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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.”

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 19126 - Posted: 01.14.2014

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

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 19121 - Posted: 01.13.2014

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

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19086 - Posted: 01.02.2014

By Regina Harrell and Pulse, I am a primary-care doctor who makes house calls in and around Tuscaloosa, Ala. Today my rounds start at a house located down a dirt road a few miles outside town. Gingerly, I cross the front walk; Mrs. Edgars told me that she killed a rattlesnake in her flowerbed last year. She is at the door, expecting my visit. Mr. Edgars sits on the couch, unable to recall that I am his doctor, or even that I am a doctor, but happy to see me nonetheless. We chat about the spring garden and the rain, then we move on to Mr. Edgars’s arthritis. Earlier on in his dementia, he wandered the woods, and his wife was afraid he would get lost and die, although the entire family agreed that this was how he would want it. Now, in a strange twist, his knee arthritis has worsened enough that it has curtailed his wanderings. I suspect that Mrs. Edgars is undertreating the pain to decrease the chance that he’ll wander off again. We talk about how anxious he grows whenever she’s out of his sight and how one of his children comes to sit with him so that she can run errands. She shows me a quilt remnant found in a log cabin on their property; it likely belonged to her husband’s grandfather, making the rough-edged fabric about a century old. I leave carrying a parting gift from her — a jar of homegrown pickled okra. When I get back to the office, I turn on the computer to write a progress note in Mr. Edgars’s electronic health record, or EHR. In addition to recording the details of our visit, I must try to meet the new federal criteria for “meaningful use,” criteria that have been adopted by my office with threats that I won’t get paid for my work if I don’t. © 1996-2013 The Washington Post

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19067 - Posted: 12.24.2013

A study in mice shows how a breakdown of the brain’s blood vessels may amplify or cause problems associated with Alzheimer’s disease. The results published in Nature Communications suggest that blood vessel cells called pericytes may provide novel targets for treatments and diagnoses. “This study helps show how the brain’s vascular system may contribute to the development of Alzheimer’s disease,” said study leader Berislav V. Zlokovic, M.D. Ph.D., director of the Zilkha Neurogenetic Institute at the Keck School of Medicine of the University of Southern California, Los Angeles. The study was co-funded by the National Institute of Neurological Diseases and Stroke (NINDS) and the National Institute on Aging (NIA), parts of the National Institutes of Health. Alzheimer’s disease is the leading cause of dementia. It is an age-related disease that gradually erodes a person’s memory, thinking, and ability to perform everyday tasks. Brains from Alzheimer’s patients typically have abnormally high levels of plaques made up of accumulations of beta-amyloid protein next to brain cells, tau protein that clumps together to form neurofibrillary tangles inside neurons, and extensive neuron loss. Vascular dementias, the second leading cause of dementia, are a diverse group of brain disorders caused by a range of blood vessel problems. Brains from Alzheimer’s patients often show evidence of vascular disease, including ischemic stroke, small hemorrhages, and diffuse white matter disease, plus a buildup of beta-amyloid protein in vessel walls. Furthermore, previous studies suggest that APOE4, a genetic risk factor for Alzheimer’s disease, is linked to brain blood vessel health and integrity.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 19033 - Posted: 12.14.2013

Taking some heartburn medications for more than two years is linked to a higher risk of vitamin B12 deficiency in adults, a U.S. study suggests. Left untreated, vitamin B12 deficiency can lead to dementia, neurological damage, anemia, and other complications. Knowing that stomach acid aids in vitamin B12 absorption, researchers set out to test whether suppressing the acids can lead to vitamin deficiency. The drugs in question are known as proton pump inhibitors and they include such well known brands as Losec, Nexium, Prabacid and Pariet. Doses of more than 1.5 pills per day were more strongly associated with vitamin D deficiency than doses of less than 0.75 pills per day, Dr. Douglas Corley, a gastroenterologist and research scientist with the Kaiser Permanente Division of Research in Broadway, Calif. and his co-authors said in Wednesday's issue of the Journal of the American Medical Association. "This research raises the question of whether people who are taking acid-depressing medications long term should be screened for vitamin B12 deficiency," Corley said in a release. "It's a relatively simple blood test, and vitamin supplements are an effective way of managing the vitamin deficiency, if it is found." For the study, researchers looked at electronic health records of 25,956 adults diagnosed with vitamin B12 deficiency in Northern California between January 1997 and June 2011, and compared them with 184,199 patients without B12 deficiency during the same time period. Among the 25,956 patients who had vitamin B12 deficiency, 12 per cent used proton pump inhibitors for at least two years, compared with 7.2 per cent of those in the control group. © CBC 2013

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 19019 - Posted: 12.11.2013

By Ingfei Chen The way doctors diagnose Alzheimer's disease may be starting to change. Traditionally clinicians have relied on tests of memory and reasoning skills and reports of social withdrawal to identify patients with Alzheimer's. Such assessments can, in expert hands, be fairly conclusive—but they are not infallible. Around one in five people who are told they have the neurodegenerative disorder actually have other forms of dementia or, sometimes, another problem altogether, such as depression. To know for certain that someone has Alzheimer's, doctors must remove small pieces of the brain, examine the cells under a microscope and count the number of protein clumps called amyloid plaques. An unusually high number of plaques is a key indicator of Alzheimer's. Because such a procedure risks further impairing a patient's mental abilities, it is almost always performed posthumously. In the past 10 years, however, scientists have developed sophisticated brain scans that can estimate the amount of plaque in the brain while people are still alive. In the laboratory, these scans have been very useful in studying the earliest stages of Alzheimer's, before overt symptoms appear. The results are reliable enough that last year the Food and Drug Administration approved one such test called Amyvid to help evaluate patients with memory deficits or other cognitive difficulties. Despite the FDA's approval, lingering doubts about the exact role of amyloid in Alzheimer's and ambivalence about the practical value of information provided by the scan have fueled debate about when to order an Amyvid test. Not everyone who has an excessive amount of amyloid plaque develops Alzheimer's, and at the moment, there is generally no way to predict whom the unlucky ones will be. Recent studies have shown that roughly one third of older citizens in good mental health have moderate to high levels of plaque, with no noticeable ill effects. And raising the specter of the disorder in the absence of symptoms may upset more people than it helps because no effective treatments exist—at least not yet. © 2013 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 19018 - Posted: 12.11.2013

Researchers striving to understand the origins of dementia are building the case against a possible culprit: lead exposure early in life. A study spanning 23 years has now revealed that monkeys who drank a lead-rich formula as infants later developed tangles of a key brain protein, called tau, linked to Alzheimer's disease. Though neuroscientists say more work is needed to confirm the connection, the research suggests that people exposed to lead as children—as many in America used to be before it was eliminated from paint, car emissions, water, and soil—could have an increased risk of the common, late-onset form of Alzheimer’s disease. Even in small doses, lead can wreak havoc on the heart, intestines, kidneys, and nervous system. Children are especially prone to its pernicious effects, as it curbs brain development. Many studies have linked early lead exposure with lower IQs. Researchers estimate that one in 38 children in the United States still have harmful levels of the metal in their systems, but evidence linking this exposure to dementia later in life has been tenuous. A team led by toxicologist Nasser Zawia, however, has vigorously pursued the lead hypothesis. In one early study, from 2008, the group showed that plaques, insoluble globs of a protein called β-amyloid, marred the brains of five macaques that had consumed a lead-enriched formula as infants. The researchers had compared the preserved brain tissues from those macaques, sacrificed in 2003 at age 23 in a National Institutes of Health lab, with four similarly aged monkeys who had had lead-free formula. The amyloid plaques closely resembled those in the brains of adults with Alzheimer's disease that are thought to contribute to the dementia. © 2013 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19012 - Posted: 12.10.2013

People with dementia who exercise improve their thinking abilities and everyday life, a body of medical research concludes. The Cochrane Collaboration carried out a systematic review of eight exercise trials involving more than 300 patients living at home or in care. Exercise did little for patients' moods, the research concluded. But it did help them carry out daily activities such as rising from a chair, and boosted their cognitive skills. Whether these benefits improve quality of life is still unclear, but the study authors say the findings are reason for optimism. Dementia affects some 800,000 people in the UK. And the number of people with the condition is steadily increasing because people are living longer. It is estimated that by 2021, the number of people with dementia in the UK will have increased to around one million. With no cure, ways to improve the lives of those living with the condition are vital. Researcher Dorothy Forbes, of the University of Alberta, and colleagues who carried out the Cochrane review, said: "Clearly, further research is needed to be able to develop best practice guidelines to enable healthcare providers to advise people with dementia living at home or in institutions. "We also need to understand what level and intensity of exercise is beneficial for someone with dementia." BBC © 2013

Related chapters from BP7e: 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: 18999 - Posted: 12.05.2013

By James Gallagher Health and science reporter, BBC News The number of people living with dementia worldwide is set to treble by 2050, according to a new analysis. Alzheimer's Disease International says 44 million people live with the disease, but that figure will increase to 135 million by 2050. The figures were released ahead of the G8 dementia summit in London next week. In the UK, dementia research receives one eighth of the amount of funding that is spent on cancer, which charities say is insufficient. Alzheimer's Disease International expects increasing life expectancies to drive a surge in cases in poor and middle-income countries, particularly in South East Asia and Africa. Currently 38% of cases are in rich countries. But that balance is predicted shift significantly by 2050, with 71% of patients being in poor and middle-income countries. The report says most governments are "woefully unprepared for the dementia epidemic". Marc Wortmann, the executive director at Alzheimer Disease International, said: "It's a global epidemic and it is only getting worse - if we look into the future the numbers of elderly people will rise dramatically." Jeremy Hughes, chief executive of the UK's Alzheimer's Society, said: "Dementia is fast becoming the biggest health and social care challenge of this generation. "We must tackle dementia now, for those currently living with the condition across the world and for those millions who will develop dementia in the future. BBC © 2013

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18998 - Posted: 12.05.2013

by Jessica Griggs HAVING type 2 diabetes may mean you are already on the path to Alzheimer's. This startling claim comes from a study linking the two diseases more intimately than ever before. There is some good news: the same research also offers a way to reverse memory problems associated with diabetes – albeit in rats – which may hint at a new treatment for Alzheimer's. "Perhaps you should use Alzheimer's drugs at the diabetes stage to prevent cognitive impairment in the first place," says Ewan McNay from the University at Albany in New York. Alzheimer's cost the US $130 billion in 2011 alone. One of the biggest risk factors is having type 2 diabetes. This kind of diabetes occurs when liver, muscle and fat cells stop responding efficiently to insulin, the hormone that tells them to absorb glucose from the blood. The illness is usually triggered by eating too many sugary and high-fat foods that cause insulin to spike, desensitising cells to its presence. As well as causing obesity, insulin resistance can also lead to cognitive problems such as memory loss and confusion. In 2005, a study by Susanne de la Monte's group at Brown University in Providence, Rhode Island, identified a reason why people with type 2 diabetes had a higher risk of developing Alzheimer's. In this kind of dementia, the hippocampus, a part of the brain involved in learning and memory, seemed to be insensitive to insulin. Not only could your liver, muscle and fat cells be "diabetic" but so it seemed, could your brain. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18987 - Posted: 11.30.2013

by Laura Sanders If you own a television, a computer or a smartphone, you may have seen ads for Lumosity, the brain-training regimen that promises to sharpen your wits and improve your life. Take the bait, and you’ll first create a profile that includes your age, how much sleep you get, the time of day you’re most productive and other minutiae about your life and habits. After this digital debriefing, you can settle in and start playing games designed to train simple cognitive skills like arithmetic, concentration and short-term recall. The 50 million people signed up for Lumosity presumably have done so because they want to improve their brains, and these games promise an easy, fun way to do that. The program also offers metrics, allowing users to chart their progress over weeks, months and years. Written in these personal digital ledgers are clues that might help people optimize their performance. With careful recordkeeping, for example, you might discover that you hit peak brainpower after precisely one-and-a-half cups of medium roast coffee at 10:34 a.m. on Tuesdays. But you’re not the only one who has access to this information. With each click, your performance data will fly by Internet into the eager hands of scientists at Lumos Labs, the San Francisco company that created Lumosity. Giant datasets like this one, created as a by-product of people paying money to learn about and improve themselves, will revolutionize research in human health and behavior, some scientists believe. Lumos Labs researchers hope that their brain-training data in particular could reveal deep truths about how the human mind works. They believe that they have a nimble, customizable and cheap way to discover things about the brain that would otherwise take huge amounts of money and many years to unearth with standard lab-based studies. Other researchers have also taken note, and some have gotten permission to use Lumosity data in their own research. Some of these researchers are hunting for subtle signatures of Alzheimer’s in the data. Others are investigating more fundamental mysteries with cross-cultural studies of how the brain builds emotions and how memory works. © Society for Science & the Public 2000 - 2013.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 10: Biological Rhythms and Sleep
Link ID: 18984 - Posted: 11.30.2013

Dara Mohammadi At the beginning of next year, Clive Holmes will attempt to do something remarkable. But you'd never guess it from meeting this mild-mannered psychiatrist with a hint of a Midlands accent. In fact, you could be sitting in his office in the Memory Assessment and Research Centre at Southampton University and be unaware that he was up to anything out of the ordinary – save for a small whiteboard behind his desk, on which he's drawn a few amorphous blobs and squiggles. These, he'll assure you, are components of the immune system. As a psychiatrist, he's had little formal training in immunology, but has spent much of his time of late trying to figure how immune cells in the body communicate with others in the brain. These signals into the brain, he thinks, accelerate the speed at which neurons – nerve cells in the brain – are killed in late-stage Alzheimer's disease and at the beginning of next year he hopes to test the idea that blocking these signals can stop or slow down disease progression. If he shows any dent on disease progression, he would be the first to do so. Despite the billions of pounds pumped into finding a cure over the last 30 years, there are currently no treatments or prevention strategies. "Drug development has been largely focused on amyloid beta," says Holmes, referring to the protein deposits that are characteristically seen in the brains of people with Alzheimer's and are thought to be toxic to neurons, "but we're seeing that even if you remove amyloid, it seems to make no difference to disease progression." © 2013 Guardian News and Media Limited

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18944 - Posted: 11.19.2013

By Melissa Hogenboom Science reporter, BBC News Changes to specific cells in the retina could help diagnose and track the progression of Alzheimer's disease, scientists say. A team found genetically engineered mice with Alzheimer's lost thickness in this layer of eye cells. As the retina is a direct extension of the brain, they say the loss of retinal neurons could be related to the loss of brain cells in Alzheimer's. The findings were revealed at the US Society for Neuroscience conference. The team believes this work could one day lead to opticians being able to detect Alzheimer's in a regular eye check, if they had the right tools. Alterations in the same retinal cells could also help detect glaucoma - which causes blindness - and is now also viewed as a neurodegenerative disease similar to Alzheimer's, the researchers report. Scott Turner, director of the memory disorders programme at Georgetown University Medical Center, said: "The retina is an extension of the brain so it makes sense to see if the same pathologic processes found in an Alzheimer's brain are also found in the eye." Dr Turner and colleagues looked at the thickness of the retina in an area that had not previously been investigated. This included the inner nuclear layer and the retinal ganglion cell layer. They found that a loss of thickness occurred only in mice with Alzheimer's. The retinal ganglion cell layer had almost halved in size and the inner nuclear layer had decreased by more than a third. BBC © 2013

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 7: Vision: From Eye to Brain
Link ID: 18925 - Posted: 11.14.2013

Kenneth S. Kosik Twenty years of research and more than US$1-billion worth of clinical trials have failed to yield an effective drug treatment for Alzheimer's disease. Most neuroscientists, clinicians and drug developers now agree that people at risk of the condition will probably need to receive medication before the onset of any cognitive symptoms. Yet a major stumbling block for early intervention is the absence of tools that can reveal the first expression of the insidious disease. So far, researchers have tended to focus on macroscopic changes associated with the disease, such as the build up of insoluble plaques of protein in certain areas of the brain, or on individual genes or molecular pathways that seem to be involved in disease progression. I contend that detecting the first disruptions to brain circuitry, and tracking the anatomical and physiological damage underlying the steady cognitive decline that is symptomatic of Alzheimer's, will require tools that operate at the 'mesoscopic' scale: techniques that probe the activity of thousands or millions of networked neurons. Although such tools are yet to be realized, several existing technologies indicate that they are within reach. Charted territory All the current approaches that are used to diagnose Alzheimer's are crude and unreliable. Take the classic biomarkers of the disease: a build up of plaques of the protein β-amyloid in a person's cerebral cortex, for instance, or elevated levels of the tau protein and dampened levels of β-amyloid in their cerebrospinal fluid. Although such markers are predictive of the disease, the interval between their appearance and the onset of cognitive problems is hugely variable, ranging from months to decades. © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 18895 - Posted: 11.08.2013

by Catherine de Lange Speak more than one language? Bravo! It seems that being bilingual helps delay the onset of several forms of dementia. Previous studies of people with Alzheimer's disease in Canada showed that those who are fluent in two languages begin to exhibit symptoms four to five years later than people who are monolingual. Thomas Bak at the University of Edinburgh, UK, wanted to know whether this was truly down to language, or whether education or immigration status might be driving the delay, since most bilingual people living in Toronto, where the first studies were conducted, tended to come from an immigrant background. He also wondered whether people suffering from other forms of dementia might experience similar benefits. He teamed up with Suvarna Alladi, a neurologist working on memory disorders at Nizam's Institute of Medical Sciences (NIMSH) in Hyderabad, India. "In India, bilingualism is part of everyday life," says Bak. The team compared the age that dementia symptoms appeared in some 650 people who visited the NIMSH over six years. About half spoke at least two languages. This group's symptoms started on average four and a half years later than those in people who were monolingual. "Incredibly the number of years in delay of symptom onset they reported in the Indian sample is identical to our findings," says Ellen Bialystok, at Toronto's York University, who conducted the original Canadian studies. What's more, the same pattern appeared in three different types of dementia: Alzheimer's, frontotemporal and vascular. The results also held true for a group of people who were illiterate, suggesting that the benefits of being bilingual don't depend on education. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 15: Language and Our Divided Brain
Link ID: 18886 - Posted: 11.07.2013

By James Gallagher Health and science reporter, BBC News A clearer picture of what causes Alzheimer's disease is emerging after the largest ever analysis of patients' DNA. A massive international collaboration has now doubled the number of genes linked to the dementia to 21. The findings, published in the journal Nature Genetics, indicate a strong role for the immune system. Alzheimer's Research UK said the findings could "significantly enhance" understanding of the disease. The number of people developing Alzheimer's is growing around the world as people live longer. However, major questions around what causes the dementia, how brain cells die, how to treat it or even diagnose it remain unanswered. "It is really difficult to treat a disease when you do not understand what causes it," one of the lead researchers, Prof Julie Williams from Cardiff University, said. Detective work The genetic code, the instructions for building and running the body, was scoured for clues. A group - involving nearly three quarters of the world's Alzheimer's geneticists from 145 academic institutions - looked at the DNA of 17,000 patients and 37,000 healthy people. They found versions of 21 genes, or sets of instructions, which made it more likely that a person would develop Alzheimer's disease. They do not guarantee Alzheimer's will develop, but they do make the disease more likely. By looking at the genes' function in the body, it allows researchers to figure out the processes going wrong in Alzheimer's disease. BBC © 2013

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18843 - Posted: 10.28.2013

Charlie Cooper Scientists have hailed an historic “turning point” in the search for a medicine that could beat Alzheimer's disease, after a drug-like compound was used to halt brain cell death in mice for the first time. Although the prospect of a pill for Alzheimer's remains a long way off, the landmark British study provides a major new pathway for future drug treatments. The compound works by blocking a faulty signal in brains affected by neurodegenerative diseases, which shuts down the production of essential proteins, leading to brain cells being unprotected and dying off. It was tested in mice with prion disease - the best animal model of human neurodegenerative disorders - but scientists said they were confident the same principles would apply in a human brain with debilitating brain diseases such as Alzheimer's or Parkinson's. The study, published today in the journal Science Translational Medicine, was carried out at the Medical Research Council's (MRC) Toxicology Unit at the University of Leicester. “It's a real step forward,” team leader Professor Giovanna Mallucci told The Independent. “It's the first time a substance has been given to mice that prevents brain disease. The fact that this is a compound that can be given orally, that gets into the brain and prevents brain disease, is a first in itself… We can go forward and develop better molecules and I can't see why preventing this process should only be restricted to mice. I think this probably will translate into other mammalian brains.” © independent.co.uk

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18775 - Posted: 10.10.2013

By Kendall Powell, Although my grandmother received a diagnosis of Alzheimer’s disease in her 80s, my family was never sure that’s what she had. She certainly suffered from dementia: She was able to recall childhood memories but couldn’t remember what she had had for lunch. But dementia and Alzheimer’s are not synonymous. Back then, the only way to look for the telltale Alzheimer’s plaques — deposits of the protein fragment beta amyloid that accumulate in the spaces between nerve cells — was through an autopsy, which we didn’t do. Over the past 15 years, researchers have developed a greater understanding of how the disease works. We now have more accurate ways of diagnosing Alzheimer’s and are moving closer to developing drugs to directly attack the disease. Much of this work is still in the early stages, but experts are growing more hopeful about dealing with the debilitating disease, which currently has no cure. Now, for example, we no longer have to rely on autopsies to confirm the existence of Alzheimer’s plaques. In a major advance last year, the Food and Drug Administration approved a method that uses a radioactive dye, known commercially as Amyvid, to light up amyloid plaques in a PET scan. The FDA approved Amyvid to rule out Alzheimer’s when the scan is negative and to confirm the presence of plaques when positive, but that does not necessarily indicate the disease is present. However, some doctors are using the scans to confirm the disease, which experts say is misdiagnosed up to a quarter of the time. Paul Aisen, director of the Alzheimer’s Disease Cooperative Study at University of California at San Diego, calls Amyvid an “enormous advance” because a positive scan, combined with his clinical diagnosis, means he can tell patients and their families the disease is “present, not probable.” © 1996-2013 The Washington Post

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18728 - Posted: 10.01.2013

Billions of dollars have been spent on clinical trials of Alzheimer’s drugs that target amyloid plaques—the hallmark protein tangles that clog brain cells in people with the memory-robbing disease. So far, all have failed, leading some frustrated researchers to say it’s time to move on to other drug targets. Others say the drugs have not yet been fairly tested because they were administered too late, after brain damage is irreversible. Yesterday, the National Institutes of Health (NIH) announced that it is giving $33 million to a study that researchers hope will either revive the amyloid hypothesis, or put it to bed. The new trial—estimated to cost at least $100 million overall, with most of the remaining funds provided by partners in the pharmaceutical industry—will be part of the Alzheimer's Prevention Initiative, a large consortium of researchers attempting to identify biomarkers and treatments that can slow or stop the disease. Lead researchers Eric Reiman and Pierre Tariot of the Banner Alzheimer’s Institute in Phoenix plan to give a yet-to-be identified anti-amyloid drug, or placebo, to 650 people who carry two copies of the APOE4 gene—a genetic double whammy that confers a 10-fold increased risk of developing Alzheimer’s late in life. All participants will be between the ages of 60 and 75 and healthy, including free of recognized Alzheimer’s symptoms. Roughly a third will likely not have much amyloid in their brains yet, allowing the researchers to track whether the drug affects its accumulation, Reiman says. © 2012 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18677 - Posted: 09.21.2013