Chapter 7. Life-Span Development of the Brain and Behavior
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By Ariana Eunjung Cha, The National Institutes of Health is undertaking an ambitious collaboration with private industry in an attempt to speed up the search for treatments for some of the world’s most devastating diseases — Alzheimer’s, type 2 diabetes, rheumatoid arthritis and lupus. The pilot projects announced Tuesday will involve the sharing of not only scientists but also of data, blood samples and tissue specimens among 10 rival companies, the federal government and several nonprofit groups and research foundations. The companies that have signed up to participate include most of the large drug makers, which in the past had resisted calls to share detailed data and samples from experiments, preferring to instead use the information to gain lucrative patents. The agreement with NIH represents a major break from how they used to do business. The competing pharmaceutical companies have said they will hold off launching commercial ventures based on discoveries from the partnership until after the data has been made publicly available. The idea behind the collaboration is similar to that of the “open source” movement among some computer scientists who believe that sharing their code with anyone who wants it is the best way to innovate. The first group of projects, which will last three to five years, will involve an investment of more than $230 million from industry participants including Bristol-Myers Squibb, GlaxoSmithKline, Johnson & Johnson, Eli Lilly, Merck, Pfizer, Sanofi and Takeda, as well as a few smaller biotech companies. © 1996-2014 The Washington Post
Link ID: 19206 - Posted: 02.05.2014
by Laura Sanders Despite seeming like a bystander, your baby is attuned to your social life (assuming you have one, which, with a baby, would be amazing). Every time you interact with someone, your wee babe is watching, eagerly slurping up social conventions. Scientists already know that babies expect some social graces: They expect people in a conversation to look at each other and talk to other people, not objects, and are eager to see good guys rewarded and bad guys punished, scientists have found. Now, a new study shows that babies are also attuned to other people’s relationships, even when those relationships have nothing to do with them. Babies are pretty good at figuring out who they want to interact with. The answer in most cases: Nice people. And that makes sense. The helpless wailers need someone reliable around to feed, change and entertain them. So to find out how good babies are at reading other people’s social relationships, University of Chicago psychologists showed 64 9-month-old babies a video of two women eating. Sometimes the women ate from the same bowl and agreed that the food was delicious, or agreed that it was gross. Sometimes the women disagreed. Later, the women interacted again, either warmly greeting each other and smiling, or giving each other the cold shoulder, arms crossed with a “hmph.” Researchers then timed how long the babies spent looking at this last scene, with the idea that the longer the baby spent looking, the more surprising the scene was. © Society for Science & the Public 2000 - 2014.
By Jennifer Ouellette It was a brisk October day in a Greenwich Village café when New York University neuroscientist David Poeppel crushed my dream of writing the definitive book on the science of the self. I had naively thought I could take a light-hearted romp through genotyping, brain scans, and a few personality tests and explain how a fully conscious unique individual emerges from the genetic primordial ooze. Instead, I found myself scrambling to navigate bumpy empirical ground that was constantly shifting beneath my feet. How could a humble science writer possibly make sense of something so elusively complex when the world’s most brilliant thinkers are still grappling with this marvelous integration that makes us us? “You can’t. Why should you?” Poeppel asked bluntly when I poured out my woes. “We work for years and years on seemingly simple problems, so why should a very complicated problem yield an intuition? It’s not going to happen that way. You’re not going to find the answer.” Well, he was right. Darn it. But while I might not have found the Ultimate Answer to the source of the self, it proved to be an exciting journey and I learned some fascinating things along the way. 1. Genes are deterministic but they are not destiny. Except for earwax consistency. My earwax is my destiny. We tend to think of our genome as following a “one gene for one trait” model, but the real story is far more complicated. True, there is one gene that codes for a protein that determines whether you will have wet or dry earwax, but most genes serve many more than one function and do not act alone. Height is a simple trait that is almost entirely hereditary, but there is no single gene helpfully labeled height. Rather, there are several genes interacting with one another that determine how tall we will be. Ditto for eye color. It’s even more complicated for personality traits, health risk factors, and behaviors, where traits are influenced, to varying degrees, by parenting, peer pressure, cultural influences, unique life experiences, and even the hormones churning around us as we develop in the womb.
Madhusree Mukerjee By displaying images on an iPad, researchers tested patients' ability to detect contrast after their vision was restored by cataract surgery. In a study of congenitally blind children who underwent surgery to restore vision, researchers have found that the brain can still learn to use the newly acquired sense much later in life than previously thought. Healthy infants start learning to discern objects, typically by their form and colour, from the moment they open their eyes. By the time a baby is a year old vision development is more or less complete, although refinements continue through childhood. But as the brain grows older, it becomes less adaptable, neuroscientists generally believe. "The dogma is that after a certain age the brain is unable to process visual inputs it has never received before," explains cognitive scientist Amy Kalia of the Massachusetts Institute of Technology (MIT) in Cambridge. Consequently, eye surgeons in India often refuse to treat children blinded by cataracts since infancy if they are over the age of seven. Such children are not usually found in wealthier countries such as the United States — where cataracts are treated as early as possible — but are tragically plentiful in India. In the study, which was published last week in Proceedings of the National Academy of Sciences1, Kalia and her collaborators followed 11 children enrolled in Project Prakash2, a humanitarian and scientific effort in India that provides corrective surgery to children with treatable cataracts and subsequently studies their visual abilities. ('Prakash' is Sanskrit for light.) © 2014 Nature Publishing Group
By GINA KOLATA For many obese adults, the die was cast by the time they were 5 years old. A major new study of more than 7,000 children has found that a third of children who were overweight in kindergarten were obese by eighth grade. And almost every child who was very obese remained that way. Some obese or overweight kindergartners lost their excess weight, and some children of normal weight got fat over the years. But every year, the chances that a child would slide into or out of being overweight or obese diminished. By age 11, there were few additional changes: Those who were obese or overweight stayed that way, and those whose weight was normal did not become fat. “The main message is that obesity is established very early in life, and that it basically tracks through adolescence to adulthood,” said Ruth Loos, a professor of preventive medicine at the Icahn School of Medicine at Mount Sinai in New York, who was not involved in the study. These results, surprising to many experts, arose from a rare study that tracked children’s body weight for years, from kindergarten through eighth grade. Experts say they may reshape approaches to combating the nation’s obesity epidemic, suggesting that efforts must start much earlier and focus more on the children at greatest risk. The findings, to be published Thursday in The New England Journal of Medicine, do not explain why the effect occurs. Researchers say it may be a combination of genetic predispositions to being heavy and environments that encourage overeating in those prone to it. But the results do provide a possible explanation for why efforts to help children lose weight have often had disappointing results. The steps may have aimed too broadly at all schoolchildren, rather than starting before children enrolled in kindergarten and concentrating on those who were already fat at very young ages. © 2014 The New York Times Company
By James Gallagher Health and science reporter, BBC News Exposure to a once widely used pesticide, DDT, may increase the chances of developing Alzheimer's disease, suggest US researchers. A study, published in JAMA Neurology, showed patients with Alzheimer's had four times the levels of DDT lingering in the body than healthy people. Some countries still use the pesticide to control malaria. Alzheimer's Research UK said more evidence was needed to prove DDT had a role in dementia. DDT was a massively successful pesticide, initially used to control malaria at the end of World War Two and then to protect crops in commercial agriculture. However, there were questions about its impact on human health and wider environmental concerns, particularly for predators. It was banned in the US in 1972 and in many other countries. But the World Health Organization still recommends using DDT to keep malaria in check. Not clear DDT also lingers in the human body where it is broken down into DDE. The team at Rutgers University and Emory University tested levels of DDE in the blood of 86 people with Alzheimer's disease and compared the results with 79 healthy people of a similar age and background. The results showed those with Alzheimer's had 3.8 times the level of DDE. However, the picture is not clear-cut. Some healthy people had high levels of DDE while some with Alzheimer's had low levels. Alzheimer's also predates the use of DDT. The researchers believe the chemical is increasing the chance of Alzheimer's and may be involved in the development of amyloid plaques in the brain, a hallmark of the disease, which contribute to the death of brain cells. BBC © 2014
By BENEDICT CAREY People of a certain age (and we know who we are) don’t spend much leisure time reviewing the research into cognitive performance and aging. The story is grim, for one thing: Memory’s speed and accuracy begin to slip around age 25 and keep on slipping. The story is familiar, too, for anyone who is over 50 and, having finally learned to live fully in the moment, discovers it’s a senior moment. The finding that the brain slows with age is one of the strongest in all of psychology. Lisa Haney Over the years, some scientists have questioned this dotage curve. But these challenges have had an ornery-old-person slant: that the tests were biased toward the young, for example. Or that older people have learned not to care about clearly trivial things, like memory tests. Or that an older mind must organize information differently from one attached to some 22-year-old who records his every Ultimate Frisbee move on Instagram. Now comes a new kind of challenge to the evidence of a cognitive decline, from a decidedly digital quarter: data mining, based on theories of information processing. In a paper published in Topics in Cognitive Science, a team of linguistic researchers from the University of Tübingen in Germany used advanced learning models to search enormous databases of words and phrases. Since educated older people generally know more words than younger people, simply by virtue of having been around longer, the experiment simulates what an older brain has to do to retrieve a word. And when the researchers incorporated that difference into the models, the aging “deficits” largely disappeared. “What shocked me, to be honest, is that for the first half of the time we were doing this project, I totally bought into the idea of age-related cognitive decline in healthy adults,” the lead author, Michael Ramscar, said by email. But the simulations, he added, “fit so well to human data that it slowly forced me to entertain this idea that I didn’t need to invoke decline at all.” © 2014 The New York Times Company
by Helen Thomson When the criteria for diagnosing autism were changed last year, concerns were raised that people already diagnosed might be re-evaluated and end up losing access to treatments and services. The American Psychiatric Association (APA), which publishes the diagnostic guidelines, recommends that children who are receiving appropriate treatment as the result of the old criteria should not be required to undergo a re-examination with the new criteria by insurance companies. But a small survey revealed to New Scientist suggests that not everyone is following the party line. In May, the APA published the DSM-5, the latest edition of what has come to be known as psychiatry's diagnostic bible. One controversial change was to the criteria used to diagnose different kinds of autism, which are now combined under the umbrella term of "Autism Spectrum Disorder" (ASD). Under the previous criteria of DSM-4, a person would be diagnosed with ASD by exhibiting at least six of 12 behaviours, which include problems with communication, interaction and repetition. Now, that same person would need to exhibit three deficits in social communication and interaction and at least two repetitive behaviours – the latter, say critics, makes the new criteria more restrictive. To see how the change in criteria was affecting people, Autism Speaks, a US science and advocacy organisation, asked users of its website to complete an online survey about their experiences. "We wanted to ensure that people are still maintaining access to the services they need," says Michael Rosanoff, Autism Speaks' associate director for public health research and scientific review. © Copyright Reed Business Information Ltd.
Link ID: 19174 - Posted: 01.27.2014
By SARAH MASLIN NIR The day after the funeral of Avonte Oquendo, the boy with autism whose remains were found this month after he disappeared at age 14 from his school in October, his mother and grandmother stood with Senator Charles E. Schumer as he announced a proposal for a new law. Called “Avonte’s law,” it would finance a program to provide optional electronic tracking devices to be worn by children with autism. “Avonte’s running away was not an isolated incident,” Mr. Schumer, Democrat of New York, said at a news conference on Sunday morning in his office on the East Side of Manhattan. “This is a high-tech solution to an age-old problem.” Citing research that suggests nearly 50 percent of children with autism wander off, often to escape the overstimulation of sounds and noise, Mr. Schumer said the new legislation would expand an existing Department of Justice program that grants money to law enforcement agencies and other groups to provide trackers for people who have Alzheimer’s disease. Mr. Schumer said he had contacted the department months ago about including children with autism in the program. There was receptiveness, he said, but money was needed to provide children with the devices, which cost $80 to $90 and a few dollars a month to operate. The legislation would allocate $10 million for the program, giving interested parents free access to the equipment, which can be worn like a watch or even sewn into clothing. Whether to use such a monitor would be up to the parents, and the exact system of employing the devices would be up to individual municipalities, Mr. Schumer said. There are different variants that could be selected, including one that alerts authorities automatically when a child has stepped across a given perimeter — for example, outside school grounds — and another that becomes activated only after authorities are called. © 2014 The New York Times Company
Link ID: 19173 - Posted: 01.27.2014
By CARL ZIMMER The term “X chromosome” has an air of mystery to it, and rightly so. It got its name in 1891 from a baffled biologist named Hermann Henking. To investigate the nature of chromosomes, Henking examined cells under a simple microscope. All the chromosomes in the cells came in pairs. All except one. Henking labeled this outlier chromosome the “X element.” No one knows for sure what he meant by the letter. Maybe he saw it as an extra chromosome. Or perhaps he thought it was an ex-chromosome. Maybe he used X the way mathematicians do, to refer to something unknown. Today, scientists know the X chromosome much better. It’s part of the system that determines whether we become male or female. If an egg inherits an X chromosome from both parents, it becomes female. If it gets an X from its mother and a Y from its father, it becomes male. But the X chromosome remains mysterious. For one thing, females shut down an X chromosome in every cell, leaving only one active. That’s a drastic step to take, given that the X chromosome has more than 1,000 genes. In some cells, the father’s goes dormant, and in others, the mother’s does. While scientists have known about this so-called X-chromosome inactivation for more than five decades, they still know little about the rules it follows, or even how it evolved. In the journal Neuron, a team of scientists has unveiled an unprecedented view of X-chromosome inactivation in the body. They found a remarkable complexity to the pattern in which the chromosomes were switched on and off. © 2014 The New York Times Company
by Laura Sanders Growing up, I loved it when my parents read aloud the stories of the Berenstain Bears living in their treehouse. So while I was pregnant with my daughter, I imagined lots of cuddly quiet time with her in a comfy chair, reading about the latest adventures of Brother and Sister. Of course, reality soon let me know just how ridiculous that idea was. My newborn couldn’t see more than a foot away, cried robustly and frequently for mysterious reasons, and didn’t really understand words yet. Baby V was simply not interested in the latest dispatch from Bear County. When I started reading child development expert Elaine Reese’s new book Tell Me a Story, I realized that I was not the only one with idyllic story time dreams. Babies and toddlers are squirmy, active people with short attention spans. “Why, then, do we cling to this soft-focus view of storytelling when we know it is unrealistic?” she writes. These days, as Baby V closes in on the 1-year mark, she has turned into a most definite book lover. But it’s not the stories that enchant her. It’s holding the book, turning its pages back to front to back again, flipping it over and generally showing it who’s in charge. Every so often I can entice Baby V to sit on my lap with a book, but we never read through a full story. Instead, we linger on the page with all the junk food that the Hungry Caterpillar chomps through, sticking our fingers in the little holes in the pages. And we make Froggy pop in and out of the bucket. And we study the little goats as they climb up and up and up on the hay bales. © Society for Science & the Public 2000 - 2014
By Melissa Healy Adolescents treated with the antidepressant fluoxetine -- better known by its commercial name, Prozac -- appear to undergo changes in brain signaling that result in changed behavior well into adulthood, says a new study. Adult mice and rats who were administered Prozac for a stretch of mid-adolescence responded to daunting social and physical challenges with less despair than animals who passed their teen years unmedicated, a team of researchers found. But, even as adults long separated from their antidepressant days, the Prozac veterans reacted to stressful situations with greater anxiety than did the adult Prozac virgins. The latest research, published Wednesday in the Journal of Neuroscience, offers evidence that treatment with a selective serotonin reuptake inhibitor -- an SSRI antidepressant -- has long-lived effects on the developing brain. It also zeroes in on how and where fluoxetine effects those lasting changes: by modifying the cascade of chemical signals issued by the brain's ventral tegmentum -- a region active in mood regulation -- in stressful situations. Yet, the new research raises more questions than it answers, since the changes in adults who were treated with Prozac as adolescents seem contradictory. Sensitivity to stress appears to predispose one to developing depression. So how does a medication that treats depression in children and teens -- and that continues to protect them from depression as adults -- also heighten their sensitivity to stress?
Dan Hurley Forget mindfulness meditation, computerized working-memory training, and learning a musical instrument; all methods recently shown by scientists to increase intelligence. There could be an easier answer. It turns out that sex might actually make you smarter. Researchers in Maryland and South Korea recently found that sexual activity in mice and rats improves mental performance and increases neurogenesis (the production of new neurons) in the hippocampus, where long-term memories are formed. In April, a team from the University of Maryland reported that middle-aged rats permitted to engage in sex showed signs of improved cognitive function and hippocampal function. In November, a group from Konkuk University in Seoul concluded that sexual activity counteracts the memory-robbing effects of chronic stress in mice. “Sexual interaction could be helpful,” they wrote, “for buffering adult hippocampal neurogenesis and recognition memory function against the suppressive actions of chronic stress.” So growing brain cells through sex does appear to have some basis in scientific fact. But there’s some debate over whether fake sex—pornography—could be harmful. Neuroscientists from the University of Texas recently argued that excessive porn viewing, like other addictions, can result in permanent “anatomical and pathological” changes to the brain. That view, however, was quickly challenged in a rebuttal from researchers at the University of California, Los Angeles, who said that the Texans "offered little, if any, convincing evidence to support their perspectives. Instead, excessive liberties and misleading interpretations of neuroscience research are used to assert that excessive pornography consumption causes brain damage." © 2014 by The Atlantic Monthly Group
Injuries to the head can leave victims susceptible to early death even years later through impaired judgement, a major analysis of survivors shows. Those with a history of psychiatric disorders before the injury are most at risk of dying prematurely. The study, in JAMA Psychiatry, of 40 years of data on more than two million people, showed that overall a brain injury trebled the risk. Suicide and fatal injuries were among the commonest causes of early death. More than one million people in Europe are taken to hospital with a traumatic brain injury each year. The study, by researchers at the University of Oxford and the Karolinska Institute in Stockholm, looked at Swedish medical records between 1969 and 2009. They followed patients who survived the initial six-month danger period after injury. The data showed that without injury 0.2% of people were dying prematurely - before the age of 56. However, the premature-death rate was three-fold higher in patients who had previously suffered traumatic brain injury. In those who also had a psychiatric disorder the rate soared to 4%. Dr Seena Fazel, one of the researchers in Oxford, said: "There are these subgroups with really high rates, and these are potentially treatable illnesses, so this is something we can do something about." BBC © 2014
A new website that helps determine whether someone might have Alzheimer's disease or dementia is so popular that the site crashed temporarily. Ohio State University's website says its Self-Administered Gerocognitive Exam (SAGE) is a test that can be done in your own home with a paper and pencil. When researchers visited 45 community events where they asked people to take the simple test, they found that of the 1, 047 who did it, 28 per cent were identified with cognitive impairment, test developer Dr. Douglas Scharre of Ohio State and his team reported Monday in The Journal of Neuropsychiatry and Clinical Neurosciences. Alzheimer's test Researchers in Ohio say the SAGE test has been shown to be effective in spotting the early signs of cognitive decline. (Ohio State University Wexner Medical Center) Participants were told the test represented their baseline level, which doctors could use for future comparisons during re-screening. "What we found was that this SAGE self-administered test correlated very well with detailed cognitive testing," Scharre said in a release. "If we catch this cognitive change really early, then we can start potential treatments much earlier than without having this test." The Alzheimer Society of Canada says early diagnosis can help with planning, care and support. © CBC 2014
Link ID: 19137 - Posted: 01.16.2014
By ANDREW POLLACK Launch media viewer Kristin Tremblay helps make dinner at home in Gainesville, Fla. She has a disorder that makes her uncontrollably hungry. Rob C. Witzel for The New York Times Lisa Tremblay still recalls in horror the time her daughter Kristin pulled a hot dog crawling with ants from the garbage at a cookout and prepared to swallow it. Kristin has a rare genetic abnormality that gives her an incessant, uncontrollable hunger. Some people with the condition, called Prader-Willi syndrome, will eat until their stomach ruptures and they die. And, not surprisingly, many are obese. “She’s eaten dog food. She’s eaten cat food,” said Ms. Tremblay, who lives in Nokomis, Fla. When Kristin, now 28, was a child, neighbors once called social welfare authorities, thinking Kristin was not being fed because she complained of being hungry so much. Once an obscure and neglected disease, Prader-Willi is starting to attract more attention from scientists and pharmaceutical companies for a simple reason: It may shed some light on the much broader public health problems of overeating and obesity. “These are remarkable human models of severe obesity,” said Dr. Steven B. Heymsfield, a professor and former executive director of the Pennington Biomedical Research Center in Baton Rouge, La. “When we discover the underlying mechanism of these very rare disorders, they will shed light on garden-variety obesity.” One drug being developed to help obese people lose weight has shown some preliminary signs of success in patients with Prader-Willi. The drug, beloranib, is believed to work by reducing fat synthesis and increasing fat use. In a small trial, it reduced weight and body fat and lowered the food-seeking urge, according to the drug’s developer, Zafgen. © 2014 The New York Times Company
Training to improve cognitive abilities in older people lasted to some degree 10 years after the training program was completed, according to results of a randomized clinical trial supported by the National Institutes of Health. The findings showed training gains for aspects of cognition involved in the ability to think and learn, but researchers said memory training did not have an effect after 10 years. The report, from the Advanced Cognitive Training for Independent and Vital Elderly (ACTIVE) study, appears in the January 2014 issue of the Journal of the American Geriatrics Society. The project was funded by the National Institute on Aging (NIA) and the National Institute of Nursing Research (NINR), components of the NIH. “Previous data from this clinical trial demonstrated that the effects of the training lasted for five years,” said NIA Director Richard J. Hodes, M.D. “Now, these longer term results indicate that particular types of cognitive training can provide a lasting benefit a decade later. They suggest that we should continue to pursue cognitive training as an intervention that might help maintain the mental abilities of older people so that they may remain independent and in the community.” “ACTIVE is an important example of intervention research aimed at enabling older people to maintain their cognitive abilities as they age,” said NINR Director Patricia Grady, Ph.D. “The average age of the individuals who have been followed over the last 10 years is now 82. Given our nation’s aging population, this type of research is an increasingly high priority.”
By Gary Stix The blood-brain barrier is the Berlin Wall of human anatomy and physiology Its closely packed cells shield neurons and the like from toxins and pathogens, while letting pass glucose and other essential chemicals for brain metabolism (caffeine?). For years, pharmaceutical companies and academic researchers have engaged in halting efforts to traverse this imposing blockade in order to deliver some of the big molecules that might potentially help slow the progression of devastating neurological diseases. Like would-be refugees from the former East Germany, many medications get snagged by border guards during the crossing—a molecular security force that either impedes or digests any invader. There have been many attempts to secure safe passage—deploying chemicals that make brain-barrier “endothelial” cells shrivel up, or wielding tiny catheters or minute bubbles that slip through minuscule breaches. Success has been mixed at best—none of these molecular cargo carriers have made their way as far as human trials. Roche, the Swiss-based drugmaker, reported in the Jan. 8 Neuron a bit of progress toward overcoming the lingering technical impediments. The study described a new technique that tricks one of the BBB’s natural checkpoints to let through an elaborately engineered drug that attacks the amyloid-beta protein fragments that may be the primary culprit inflicting the damage wrought by Alzheimer’s. The subterfuge involves the transferrin receptor, a docking site used to transport iron into the brain. Roche took a fragment of an antibody that binds the transferrin receptor and latched it onto another antibody that, once on the other side of the BBB, attaches to and then removes amyloid. © 2014 Scientific American
Link ID: 19121 - Posted: 01.13.2014
by Bethany Brookshire When most people think of the quintessential lab mouse, they think of a little white mouse with red eyes. Soft fur. A timid nature. But scientists think of something very different. This mouse is black, small and fast, with pink ears and a pinkish tail. It’s got black eyes to match. The fur may be soft, but the temper sure isn’t. This is the C57 Black 6 mouse. Each Black 6 mouse should be almost identical to every other Black 6 mouse. They have been bred to their own siblings for hundreds of generations, so there should be very few genetic differences left. But even supposedly identical mouse strains have their differences. These take the form of mutations in single DNA base pairs that accumulate in different populations. Recently, researchers showed that one of these tiny changes in a single gene was enough to produce a huge difference in how two groups of Black 6 mice respond to drugs. And the authors identified a surprising number of other small DNA differences still waiting to be explored. On one level, the new work offers scientists a novel tool for identifying genes that could relate to behaviors. But it also serves as a warning. “Identical” mouse populations aren’t as alike as many scientists had assumed. The Black 6, the most common lab mouse in the United States, is used for everything from drug abuse studies to cancer research. The Black 6 is also the reference strain for the Mouse Genome Sequencing Consortium. Whenever scientists discover a new genetic change in a mouse strain, they compare it first against the Black 6. And it’s the mouse used by the International Knockout Mouse Consortium (now the International Mouse Phenotyping Consortium), which keep a library of mouse embryos with different deleted genes. The Allen Brain Atlas, a database of neuroanatomy and gene activity throughout the mouse brain, relies on the Black 6 as well. © Society for Science & the Public 2000 - 2014
By PAM BELLUCK Does vitamin E help people with Alzheimer’s disease? For years, scientists have been trying to find out, guessing that the vitamin’s antioxidant properties might be beneficial. But the results from clinical trials have been mixed and — following a report that high doses of vitamin E may increase the risk of death — cautionary. Now a study suggests that vitamin E supplements may be good for some Alzheimer’s patients after all. The benefit was not huge, but for a devastating disease that has proved almost impervious to treatment, it was notable. The study, published in Wednesday’s issue of JAMA, The Journal of the American Medical Association, found that over a little more than two years, high-dose vitamin E slowed the decline of people with mild to moderate Alzheimer’s by about six months on average. Vitamin E did not delay cognitive or memory deterioration, however. Instead, it seemed to temporarily protect something many patients consider especially valuable: their ability to perform daily activities like putting on clothes and feeding themselves. Compared with other study participants, people who took vitamin E also required about two fewer hours of help from caregivers per day, the researchers said. “Is it really going to dramatically alter the lives of Alzheimer’s patients? That’s unclear,” said Dr. Scott Small, director of Columbia University’s Alzheimer’s Disease Research Center, who was not involved in the study. “But it might improve patients’ ability to bathe themselves and dress themselves.” © 2014 The New York Times Company
Link ID: 19086 - Posted: 01.02.2014