minds. Bob Woods, a professor at Bangor University in the UK who led the study, said that researchers in this field had considered cognitive stimulation to be helpful for people with dementia, based on earlier work. SOURCE: http://bit.ly/Af8nyY Cochrane Database of Systematic Reviews, February 2012. Copyright © 2012, Reuters

Alzheimer's Disease Symptoms Reversed in Mice

By Gary Stix A nearly 13-year-old skin cancer drug rapidly alleviates molecular signs of Alzheimer's disease and improves brain function, according to the results of a new mouse study being hailed as extremely promising. Early-stage human clinical trials could begin within months. In the study, published online February 9 by Science, researchers from Case Western Reserve University in Cleveland and colleagues used mice genetically engineered to exhibit some of the symptoms of Alzheimer's. Most notably, the mice produced amyloid beta peptides—toxic protein fragments that gum up neurons and lead to cell death—and showed signs of forgetfulness. The Case Western team, led by Gary Landreth, decided to try the drug bexarotene (Targretin), approved in 1999 for cutaneous T cell lymphomas. The team chose this drug because of its long experience working with proteins in the nucleus of brain cells that can induce biochemical processes that affect amyloid beta. Landreth and his colleagues fed bexarotene to the demented mice, and with just a single dose it lowered the most toxic form of the amyloid beta peptide by 25 percent within six hours, an effect that lasted for up to three days. Mice that were cognitively impaired by the amyloid buildup resumed normal behaviors after 72 hours: They began to crinkle toilet paper placed nearby to make nests, a skill lost as amyloid increased in their brains. © 2012 Scientific American,

Cracks in the Plaques: Mysteries of Alzheimer's Slowly Yielding to New Research

By Daisy Yuhas This has been a big week in Alzheimer's news as scientists put together a clearer picture than ever before of how the disease affects the brain. Three recently published studies have detected the disease with new technologies, hinted at its prevalence, and described at last how it makes its lethal progress through the brain. The existence of two forms of Alzheimer's—early- and late-onset—has long baffled scientists. Of the estimated five million Americans who suffer from Alzheimer's, only a few thousand are diagnosed with an early-onset form of the affliction, which affects people before the age of 65. This rare early-onset form is thought to be hereditary and scientists have associated multiple genetic mutations contributing to its occurrence. Late-onset Alzheimer's, although more common, has been the bigger mystery. One variant of the APOE gene-—sometimes known as the Alzheimer's gene—is linked to the late-onset disease. But the APOE gene, unlike dominant early-onset genes, does not determine whether a person will ultimately have dementia. Now there's evidence that late-onset Alzheimer's has a genetic basis similar to that of early-onset Alzheimer's. By sequencing select genes associated with the latter, along with frontotemporal dementia, researchers at Washington University in Saint Louis and other institutions found that patients with late-onset Alzheimer's carry some of the same genetic mutations as those with the early-onset form. The evidence, published on Wednesday in PLoS ONE, bolsters the argument that the forms of Alzheimer's that appear at different life stages should be classified as the same disease. As to why the disease appears earlier in some cases, the scientists speculated that those patients diagnosed relatively early in life carry more genetic risk factors for the disease. © 2012 Scientific American,

Path Is Found for the Spread of Alzheimer’s

By GINA KOLATA Alzheimer’s disease seems to spread like an infection from brain cell to brain cell, two new studies in mice have found. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau. The surprising finding answers a longstanding question and has immediate implications for developing treatments, researchers said. And they suspect that other degenerative brain diseases like Parkinson’s may spread in a similar way. Alzheimer’s researchers have long known that dying, tau-filled cells first emerge in a small area of the brain where memories are made and stored. The disease then slowly moves outward to larger areas that involve remembering and reasoning. But for more than a quarter-century, researchers have been unable to decide between two explanations. One is that the spread may mean that the disease is transmitted from neuron to neuron, perhaps along the paths that nerve cells use to communicate with one another. Or it could simply mean that some brain areas are more resilient than others and resist the disease longer. The new studies provide an answer. And they indicate it may be possible to bring Alzheimer’s disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau. © 2012 The New York Times Company

How Exercise May Keep Alzheimer’s at Bay

By GRETCHEN REYNOLDS Alzheimer’s disease, with its inexorable loss of memory and self, understandably alarms most of us. This is especially so since, at the moment, there are no cures for the condition and few promising drug treatments. But a cautiously encouraging new study from The Archives of Neurology suggests that for some people, a daily walk or jog could alter the risk of developing Alzheimer’s or change the course of the disease if it begins. For the experiment, researchers at Washington University in St. Louis recruited 201 adults, ages 45 to 88, who were part of a continuing study at the university’s Knight Alzheimer’s Disease Research Center. Some of the participants had a family history of Alzheimer’s, but none, as the study began, showed clinical symptoms of the disease. They performed well on tests of memory and thinking. “They were, as far as we could determine, cognitively normal,” says Denise Head, an associate professor of psychology at Washington University who led the study. The volunteers had not had their brains scanned, however, so the Washington University scientists began their experiment by using positron emission tomography, an advanced scanning technique, to look inside the volunteers’ brains for signs of amyloid plaques, the deposits that are a hallmark of Alzheimer’s. People with a lot of plaque tend to have more memory loss, though the relation is complex. Next they genetically typed their volunteers for APOE, a gene involved in cholesterol metabolism. Everyone carries the APOE gene, but scientists have determined that those who have a particular variation of the gene known as e4 are at 15 times the risk of developing Alzheimer’s compared with those who do not carry the variant. © 2012 The New York Times Company

Alzheimer's 'in a dish' shows promise

Ewen Callaway Skin cells from patients with Alzheimer’s disease have been reprogrammed to form brain cells, offering clues to their dementia and, for others, the prospect of early diagnosis and new ways of finding treatments. An estimated 30 million people worldwide have Alzheimer’s disease, which causes neurodegeneration and typically strikes late in life. The disease is nearly impossible to diagnose before symptoms develop, and no drugs exist at present that can change its course. Scientists aiming to learn the causes of Alzheimer’s have looked to brain biopsies of patients after they die, blood tests and animals as diverse as fruitflies and fish. Until recently, it has not been possible to probe the neurons of Alzheimer’s patients before they show symptoms. “By the time you can see dementia in a person, their brain cells have been behaving in an abnormal way for years, perhaps decades or longer,” says Larry Goldstein, a neuroscientist at the University of California, San Diego, who led the study published online today in Nature1. Goldstein and his team created induced pluripotent stem (iPS) cells from four patients with Alzheimer’s and two people without dementia. iPS cells are made by treating fibroblasts, a type of skin cell, with reprogramming factors to revert them to an embryonic-like state. Like the stem cells in early embryos, iPS cells can form any tissue in the body — including neurons. © 2012 Nature Publishing Group

Mental decline can begin as early as 45, study finds

By Linda Thrasybule The brain's abilities to reason, comprehend and remember may start to worsen as early as age 45, a new study from England suggests. Researchers gave tests of thinking skills to about 5,100 men and 2,200 women between the ages of 45 and 70 years over a 10-year period. They found people ages 45 to 49 years experienced a notable decline in mental functioning. " 'Senior' moments that people often joke about are true," said Dr. Gary Small, geriatric psychiatrist David Geffen School of Medicine at the University of California, Los Angeles, who was not involved with the work. "If you follow people over time, you'll see there are structural changes that happen in the brain as they age," he said. The study was published today (Jan. 5) in the British Medical Journal. Previous evidence suggests that impaired cognitive function could be an early sign of dementia. One recent study showed cognitive performance strongly predicted a 75 percent diagnosis of Alzheimer's disease, a common form of dementia, after six years. About 1 in 8 older Americans have Alzheimer's disease, according to the Alzheimer's Association. They anticipate the numbers will grow each year as more and more people continue to live longer. © 2012 msnbc.com

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