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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

David Hilfiker knows what's coming. He was diagnosed with Alzheimer's so early that he's had time to tell his family what he wants to happen once forgetfulness turns incapacitating. "When it's time to put me in an institution, don't have me at home and destroy your own life," said the retired physician, who is still well enough that he blogs about the insidious progress of the disease. "Watching the Lights Go Out," it's titled. Nearly half of all seniors who need some form of long-term care -— from help at home to full-time care in a facility — have dementia, the World Alzheimer Report said Thursday. It's a staggering problem as the global population ages, placing enormous strain on families who provide the bulk of that care at least early on, and on national economies alike. Indeed, cognitive impairment is the strongest predictor of who will move into a care facility within the next two years, 7.5 times more likely than people with cancer, heart disease or other chronic ailments of older adults, the report found. "It's astonishing," said Marc Wortmann, executive director of Alzheimer's Disease International, which commissioned the report and focused on the problems of caregiving. "What many countries try to do is keep people away from care homes because they say that's cheaper. Yes it's cheaper for the government or the health system, but it's not always the best solution." And dropping birth rates mean there are fewer children in families to take care of aging parents, too, said Michael Hodin of the Global Coalition on Aging. © CBC 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: 18676 - Posted: 09.21.2013

by Andy Coghlan The two major brain abnormalities that underlie Alzheimer's disease can now be viewed simultaneously in brain scans while people are still alive, providing new insight into how the disease develops and whether drugs are working. The breakthrough comes from the development of a harmless tracer chemical that is injected into the bloodstream and accumulates exclusively in "tau tangles" – one type of abnormality that occurs in the brains of people with Alzheimer's and other kinds of dementia. Fluorescent light emitted from the chemical is picked up using positron emission tomography (PET), showing exactly where the tangles are. The tracer remains in the brain for a few hours before being broken down and expelled from the body. Similar tracers already exist for beta amyloid plaques, the other major anatomical feature of Alzheimer's, so the one for tau tangles completes the picture. "This is a big step forward," says John Hardy, an Alzheimer's researcher at University College London. "This is of critical significance, as tau lesions are known to be more intimately associated with neuronal loss than plaques," says Makoto Higuchi of the National Institute of Radiological Sciences in Chiba, Japan, and head of the team who developed the new tracer. The tracer could help researchers unravel exactly how Alzheimer's develops, and enable earlier diagnosis and monitoring of treatments. © Copyright Reed Business Information Ltd.

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: 18673 - Posted: 09.19.2013

By PAM BELLUCK In the most significant sign yet of a broad shift in the focus of Alzheimer’s research from treating to preventing the disease, the federal government announced on Wednesday its largest grant so far to test an Alzheimer’s drug on healthy people at greatest risk for the most common form of the disease. The $33.2 million grant, and several other prevention studies awarded federal money in the last year, follow years of unsuccessful trials of treatments on people who already have dementia. Those failures have led to the realization that these drugs appear to be ineffective by the time memory and thinking problems have taken hold. At the same time, scientific advances have allowed researchers to identify people at risk for Alzheimer’s long before symptoms emerge. With five million Americans suffering from Alzheimer’s and their ranks projected to surge as baby boomers age, federal health officials consider the disease such a priority that Dr. Francis S. Collins, director of the National Institutes of Health, scraped money together when forced budget cuts slashed the Obama administration’s promise of $100 million in additional funding for Alzheimer’s for 2013. Dr. Collins said he dipped into the budgets of the 27 N.I.H. agencies to supply $40 million awarded Wednesday for several Alzheimer’s research projects. Another $5 million was provided by the National Institute on Aging. “The worst thing we could do would be to just hunker down and hold off tackling very important problems,” Dr. Collins said, adding, “Obviously, this is high-risk research, but goodness, the stakes are so high that we felt we had to go forward even in the face of the most difficult budget environment that anyone can remember in the N.I.H.” © 2013 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: 18672 - Posted: 09.19.2013

Drugs to treat Alzheimer's disease don't help patients with mild cognitive impairment and are linked to greater risk of harm, a Canadian review concludes. People with mild cognitive impairment show symptoms of memory problems that are not severe enough to be considered dementia or to interfere with day-to-day functioning. Each year, three to 17 per cent of people with mild cognitive impairment deteriorate to dementia, research suggests. It was hoped that "cognitive enhancers" used to treat dementia might delay progression to dementia. Dr. Sharon Straus of the department of geriatric medicine at the University of Toronto and her team reviewed clinical trials and reports on the effects of four cognitive enhancers. "Cognitive enhancers did not improve cognition or function among patients with mild cognitive impairment and were associated with a greater risk of gastrointestinal harms," the reviewers concluded in Monday's issue of the Canadian Medical Association Journal. "Our findings do not support the use of cognitive enhancers for mild cognitive impairment." The medications act on different neurotransmitters in the brain, such as acetylcholine. © 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: 18658 - Posted: 09.17.2013

Kelly Servick If keeping the brain spry were as simple as pumping iron, everyone would want to own the ultimate piece of cognitive exercise equipment. But designing activities to reverse the mental effects of aging is tricky. A new video game created by neuroscientists shows promise in reversing some signs of decline. Now, the researchers behind it aim to prove that video game training can be more than the latest workout craze. Games designed to keep the brain healthy as it ages have found an eager audience. “Many, many people have gotten into the business,” says neuropsychologist Glenn Smith of the Mayo Clinic in Rochester, Minnesota. The brain does appear to be capable of changing its structure and developing new skills over the course of a lifetime. But not all the products on the market are designed using scientific knowledge of the aging brain, and their ability to make meaningful, lasting changes hasn’t been proven, says Smith, who studies games as treatment for early signs of dementia. “There’s an awful lot of skepticism out there,” he says. The heart of the issue is whether practicing a video game can strengthen skills that are useful away from a computer. Early research showed that people could improve on computerized memory and speed tasks in the lab, Smith says. But it’s not clear whether these gains translate to everyday life. A recent trend puts more value in games that target the underlying problem—the decline in ability to remember and react as people age. © 2012 American Association for the Advancement of Science.

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: 18611 - Posted: 09.05.2013

By Caitlin Shure The newest chemical under investigation for managing Alzheimer’s disease (AD) is actually not new at all. Insulin, the therapeutic hormone all-too familiar to individuals with diabetes, has been around for decades. In fact December will mark 90 years since its discoverers earned the Nobel Prize in Physiology or Medicine for the extraction of insulin for clinical use. Yet to say that insulin has been under our noses all these years wouldn’t exactly be correct. Because if it had been under our noses, we might have sensed its neurologic benefits sooner. The latest insulin therapy is not delivered via injection like its diabetes-treating counterparts, nor does it come in the form of a pill or a patch like the cholinesterase inhibitors often prescribed to patients with AD. Instead this novel therapeutic enters the body through the nose—the only entry point that gives insulin a chance of reaching the brain. A large peptide molecule, insulin from the blood cannot float easily into the brain because the blood brain barrier (BBB), a sort of neuroprotective moat, prevents its transport. Fortified by cellular guards called tight junctions, the BBB rejects many pharmacologic hopefuls, allowing entrance only to certain types of substances. Namely small or lipophilic molecules can be administered orally (or via injection, or through the skin) and as long as the relevant chemicals end up in the blood stream, they can casually saunter across the BBB and act on the brain. Large and cumbersome, insulin does not have this luxury and must therefore take a more creative route across the moat. © 2013 Scientific American

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: 18546 - Posted: 08.22.2013

By James Gallagher Health and science reporter, BBC News A lifetime of too much copper in our diets may be contributing to Alzheimer's disease, US scientists say. However, research is divided, with other studies suggesting copper may actually protect the brain. The latest study in Proceedings of the National Academy of Sciences showed high levels of copper left the brain struggling to get rid of a protein thought to cause the dementia. Copper is a vital part of our diet and necessary for a healthy body. Tap water coming through copper pipes, red meat and shellfish as well as fruit and vegetables are all sources of dietary copper. Barrier The study on mice, by a team at the University of Rochester in New York, suggested that copper interfered with the brain's shielding - the blood brain barrier. Mice that were fed more copper in their water had a greater build-up of the metal in the blood vessels in the brain. The team said this interfered with the way the barrier functioned and made it harder for the brain to get rid of a protein call beta amyloid. One of the hallmarks of Alzheimer's disease is the formation of plaques of amyloid in the dying brain. Lead researcher Dr Rashid Deane said: "It is clear that, over time, copper's cumulative effect is to impair the systems by which amyloid beta is removed from the brain." BBC © 2013

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18532 - Posted: 08.20.2013

For most people, seeing a picture of a famous face — Oprah Winfrey, the Queen or Einstein, for instance — sparks immediate recognition and brings the name readily to the lips. But for people with a rare form of early-onset dementia called primary progressive aphasia, or PPA, the ability to identify a face or the person's name can be impaired. PPA strikes people aged about 40 to 65, much earlier than is typical for other forms of dementia like Alzheimer's disease. The condition is characterized by a deterioration in language and eventually the ability to communicate, although at least initially cognitive function in other areas remains intact, said Tamar Gefen, a PhD candidate in clinical neuropsychology at Northwestern University in Chicago. "Memory is fine, attention is fine and their planning, their judgment, their personality, their emotions — they're intact," explained Gefen, adding that early symptoms can include being unable to recall the names of familiar people or in some cases everyday objects. "Someone will come in and say: 'I can't remember my co-worker's name. I see her every day and I cannot remember it,"' she said. As the disease progresses, the person has difficulty speaking coherently and eventually stops talking altogether. Since the inability to put a name to a face can be an early sign of Alzheimer's disease, Gefen said it's important to properly diagnose the cause using specific tests that can identify PPA. © CBC 2013

Related chapters from BP7e: 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: 18498 - Posted: 08.13.2013