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How Do You Live Knowing You Might Have an Alzheimer’s Gene?

By GINA KOLATA It seemed as if it would be a perfectly ordinary occasion, that hot August day in 1959. Three generations of a large Oklahoma family gathered at a studio in nearby Perryton, Tex., to have a photo taken of the elders, 14 siblings ranging in age from 29 to 52. Afterward, everyone went to a nearby park for a picnic. Among the group were two cousins, Doug Whitney, who was 10, and Gary Reiswig, who was 19. Doug’s mother and Gary’s father were brother and sister. Doug does not remember any details of that day, but Gary says he can never forget it. His father, and some of his aunts and uncles, just did not seem right. They stared blankly. They were confused, smiling and nodding, even though it seemed as if they weren’t really following the conversation. Seeing them like that reminded Gary of what his grandfather had been like years before. In 1936, at the age of 53, his grandfather was driving with his grandmother and inexplicably steered into the path of a train. He survived, but his wife did not. Over the next decade, he grew more and more confused. By the time he died at 63, he was unable to speak, unable to care for himself, unable to find his way around his house. Now here were the first signs of what looked like the same condition in several of his children. “We were looking at the grimness face to face,” Gary says. “After that, we gradually stopped getting together.” It was the start of a long decline for Gary’s father and his siblings. Their memories became worse, their judgment faltered, they were disoriented. © 2012 The New York Times Company

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: 16891 - Posted: 06.09.2012

US government sets out Alzheimer’s plan

Meredith Wadman Of the top ten leading causes of death in the United States, Alzheimer’s disease — which ranks sixth — is particularly devastating in that there is no cure, no way to prevent it and no proven way to slow its progression. And with at least 11 million Americans expected to have the disease by the middle of the century (see ‘Degeneration generation’) — boosting the annual costs of health care to more than US$1 trillion — the US government is anxiously looking to researchers to improve the prognosis. Last week, the government set out how it planned to spend a $50-million top-up to this year’s funding for the National Institutes of Health (NIH) in Bethesda, Maryland, announced in February as part of a bid to “prevent and effectively treat Alzheimer’s disease by 2025”. The money adds to the $448 million that the NIH was allocated to spend on the disease this year, and roughly half of it is already being used by scientists funded by the National Human Genome Research Institute and the National Institute on Aging. They are preparing to conduct whole-genome and whole-exome studies to discover mutations that may predispose someone to the disease or protect against it. The scientists are assembling a bank of thousands of DNA samples from patients and other people whose DNA could be informative — such as elderly individuals who carry predisposing mutations but show no sign of the disease. The first results from the effort are expected as early the end of this year. © 2012 Nature Publishing Group,

Some Fats May Harm the Brain More

By NICHOLAS BAKALAR Some studies have linked dietary fat to the development of dementia later in life. A new study suggests that the risk may depend on the type of fat consumed. Scientists studied 6,183 women over age 65, tracking their fat consumption and changes in their mental abilities over four years. The women completed a food questionnaire at the start of the study, then periodically took tests of mental ability. The researchers assigned a “change score” to each volunteer, summarizing changes in memory and abstract thinking over time — the lower the score, the greater the decline. The study appeared online Thursday in the journal Annals of Neurology. After controlling for many health and socioeconomic factors, the researchers found that women who consumed the most saturated fat were 60 percent more likely than those consuming the least to have change scores that put them below the 10th percentile. On the other hand, women who reported consuming the most monounsaturated fat were 44 percent less likely to have change scores in lowest one-tenth. Consumption of polyunsaturated fats and trans fats was not associated with any change, nor was total fat. “People might consider making changes or substitutions in their diet, switching out saturated fats in favor of monounsaturated fats,” said the lead author, Dr. Olivia I. Okereke, an assistant professor of psychiatry at Harvard. Copyright 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: 16824 - Posted: 05.22.2012

NIH-funded research provides new clues on how ApoE4 affects Alzheimer's risk

Common variants of the ApoE gene are strongly associated with the risk of developing late-onset Alzheimer's disease, but the gene's role in the disease has been unclear. Now, researchers funded by the National Institutes of Health have found that in mice, having the most risky variant of ApoE damages the blood vessels that feed the brain. The researchers found that the high-risk variant, ApoE4, triggers an inflammatory reaction that weakens the blood-brain barrier, a network of cells and other components that lines brain's brain vessels. Normally, this barrier allows nutrients into the brain and keeps harmful substances out. The study appears today in Nature, and was led by Berislav Zlokovic, M.D., Ph.D., director of the Center for Neurodegeneration and Regeneration at the Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles. “Understanding the role of ApoE4 in Alzheimer's disease may be one of the most important avenues to a new therapy," Dr. Zlokovic said. "Our study shows that ApoE4 triggers a cascade of events that damages the brain's vascular system," he said, referring to the system of blood vessels that supply the brain. The ApoE gene encodes a protein that helps regulate the levels and distribution of cholesterol and other lipids in the body. The gene exists in three varieties. ApoE2 is thought to play a protective role against both Alzheimer's and heart disease, ApoE3 is believed to be neutral, and ApoE4 confers a higher risk for both conditions. Outside the brain, the ApoE4 protein appears to be less effective than other versions at clearing away cholesterol; however,inside the brain, exactly how ApoE4 contributes to Alzheimer's disease has been a mystery.

New Drug Trial Seeks to Stop Alzheimer’s Before It Starts

By PAM BELLUCK In a clinical trial that could lead to treatments that prevent Alzheimer’s, people who are genetically guaranteed to develop the disease — but who do not yet have any symptoms — will for the first time be given a drug intended to stop it, federal officials announced Tuesday. Experts say the study will be one of the few ever conducted to test prevention treatments for any genetically predestined disease. For Alzheimer’s, the trial is unprecedented, “the first to focus on people who are cognitively normal but at very high risk for Alzheimer’s disease,” said Dr. Francis S. Collins, director of the National Institutes of Health. Most participants will come from the world’s largest family to experience Alzheimer’s, an extended clan of 5,000 people who live in Medellín, Colombia, and remote mountain villages outside that city. Family members with a specific genetic mutation begin showing cognitive impairment around age 45, and full dementia around age 51, debilitated in their prime working years as their memories fade and the disease quickly assaults their ability to move, eat, speak and communicate. Three hundred family members will participate in the initial trial. Those with the mutation will be years away from symptoms, some as young as 30. “Because of this study, we do not feel as alone,” said Gladys Betancur, 39, a family member. Her mother died of Alzheimer’s, three of her siblings already have symptoms, and she had a hysterectomy because of her fears that she has the mutation and would pass it on to her children. “Sometimes we think that life is ending, but now we feel that people are trying to help us.” The $100 million study will last five years, but sophisticated tests may indicate in two years whether the drug helps delay memory decline or brain changes, said Dr. Eric M. Reiman, executive director of the Banner Alzheimer’s Institute in Phoenix and a study leader. © 2012 The New York Times Company

More Omega-3s in Diet, Less of an Alzheimer’s Protein

By NICHOLAS BAKALAR A new study has found that consumption of omega-3 fatty acids, plentiful in fish and nuts, is associated with lower blood levels of beta-amyloid protein. Amyloid plaques and tangles in the brain are characteristic of Alzheimer’s disease and are known to increase the risk for mental decline; blood levels of the protein may reflect levels of its deposits in the brain. Researchers studied 1,219 mentally healthy people over 65, recording their diet over one and a half years and testing their blood for beta-amyloid and for vitamins and other nutrients. The study appeared online last week in Neurology. None of the nutrients was associated with reduced beta-amyloid levels except for omega-3 fatty acid. After controlling for age, education, ethnicity, alcohol intake and apolipoprotein E genotype (a genetic marker for dementia risk), the scientists found that higher levels of omega-3 intake were associated with significantly lower beta-amyloid blood levels. The subjects got their omega-3 mainly from fish, poultry, margarine and nuts, but Dr. Nikolaos Scarmeas, the senior author, was unwilling to offer diet advice. “The aim of this study is to try and confirm or disprove mechanisms by which omega-3 may affect brain function,” he said. “But it is not intended to derive public health recommendations.” Dr. Scarmeas is an associate professor of clinical neurology at Columbia University. Copyright 2012 The New York Times Company

When Illness Makes a Spouse a Stranger

By DENISE GRADY He threw away tax documents, got a ticket for trying to pass an ambulance and bought stock in companies that were obviously in trouble. Once a good cook, he burned every pot in the house. He became withdrawn and silent, and no longer spoke to his wife over dinner. That same failure to communicate got him fired from his job at a consulting firm. By 2006, Michael French — a smart, good-natured, hardworking man — had become someone his wife, Ruth, felt she hardly knew. Infuriated, she considered divorce. But in 2007, she found out what was wrong. “I cried,” Mrs. French said. “I can’t tell you how much I cried, and how much I apologized to him for every perceived wrong or misunderstanding.” Mr. French, now 71, has frontotemporal dementia — a little-known, poorly understood and frequently misdiagnosed group of brain diseases that eat away at personality and language. Although it was first recognized more than 100 years ago, there is still no cure or treatment, and patients survive an average of only eight years after the diagnosis. But recently, researchers have been making important discoveries about the biochemical and genetic defects that cause some forms of the disease. And for the first time, they have identified drugs that may be able to treat one of those defects, the buildup of abnormal proteins in the brain. Tests in people, the first ever such drug trials in this disease, could begin as soon as early next year at the University of California, San Francisco. © 2012 The New York Times Company

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 16756 - Posted: 05.07.2012

Protein tweak may trigger Alzheimer’s

By Laura Sanders Scientists have caught tiny amounts of a strangely shaped protein — a relative of a well-known suspect in Alzheimer’s disease —spreading destruction throughout the brains of mice. If a similar process happens in the human brain, it could help explain how Alzheimer’s starts, and even suggest new ways to stop the dangerous molecule’s spread. Many Alzheimer’s researchers believe the abundance of a molecule called A-beta in the brain is one of the key steps in developing the disease. A-beta commonly takes the form of a chain of 42 protein building blocks called amino acids. The new study chronicles the dangers of a modified A-beta that lacks the first two amino acids in the chain. Capping this stub is a rare, circular amino acid called pyroglutamate. Until recently, this form “has been largely ignored as some minor mysterious form of amyloid-beta,” says study coauthor George Bloom of the University of Virginia. Yet even trace amounts of this version, called pyroglutamylated A-beta, or pE A-beta, are devastating to mouse nerve cells, he and colleagues report online May 2 in Nature. “This opens up a whole new view of the disease,” says neurogeneticist Rudy Tanzi of Harvard Medical School. Instead of focusing just on the amount of A-beta in the brain, scientists need to pay attention to modifications of the molecule, too, he says. © Society for Science & the Public 2000 - 2012

Finding alternatives to potent sedatives

By Kay Lazar LITTLETON - Marjorie Bontempo was a changed woman after moving into Life Care Center of Nashoba Valley, a Littleton nursing home where the staff doesn’t believe in using antipsychotic drugs simply to calm residents. A physician had prescribed an antipsychotic for Bontempo a year earlier, after Alzheimer’s disease had transformed her from an accomplished seamstress and demure family peacekeeper into a cantankerous, confused woman who refused to eat. The medicine eased her aggression but left her dazed, said her daughter, Patty Sinnett. Nashoba’s nurses took Bontempo off the powerful sedative. Sinnett went to visit soon after and found her mother in the activity room watching a Clark Gable movie. “She started explaining the whole movie to me, like a normal person would,’’ Sinnett said. “It was the first time I had had a conversation with her in a year. It was incredible.’’ The Littleton facility is one of a small but growing number of nursing homes that are treating the agitation and disruptive behavior that often accompany dementia without resorting to antipsychotics. Instead, Life Care Center and similar homes try to tailor care to each resident, to make it familiar and comforting. Staffers comb residents’ pasts to learn their preferences, hobbies, and accomplishments, tapping bedrock emotions that endure long after memory fades. © 2012 NY Times Co

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: 16727 - Posted: 04.30.2012

Don’t Just Sit There

By GRETCHEN REYNOLDS ONE lesson I’ve learned while writing about fitness is that few things impinge on an active life as much as writing about fitness — all that time spent hunched before a computer or puzzling over scientific journals, the countless hours of feckless, seated procrastination. While writing about the benefits of exercise, my muscles slackened. Fat seeped insidiously into my blood, liver and ventricles. Stupor infiltrated my brain. We all know by now that being inactive is unhealthy. But far too many of us think that being inactive is something that happens to other people. Studies of daily movement patterns, though, show that your typical modern exerciser, even someone who runs, subsequently sits for hours afterward, often moving less over all than on days when he or she does not work out. The health consequences are swift, pervasive and punishing. In a noteworthy recent experiment conducted by scientists at the University of Massachusetts and other institutions, a group of healthy young men donned a clunky platform shoe with a 4-inch heel on their right foot, leaving the left leg to dangle above the ground. For two days, the men hopped about using crutches (and presumably gained some respect for those people who regularly toddle about in platform heels). Each man’s left leg never touched the ground. Its muscles didn’t contract. It was fully sedentary. © 2012 The New York Times Company

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: 16717 - Posted: 04.28.2012

Taking On Dementia With the Experiences of Normal Life

By JOHN TAGLIABUE WEESP, the Netherlands — The sparkling-new 23-unit Hogewey complex here is virtually indistinguishable from other residential developments in the area. The apartments open onto a courtyard with benches, ponds and fountains, with beds of flowers in season (this is the Netherlands, after all). One kidney-shaped pond planted with reeds and other vegetation occasionally attracts wild ducks. There are plenty of amenities: a small supermarket, a theater and a restaurant and cafe that attract people from around the area. Again, nice, but nothing out of the ordinary. The residents can also participate in a variety of activities, like clubs for music, baking, painting and gardening. Yet, if Hogewey does not sound all that different from a typical residential complex, that is exactly the point. The residents are older men and women suffering from severe dementia, but instead of being constrained in a typical nursing home, they live here for $6,555 a month, six to eight to an apartment, where they are cared for by two or more trained professionals. The residents are confined to Hogewey for their own safety. But within the complex they are allowed to move around freely, to the extent that they are able. On a recent unseasonably chilly afternoon, the residents of one apartment, designated as “urban” to reflect its residents’ tastes, gathered around a dining room table for tea. Most sat quietly, smiling, some in wheelchairs. Jo Verhoef, a woman known as Aunt Jo, sat upright in a comfortable armchair. © 2012 The New York Times Company

The Faces of Alzheimer’s

By ANAHAD O'CONNOR The prevailing view of people with Alzheimer’s is often a depressing one: the patient slumped in a chair or parked in front of a television set. But a new book and photo exhibition this month in New York show another side of the disease, one in which people with dementia can still be engaged, lead active lives and experience love and joy. The book, “Love, Loss and Laughter: Seeing Alzheimer’s Differently,” was written by Cathy Greenblat, a professor emerita of sociology at Rutgers University who found a second career as a photographer. The exhibition has toured the world and is currently on display at the Michael Schimmel Center for the Arts at Pace University in Manhattan. “I wanted to show what many people don’t know about Alzheimer’s,” Ms. Greenblat said, “that there are ways we can take care of people that build on their remaining capacities instead of just protecting them from danger.” In one of the many vivid photographs in her book, Ms. Greenblat shows an elderly Houston woman named Luleene, a former musician who played the organ, sang and loved animals, with her husband, Joe. To help her feel connected to her past, the hospice that assists her includes sessions with a music therapist in her weekly program as well as visits with pets. In India, a former math teacher, now with dementia, is shown dutifully scribbling numbers on a blackboard purchased by the staff at her day care center to help her experience old pleasures. Each line, perhaps inscrutable to the staff, is nonetheless a victory for the former teacher. Copyright 2012 The New York Times Company

WHO: Dementia cases worldwide will triple by 2050

By Frank Jordans GENEVA—Cases of dementia -- and the heavy social and financial burdens associated with them -- are set to soar in the coming decades as life expectancy and medical care improve in poorer countries, the World Health Organization says. Some 35.6 million people were living with dementia in 2010, but that figure is set to double to 65.7 million by 2030, the U.N. health agency said Wednesday. In 2050, it expects dementia cases to triple to 115.4 million. "The numbers are already large and are increasing rather rapidly," said Dr. Shekhar Saxena, the head of WHO's mental health division. Most dementia patients are cared for by relatives who shoulder the bulk of the current estimated annual cost of $604 billion. And the financial burden is expected to rise even faster than the number of cases, WHO said in its first substantial report on the issue. "The catastrophic cost drives millions of households below the poverty line," warned the agency's director-general, Margaret Chan. Dementia, a brain illness that affects memory, behavior and the ability to perform even common tasks, affects mostly older people. About 70 percent of cases are believed to be caused by Alzheimer's. In the last few decades, dementia has become a major public health issue in rich countries. But with populations in poor and middle-income countries projected to grow and age rapidly over the coming decades, WHO appealed for greater public awareness and better support programs everywhere. © 2012 NY Times Co.

Unflinching View of a Wandering Mind, No Breadcrumb Trail in Sight

By NEIL GENZLINGER Perhaps years from now, after a scientific breakthrough has turned Alzheimer’s disease into a memory as distant as polio wards are to younger Americans today, someone will stumble upon Scott Kirschenbaum’s hard-to-watch documentary, “You’re Looking at Me Like I Live Here and I Don’t,” and be stunned. “I’ve read about Alzheimer’s,” this person will say, “but I had no idea what it was actually like.” Alzheimer’s has been a trendy topic for writers of plays and television scripts in recent years. But those stories have often been primarily about the people surrounding the patient — family members, friends — and the effect of the disease on their lives. Mr. Kirschenbaum, whose film will be broadcast nationally on PBS’s “Independent Lens” on Thursday (on Sunday on Channel 13 in New York), takes the simple but bold step of making Alzheimer’s the only thing in his tale. It’s not a plot point that propels a narrative; it’s an inescapable box. The film zeros in on one woman, Lee Gorewitz, in a residential care center in Danville, Calif., and follows her through her daily routines. There are no talking heads describing current research into the disease, no family members waxing nostalgic about Ms. Gorewitz’s life before Alzheimer’s. Mr. Kirschenbaum sprinkles in some unobtrusive music and prods with an occasional question from behind the camera, but that’s it. © 2012 The New York Times Company

Chronic Stress and Phosphorylated Tau: suggestions for Alzheimer’s

By Scicurious Could stress play a role in the development of Alzheimer’s? Right now we’re not sure, but this latest study shows that it may play a role, though exactly how? Well, we’re still not sure. So what does stress have to do with Alzheimer’s? To look at this we’ll have to start by bringing two areas of study together: stress, and Tau. Alzheimer’s Disease is characterized by the development of two different globs of proteins, beta-amyloid plaques and neurofibrillary tangles. This study focuses on neurofibrillary tangles, or NFTs, which are made up of aggregates of a protein called tau. Tau is normally a protein used in the cytoskeleton to build and maintain cellular structure. In the case of Alzheimer’s Disease, tau proteins end up getting phosphorylated, have phosphorous attached to them, which causes them to be able to aggregate in groups, and if those get large enough, into neurofibrillary tangles. These tangles in your brain cells correlate with the cognitive decline associated with Alzheimer’s (though as yet we have no definitive proof that they CAUSE Alzheimer’s). Studying the tau protein, how it becomes phosphorylated and then aggregates, could thus allow us to study one of the hallmarks of Alzheimer’s disease, and if these tangles cause some of the symptoms of Alzheimer’s, studies of tau could also provide us with new methods to attack the development of the disease. And now what about stress? Stress has been linked to the development of many psychiatric diseases such as anxiety and depression, but it is also a natural response to, well, stressful situations. © 2012 Scientific American,

Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 16581 - Posted: 03.27.2012

Drug Dosage Was Approved Despite Warning

By KATIE THOMAS Four months before a best-selling Alzheimer’s drug was set to lose its patent protection, its makers received approval for a higher dosage that extended their exclusive right to sell the drug. But the higher dosage caused potentially dangerous side effects and worked only slightly better than the existing drugs, according to an article published Thursday in the British Medical Journal. The drug, Aricept 23, was approved in July 2010 against the advice of reviewers at the Food and Drug Administration. They noted that the clinical trial had failed to show that the higher dosage — 23 milligrams versus the previous dosages of 5 and 10 milligrams — met its goals of improving both cognitive and overall functioning in people with moderate to severe Alzheimer’s disease. The single clinical trial of 1,400 patients also found that the larger dosage led to substantially more nausea and vomiting, potentially dangerous side effects for elderly patients struggling with advanced Alzheimer’s disease. The drug was developed by the Japanese pharmaceutical company Eisai but is marketed in the United States in a partnership with Pfizer. “It doesn’t really have much benefit, but does substantially more harm,” said Dr. Steven Woloshin, one of the co-authors of the journal article and a professor of medicine at the Dartmouth Institute for Health Policy and Clinical Practice. Aricept generated more than $2 billion in annual sales since its first approval in 1996, according to the journal article, but it was set to lose its patent protection in November 2010, opening the door to cheaper generic versions of the drug. © 2012 The New York Times Company

Dementia's youngest victims defy stereotypes

By MATT SEDENSKY LEESBURG, Fla. — Doreen Watson-Beard cared for more people with dementia than she could count. The nurse was so moved by her patients that she led Alzheimer's support groups. She knew the warning signs and understood there was no cure. But the 49-year-old never thought the disease would affect someone her age. The first clues surfaced around five years ago, when she was 44. She'd forget to pick up her grandchildren at school or plans she made with her husband. She wrote down the wrong medication dosage for a patient. "I have no idea what's going on," she remembered telling her doctor. About 200,000 Americans under 65 are among the 5.4 million Americans suffering from Alzheimer's disease, according to the Alzheimer's Association. Experts' estimates suggest there's a similar number of younger people with other types of dementia, meaning about a half-million Americans, some as young as their 30s, suffer from early-onset or younger-onset dementia. The number of people suffering from all types of dementia is rapidly increasing because of the aging of the baby boom generation — the 78 million Americans born between 1946 and 1964 — though there's no sign the percentage of younger people with dementia is going up. Pat Summit, the 59-year-old Hall of Fame college women's basketball coach, is among the most famous to suffer publicly with it. Watson-Beard is one of a tiny minority, a fascinating, sorrowful subset to a disease trademarked by its slow, cruel overtaking of the mind. Copyright 2012 The Associated Press

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.

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

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