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by Judith Graham You’ve turned 65 and exited middle age. What are the chances you’ll develop cognitive impairment or dementia in the years ahead? New research about “cognitive life expectancy” — how long older adults live with good vs. declining brain health — shows that after age 65, men and women spend more than a dozen years in good cognitive health, on average. And, over the past decade, that time span has been expanding. By contrast, cognitive challenges arise in a more compressed time frame in later life, with mild cognitive impairment (problems with memory, decision-making or thinking skills) lasting about four years, on average, and dementia (Alzheimer’s disease or other related conditions) occurring over 1½ to two years. Even when these conditions surface, many seniors retain an overall sense of well-being, according to new research presented in April at the Population Association of America’s annual meeting. “The majority of cognitively impaired years are happy ones, not unhappy ones,” said Anthony Bardo, a co-author of that study and an assistant professor of sociology at the University of Kentucky at Lexington. Recent research finds that: Most seniors don’t have cognitive impairment or dementia. Of Americans 65 and older, about 20 to 25 percent have mild cognitive impairment while about 10 percent have dementia, according to Kenneth Langa, an expert in the demography of aging and a professor of medicine at the University of Michigan. Risks rise with advanced age, and the portion of the population affected is significantly higher for people older than 85. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25099 - Posted: 06.18.2018

By Judith Graham, You’ve turned 65 and exited middle age. What are the chances you’ll develop cognitive impairment or dementia in the years ahead? New research about “cognitive life expectancy”—how long older adults live with good versus declining brain health—shows that after age 65 men and women spend more than a dozen years in good cognitive health, on average. And, over the past decade, that time span has been expanding. By contrast, cognitive challenges arise in a more compressed time frame in later life, with mild cognitive impairment (problems with memory, decision-making or thinking skills) lasting about four years, on average, and dementia (Alzheimer’s disease or other related conditions) occurring over 1½ to two years. Even when these conditions surface, many seniors retain an overall sense of well-being, according to new research presented last month at the Population Association of America’s annual meeting. “The majority of cognitively impaired years are happy ones, not unhappy ones,” said Anthony Bardo, a co-author of that study and assistant professor of sociology at the University of Kentucky-Lexington. Recent research finds that: Most seniors don’t have cognitive impairment or dementia. Of Americans 65 and older, about 20 to 25 percent have mild cognitive impairment while about 10 percent have dementia, according to Dr. Kenneth Langa, an expert in the demography of aging and a professor of medicine at the University of Michigan. Risks rise with advanced age, and the portion of the population affected is significantly higher for people over 85. © 2018 Scientific American

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25022 - Posted: 05.25.2018

Kelly Crowe · In a darkened room at Toronto's Krembil Research Institute, Dr. Donald Weaver is looking at a screen covered in green fluorescent dots. That's not a good thing. Those glowing green dots are exactly what this Alzheimer's researcher did not want to see. "Weeks if not months of work went into this compound and it failed," he said. "It's done." Weaver, a neurologist and chemist, was testing a compound to see if it could prevent the clumping of a protein called tau which creates distinctive tangles in the brains of people with Alzheimer's disease. If it had worked, it might have been a candidate for a new drug. But it didn't work, just like the thousands of others he's already tried. Failure is normal for researchers engaged in the frustrating search for drugs to treat Alzheimer's disease. "You have to be passionate," Weaver said. "This is a disease in which so many approaches have failed. You really have to deeply believe that your approach is correct just to get up every day and keep working at it." Many promising drugs have failed But after a series of high-profile drug failures over the past few years, scientists are facing the disturbing possibility that their leading theory of Alzheimer's might be fatally flawed. It's called the amyloid hypothesis, and it was an obvious target for researchers because the amyloid protein forms distinctive plaques in the brains of people with Alzheimer's. "That led to the conclusion it must be playing a pretty important role in the disease," Weaver said. The amyloid hypothesis was first proposed in 1992, and for the past 25 years research has focused on finding compounds that clear amyloid from the brain or slow down its production. ©2018 CBC/Radio-Canada.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25015 - Posted: 05.24.2018

by Erin Blakemore Want to cure Alzheimer’s? Get in line. Researchers have long been puzzled by the disease and vexed by how long it’s taking to unravel its mysteries. One group of scientists is helping speed up that process with assistance from the public. “Stall Catchers,” a game created by Cornell University’s Human Computation Institute, turns the hunt for a cure from frustrating to fun. In the game, players watch short movies — made using a multiphoton microscope — that show blood flowing through the brains of living mice. Players work on a data set of thousands of images to point out “stalls” — areas of reduced blood flow caused by white blood cells accumulating on the sides of the vessels. The films might seem far removed from the experience typical of people with Alzheimer’s disease: difficulty concentrating, jumbled speech and confusion. But they may be closely linked: It’s thought that reduced blood flow in the brain is at least partially responsible for Alzheimer’s symptoms. When a blood vessel in the brain gets stalled, blood doesn’t flow as it should. A single stalled capillary might seem like no big deal, but in mice with Alzheimer’s disease, up to 2 percent of brain capillaries can be stalled. Because vessels in the brain are so interconnected, that can restrict overall brain blood flow by up to 30 percent. Reduced blood flow has been found in the brains of humans with Alzheimer’s disease, too. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24945 - Posted: 05.07.2018

By JANE E. BRODY I had hoped that by now most adults in this country would have completed an advance directive for medical care and assigned someone they trusted to represent their wishes if and when they are unable to speak for themselves. Alas, at last count, barely more than one-third have done so, with the rest of Americans leaving it up to the medical profession and ill-prepared family members to decide when and how to provide life-prolonging treatments. But even the many who, like me, have done due diligence — completed the appropriate forms, selected a health care agent and expressed their wishes to whoever may have to make medical decisions for them — may not realize that the documents typically do not cover a likely scenario for one of the leading causes of death in this country: dementia. Missing in standard documents, for example, are specific instructions about providing food and drink by hand as opposed to through a tube. Advanced dementia, including Alzheimer’s disease, is the sixth leading cause of death overall in the United States. It is the fifth leading cause for people over 65, and the third for those over 85. Yet once the disease approaches its terminal stages, patients are unable to communicate their desires for or against life-prolonging therapies, some of which can actually make their last days more painful and hasten their demise. End of Life Choices New York is trying to change that and has created an advance directive that it hopes will become a prototype for the rest of the country. (Washington State has already developed its own, though somewhat different, document.) © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24936 - Posted: 05.03.2018

Sarah Boseley Health editor Some antidepressants and bladder medicines could be linked to dementia, according to a team of scientists who are calling for doctors to think about “de-prescribing” them where possible. Tricyclic antidepressants such as amitriptyline, which are also prescribed for pain and to help with sleeping, and one of the SSRI class, paroxetine (also known as Seroxat), are implicated by the largest ever study to look at this possible risk. Amitriptyline was in the news in February, named as the most effective of the antidepressants in a study. Some Parkinson’s drugs are also linked to a raised dementia risk. As a group, these are known as anticholinergic drugs. There are 1.5 to 2 million people in England alone on this type of drug. It is already known that they can cause short-term confusion and raise people’s risk of a fall. One in five people taking an antidepressant is on an anticholinergic drug, usually amitriptyline. The researchers warn that the increasing tendency for older people to be taking a cocktail of drugs for different conditions may be part of the problem. “In the last 20 years, the number of older individuals taking five or more medicines has quadrupled,” said Dr Ian Maidment, senior lecturer in clinical pharmacy at Aston University. “Many of these medicines will have some anticholinergic activity and, in the light of today’s findings, we have to consider whether the risks of dementia outweigh the benefits from taking a cocktail of prescribed drugs. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 24905 - Posted: 04.26.2018

Alison Abbott Neuroscientist Michael Heneka knows that radical ideas require convincing data. In 2010, very few colleagues shared his belief that the brain’s immune system has a crucial role in dementia. So in May of that year, when a batch of new results provided the strongest evidence he had yet seen for his theory, he wanted to be excited, but instead felt nervous. He and his team had eliminated a key inflammation gene from a strain of mouse that usually develops symptoms of Alzheimer’s disease. The modified mice seemed perfectly healthy. They sailed through memory tests and showed barely a sign of the sticky protein plaques that are a hallmark of the disease. Yet Heneka knew that his colleagues would consider the results too good to be true. Even he was surprised how well the mice fared; he had expected that removal of the gene, known as Nlpr3, would protect their brains a little, but not that it would come close to preventing dementia symptoms. “I thought something must have gone wrong with the experiments,” says Heneka, from the German Center for Neurodegenerative Diseases in Bonn. He reanalysed the results again and again. It was past midnight when he finally conceded that they might actually be true. Over the next couple of years, he confirmed that nothing had gone wrong with the experiments. Together with his colleagues, he replicated and elaborated on the results1. © 2018 Macmillan Publishers Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 24899 - Posted: 04.25.2018

by Lauren Neergaard It’s pretty extraordinary for people in their 80s and 90s to keep the same sharp memory as someone several decades younger, so scientists are peeking into the brains of“superagers” who do to uncover their secret. The work is the flip side of the disappointing hunt for new drugs to fight or prevent Alzheimer’s disease. Instead of tackling that problem, “why don’t we figure out what it is we might need to do to maximize our memory?” said neuro­scientist Emily Rogalski, who leads the SuperAging study at Northwestern University in Chicago. Parts of the brain shrink with age, one of the reasons that most people experience a gradual slowing of at least some types of memory late in life. But it turns out that superagers’ brains aren’t shrinking nearly as fast as their peers’. And autopsies of the first superagers to die during the study show they harbor a lot more of a special kind of nerve cell in a deep-brain region that’s important for attention, Rogalski told a recent meeting of the American Association for the Advancement of Science. These elite elders are “more than just an oddity or a rarity,” said neuroscientist Molly Wagster of the National Institute on Aging, which helps fund the research. “There’s the potential for learning an enormous amount and applying it to the rest of us, and even to those who may be on a trajectory for some type of neurodegenerative disease.” © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 24874 - Posted: 04.17.2018

Jon Hamilton An international coalition of brain researchers is suggesting a new way of looking at Alzheimer's. Instead of defining the disease through symptoms like memory problems or fuzzy thinking, the scientists want to focus on biological changes in the brain associated with Alzheimer's. These include the plaques and tangles that build up in the brains of people with the disease. But they say the new approach is intended only for research studies, and isn't yet ready for use by most doctors who treat Alzheimer's patients. If the new approach is widely adopted, it would help researchers study patients whose brain function is still normal, but are likely to develop dementia caused by Alzheimer's. "There is a stage of the disease where there are no symptoms and we need to have some sort of a marker," says Eliezer Masliah, who directs the Division of Neuroscience at the National Institute on Aging. The new approach would be a dramatic departure from the traditional way of looking at Alzheimer's, says Clifford Jack, an Alzheimer's researcher at Mayo Clinic Rochester. In the past, "a person displayed a certain set of signs and symptoms and it was expected that they had Alzheimer's pathology," says Jack, who is the first author of the central paper describing the proposed new "research framework." © 2018 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24846 - Posted: 04.10.2018

By NICHOLAS BAKALAR Being physically fit in midlife may reduce a woman’s risk for dementia. In 1968, Swedish researchers evaluated the cardiovascular fitness of 191 women ages 38 to 60, testing their endurance with an ergometer cycling test. Then they examined them periodically through 2012. Over the years, 44 women developed dementia. They categorized the women into three fitness groups based on peak workload in their cycling tests: low, medium and high. The incidence of all-cause dementia was 32 percent in the low fitness group, 25 percent for the medium, and 5 percent among those with a high fitness level. The average age at dementia was 11 years older in the high-fitness group than in the medium fitness group. Compared with medium fitness, high fitness decreased the risk of dementia by 88 percent. The study, in Neurology, controlled for many variables, including smoking, drinking, blood pressure and cholesterol, and the follow-up was very long. But the sample was small and the study is observational, and the authors draw no conclusions about cause and effect. Still, the senior author, Dr. Ingmar Skoog, a professor of psychiatry at the University of Gothenburg, said that women should get moving for many reasons. “If you start exercising,” he said, “you reduce your risk for cardiovascular disease, cancer and dementia. And you get immediate gratification by feeling better.” © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24794 - Posted: 03.29.2018

Sara Reardon Jhon Kennedy was building a house for his family when he realized that his 45-year-old father was beginning to struggle with daily life. His dad tried to help with the construction project but often forgot to complete simple tasks. And he kept getting lost on the way home from work. Jhon Kennedy wasn’t surprised: his four uncles had also started to lose their memories, one by one. But their doctors in Colombia's rural Antioquia region, which is known for its mountainous terrain and coffee plantations, had never heard of early-onset dementia. It wasn’t until a cousin learned about a study of Alzheimer’s disease at the University of Antioquia in Medellín that Jhon Kennedy’s relatives understood the illness they faced. For more than three decades, researchers there have been tracking a genetic mutation — common in the region — that causes Alzheimer’s to strike people in their 40s and 50s. Later this year, a team at the university will begin scanning the brains of some Alzheimer’s-study participants with a technique that is available only in a few major medical centres worldwide. It will allow the researchers to track a protein called tau, which accumulates rapidly in the brains of people with the disease as symptoms begin to emerge. Watching tau form in real time could reveal the role it plays in Alzheimer’s, says Francisco Lopera, the neurologist who is leading the research. Many scientists have long believed that the disease is triggered by another protein, amyloid, that builds up in the brains of people with Alzheimer’s. But several drugs that reduce amyloid levels have failed to relieve the symptoms of the disease in clinical trials, increasing researchers’ interest in the role of tau. © 2018 Macmillan Publishers Limited,

Related chapters from BN8e: 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: 24793 - Posted: 03.28.2018

By Michelle Roberts Health editor, BBC News online Four dementia scientists have shared this year's 1m Euro brain prize for pivotal work that has changed our understanding of Alzheimer's disease. Profs John Hardy, Bart De Strooper, Michel Goedert, based in the UK, and Prof Christian Haass, from Germany, unpicked key protein changes that lead to this most common type of dementia. On getting the award, Prof Hardy said he hoped new treatments could be found. He is donating some of his prize money to care for Alzheimer's patients. Much of the drug discovery research that's done today builds on their pioneering work, looking for ways to stop the build-up of damaging proteins, such as amyloid and tau. Alzheimer's and other dementias affect 50 million people around the world, and none of the treatments currently available can stop the disease. Path to beating Alzheimer's Prof Hardy's work includes finding rare, faulty genes linked to Alzheimer's disease. These genetic errors implicated a build-up of amyloid as the event that kick-starts damage to nerve cells in Alzheimer's. This idea, known as the amyloid cascade hypothesis, has been central to Alzheimer's research for nearly 30 years. Together with Prof Haass, who is from the University of Munich, Prof Hardy, who's now at University College London, then discovered how amyloid production changes in people with rare inherited forms of Alzheimer's dementia. How one woman and her family transformed Alzheimer's research Prof Goedert's research at Cambridge University, meanwhile, revealed the importance of another damaging protein, called tau, while Prof De Stooper, who is the new director of the UK Dementia Research Institute at UCL, discovered how genetic errors that alter the activity of proteins called secretases can lead to Alzheimer's processes. Dr David Reynolds, Chief Scientific Officer at Alzheimer's Research UK, said: "Our congratulations go to all four of these outstanding scientists whose vital contributions have transformed our understanding of the complex causes of Alzheimer's disease. © 2018 BBC.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24730 - Posted: 03.08.2018

Helen Thomson In March 2015, Li-Huei Tsai set up a tiny disco for some of the mice in her laboratory. For an hour each day, she placed them in a box lit only by a flickering strobe. The mice — which had been engineered to produce plaques of the peptide amyloid-β in the brain, a hallmark of Alzheimer’s disease — crawled about curiously. When Tsai later dissected them, those that had been to the mini dance parties had significantly lower levels of plaque than mice that had spent the same time in the dark1. Tsai, a neuroscientist at Massachusetts Institute of Technology (MIT) in Cambridge, says she checked the result; then checked it again. “For the longest time, I didn’t believe it,” she says. Her team had managed to clear amyloid from part of the brain with a flickering light. The strobe was tuned to 40 hertz and was designed to manipulate the rodents’ brainwaves, triggering a host of biological effects that eliminated the plaque-forming proteins. Although promising findings in mouse models of Alzheimer’s disease have been notoriously difficult to replicate in humans, the experiment offered some tantalizing possibilities. “The result was so mind-boggling and so robust, it took a while for the idea to sink in, but we knew we needed to work out a way of trying out the same thing in humans,” Tsai says. “There’s been an explosion in brain wave research…pick your area and different people are trying to apply extra cranial stimulation.” The neuroscience that’s making waves for a wide range of conditions. © 2018 Macmillan Publishers Limited,

Related chapters from BN8e: 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: 24710 - Posted: 02.28.2018

By Natalie Crockett BBC News Older people in Wales are being urged to think about donating their brains after they die to help scientists researching dementia. Researchers at Cardiff University are not actively recruiting at the moment but are still keen to hear from people aged over 85 without a diagnosis. While they also recruit donors with dementia as healthy brains are needed for comparisons. Donor Ken Baxter, 75, said: "When I'm finished, it isn't any use to me." Since 2009, 460 people in Wales have signed up, with 79 successful donations made to the Brains for Dementia Research project so far. They are recruited through its team at the university, which is working to identify which genes contribute to a person's susceptibility to developing Alzheimer's disease. It is hoped they will then be able to predict which people are more likely to get it. But to do this they need to study human brain tissue, as looking at the distribution of protein deposits on the brain is the only way to get a definitive diagnosis of the disease. While donors who have dementia often find out about brain donation from medical professionals, it can be harder to attract those with healthy brains. Mr Baxter is one such donor and decided to donate his brain after seeing how dementia affected a friend. He saw it as a way to help others but admitted he does not always get a positive reaction to his plans. He said: "'[People say] are you sure? It's not something I want to do'. And some people are horrified when you tell them - I can't see a reason why but a lot of people take it the wrong way. "They think 'I've never thought of that' - but you're helping someone. If we can overcome these diseases, so much the better." © 2018 BBC.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24696 - Posted: 02.26.2018

Jon Hamilton Beer has fueled a lot of bad ideas. But on a Friday afternoon in 2007, it helped two Alzheimer's researchers come up with a really a good one. Neuroscientists Robert Moir and Rudolph Tanzi were sipping Coronas in separate offices during "attitude adjustment hour" at Massachusetts General Hospital, Harvard's largest teaching hospital. And, by chance, each scientist found himself wondering about an apparent link between Alzheimer's disease and the immune system. Moir had been surfing through random scientific papers online — something he does for an hour or so on most Fridays. "I cruise wherever my fancy takes me," he says. And on this day, he cruised to research on molecules known as antimicrobial peptides. They're part of the ancient immune system that's found in all forms of life and plays an important role in protecting the human brain. One way antimicrobial peptides protect us is by engulfing and neutralizing a germ or some other foreign invader. That gives newer parts of the immune system time to get mobilized. These peptides are "extremely important," Moir says. "They're not like legacies from an immune system we don't use anymore. If you don't have them, you're going to die in a couple of hours." As Moir surfed through paper after paper, he realized that one of these ancient molecules, known as LL-37, looked a lot like a molecule closely associated with Alzheimer's. That molecule is called amyloid-beta and it forms the sticky plaques that tend to build up in the brains of people with dementia. © 2018 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 24680 - Posted: 02.19.2018

By John Carroll, For years now the gold standard for R&D in Alzheimer’s disease has focused on generating convincing evidence that any new therapy being studied could slow the cognitive decline of patients and help preserve their ability to perform the kind of daily functions that can keep a patient independent for a longer period of time. That’s a hurdle no one has managed to clear for well over a decade. So now, with late-stage clinical failures piling up, the U.S. Food and Drug Administration (FDA) has set off down a path to adapt those standards as researchers are pushed inexorably into earlier and earlier forms of the disease, ahead of the brain damage inflicted by Alzheimer’s. In a set of draft guidances, the agency essentially proposed to offer an approval pathway for new drugs that could prevent the onset of the devastating symptoms of Alzheimer’s if drug developers could hit acceptable biomarkers that indicate the drug is working. And they’re likely going to continue with a new gold standard that will focus on long-term cognition alone, lowering the bar for drugs for an enormous and growing market. David Miller, the clinical vice president of Bracket, a Washington, D.C.-based tech provider which specializes in Alzheimer’s studies, tells me the draft guidance hit just after a meeting of the Washington, D.C.-based Alzheimer’s Association research group, which was discussing how you might be able to use a mix of markers for amyloid β and tau—two toxic proteins frequently cited as likely triggers—alongside neurodegenerative markers to identify patients who could be enrolled at a very early point in the disease. © 2018 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24674 - Posted: 02.17.2018

Aimee Cunningham Knocking back an enzyme swept mouse brains clean of protein globs that are a sign of Alzheimer’s disease. Reducing the enzyme is known to keep these nerve-damaging plaques from forming. But the disappearance of existing plaques was unexpected, researchers report online February 14 in the Journal of Experimental Medicine. The brains of mice engineered to develop Alzheimer’s disease were riddled with these plaques, clumps of amyloid-beta protein fragments, by the time the animals were 10 months old. But the brains of 10-month-old Alzheimer’s mice that had a severely reduced amount of an enzyme called BACE1 were essentially clear of new and old plaques. Studies rarely demonstrate the removal of existing plaques, says neuroscientist John Cirrito of Washington University in St. Louis who was not involved in the study. “It suggests there is something special about BACE1,” he says, but exactly what that might be remains unclear. One theory to how Alzheimer’s develops is called the amyloid cascade hypothesis. Accumulation of globs of A-beta protein bits, the idea goes, drives the nerve cell loss and dementia seen in the disease, which an estimated 5.5 million Americans had in 2017. If the theory is right, then targeting the BACE1 enzyme, which cuts up another protein to make A-beta, may help patients. |© Society for Science & the Public 2000 - 2018.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24666 - Posted: 02.15.2018

By Andy Coghlan Surgical instruments may need to be cleaned more thoroughly after brain operations, following the news that they might be spreading proteins linked to Alzheimer’s disease. There’s no evidence yet that spreading these proteins from one person to another can cause Alzheimer’s disease itself. But a study of eight people suggests that unclean instruments may sometimes lead to a rare and potentially fatal kind of brain bleeding disorder. People who have Alzheimer’s disease typically have plaques of sticky amyloid proteins in their brains, although it remains unclear whether these are a cause or a consequence of the condition. But when amyloid builds up in blood vessels in the brain, it can sometimes make them so brittle that they leak or burst. This condition, called cerebral amyloid angiopathy (CAA), usually doesn’t develop until people reach their sixties or older. But Sebastian Brandner, at University College London, and his team have been investigating the cases of eight people who developed CAA under the age of 60. Scouring their medical records, the team found that all eight of these people had undergone brain surgery during childhood or their teenage years for a variety of reasons. Of the eight people, at least three have already died from strokes, which can be caused by CAA. They died between the ages of 37 and 57. © Copyright New Scientist Ltd.

Related chapters from BN8e: 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: 24665 - Posted: 02.15.2018

The supplement nicotinamide riboside (NR) – a form of vitamin B3 – prevented neurological damage and improved cognitive and physical function in a new mouse model of Alzheimer’s disease. The results of the study, conducted by researchers at the National Institute on Aging (NIA) part of the National Institutes of Health, suggest a potential new target for treating Alzheimer’s disease. The findings appear in the Feb. 5, 2018, issue of Proceedings of the National Academy of Sciences. NR acts on the brain by normalizing levels of nicotinamide adenine dinucleotide (NAD+), a metabolite vital to cellular energy, stem cell self-renewal, resistance to neuronal stress and DNA repair. In Alzheimer’s disease, the brain’s usual DNA repair activity is impaired, leading to mitochondrial dysfunction, lower neuron production, and increased neuronal dysfunction and inflammation. “The pursuit of interventions to prevent or delay Alzheimer’s and related dementias is an important national priority,” said Richard J. Hodes, M.D., director of the NIA. “We are encouraging the testing of a variety of new approaches, and this study’s positive results suggest one avenue to pursue further.” Based on their studies in human postmortem brain, they developed a new strain of mice mimicking major features of human Alzheimer’s such as tau pathology, failing synapses, neuronal death and cognitive impairment. Using this animal model, the researchers tested the effects of an NR supplement by adding it to the drinking water of the mice. Over a three-month period, researchers found that mice who received NR showed reduced tau in their brains, but no change in amyloid-beta.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24627 - Posted: 02.07.2018

Ina Jaffe A study published Monday by Human Rights Watch finds that about 179,000 nursing home residents are being given antipsychotic drugs, even though they don't have schizophrenia or other serious mental illnesses that those drugs are designed to treat. Most of these residents have Alzheimer's disease or another form of dementia and antipsychotics aren't approved for that. What's more, antipsychotic drugs come with a "black box warning" from the FDA, stating that they increase the risk of death in older people with dementia. The study concluded that antipsychotic drugs were often administered without informed consent and for the purpose of making dementia patients easier to handle in understaffed facilities. Researchers focused on six states, including California and Texas, which have the most skilled nursing facilities. They used publicly available data, along with hundreds of interviews with residents, families and state ombudsmen, the officials who deal with complaints about long term care facilities. In 2012, the federal government began a program to reduce the use of antipsychotic drugs in nursing homes, in partnership with the nursing home industry, and advocacy organizations. Since then, the use of the drugs has dropped by about a third nationwide, from 23.9 percent of residents in 2012 to 15.7 percent at the beginning of 2017. The Centers for Medicare and Medicaid Services have called for an additional 15 percent reduction by 2019 for those nursing homes that have lagged in curtailing their use of antipsychotics. © 2018 npr

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 24620 - Posted: 02.06.2018