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Hannah Devlin Scientists have developed a new genetic test for Alzheimer’s risk that can be used to predict the age at which a person will develop the disease. A high score on the test, which is based on 31 genetic markers, can translate to being diagnosed many years earlier than those with a low-risk genetic profile, the study found. Those ranked in the top 10% in terms of risk were more than three times as likely to develop Alzheimer’s during the course of the study, and did so more than a decade before those who ranked in the lowest 10%. Strobe lighting provides a flicker of hope in the fight against Alzheimer’s Read more Rahul Desikan, of the University of California – who led the international effort, said the test could be used to calculate any individual’s risk of developing Alzheimer’s that year. “That is, if you don’t already have dementia, what is your yearly risk for AD onset, based on your age and genetic information,” he said. The so-called polygenic hazard score test was developed using genetic data from more than 70,000 individuals, including patients with Alzheimer’s disease and healthy elderly people. It is already known that genetics plays a powerful role in Alzheimer’s. Around a quarter of patients have a strong family history of the disease, and scientists have shown this is partly explained by a gene called ApoE, which comes in three versions, and is known to have a powerful influence on the risk of getting the most common late-onset type of Alzheimer’s. One version of ApoE appears to reduce risk by up to 40%, while those with two copies (one from each parent) of the high-risk version can increase risk by 12 times.

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: 23390 - Posted: 03.22.2017

By KIM SEVERSON SONOMA, Calif. — The first thing Paula Wolfert wants to make a guest is coffee blended with butter from grass-fed cows and something called brain octane oil. She waves a greasy plastic bottle of the oil around her jumble of a kitchen like a preacher who has taken up a serpent. Never mind that this is the woman who introduced tagines, Aleppo pepper and cassoulet to American kitchens, wrote nine cookbooks and once possessed a palate the food writer Ruth Reichl declared the best she’d ever encountered. Ms. Wolfert, 78, has dementia. She can’t cook much, even if she wanted to. Which, by the way, she doesn’t. She learned she probably had Alzheimer’s disease in 2013, but she suspected something wasn’t right long before. Words on a page sometimes made no sense. Complex questions started to baffle her. Since she has always been an audacious and kinetic conversationalist with a touch of hypochondria, friends didn’t notice anything was wrong. Doctors spoke of “senior moments.” But she knew. One day, Ms. Wolfert went to make an omelet for her husband, the crime novelist William Bayer. She had to ask him how. The woman who once marched up to the French chef Jean-Louis Palladin and told him a dish didn’t have enough salt can no longer taste the difference between a walnut and a pecan, or smell whether the mushrooms are burning. The list of eight languages she once understood has been reduced to English. Maybe 40 percent of the words she knew have evaporated. “What am I going to do, cry about it?” Ms. Wolfert said in an interview at her home this month, the slap of her Brooklyn accent still sharp. After all, she points out, her first husband left her in Morocco with two small children and $2,000: “I cried for 20 minutes and I thought, ‘This isn’t going to do any good.’” © 2017 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: 23389 - Posted: 03.22.2017

By NICHOLAS BAKALAR Some research has suggested that vitamin E and selenium supplements might lower the risk for Alzheimer’s disease, but a new long-term trial has found no evidence that they will. The study began as a randomized clinical trial in 2002 testing the supplements for the prevention of prostate cancer. When that study was stopped in 2009 because no effect was found, 3,786 of the original 7,540 men participated in a continuing study to test the antioxidants as a preventive for Alzheimer’s. The study, in JAMA Neurology, randomly assigned the men, whose average age was 67 at the start, to take either vitamin E, selenium, both supplements, or a placebo. By 2015, 4.4 percent of the men had dementia, but there was no difference between the groups. Neither selenium, vitamin E, nor both in combination were any more effective than a placebo. The study controlled for age, family history of Alzheimer’s disease, education, race, diabetes and other factors. The lead author, Richard J. Kryscio, a professor of statistics at the University of Kentucky, said that it is possible that different dosages or different types of selenium or vitamin E might show an effect. “We could have picked the wrong version or the wrong dose,” he said. “But there’s really no evidence that these supplements will make a difference down the road in preventing dementia.” © 2017 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: 23388 - Posted: 03.22.2017

Heidi Ledford Like a zombie that keeps on kicking, legal battles over mutant mice used for Alzheimer’s research are haunting the field once again — four years after the last round of lawsuits. In the latest case, the University of South Florida (USF) in Tampa has sued the US National Institutes of Health (NIH) for authorizing the distribution of a particular type of mouse used in the field. The first pre-trial hearing in the case is set to begin in a federal court on 21 March. The university holds a patent on the mouse, but the NIH has contracted the Jackson Laboratory, a non-profit organization in Bar Harbor, Maine, to supply the animals to researchers. The USF is now claiming that it deserves some of the money that went to the contractor. If the suit, filed in December 2015, is successful, it could set a precedent for other universities, cautions Robert Cook-Deegan, an intellectual-property scholar at the Washington DC centre of Arizona State University in Tempe. And that would threaten the affordability of and access to lab animals used to investigate. “It feels greedy to me,” Cook-Deegan says. “If other universities start doing this, all it does is push up the cost of research tools.” The mice, on which the USF filed a patent in 1997, express mutated forms of two genes1. These modifications help researchers to study how amyloid plaques develop in the brain, and enable them to investigate behavioural changes that manifest before those plaques appear. © 2017 Macmillan Publishers 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: 23356 - Posted: 03.15.2017

By Andy Coghlan People who have autoimmune disorders may be 20 per cent more likely to develop dementia. That’s according to an analysis of 1.8 million hospital cases in England. Based on data collected between 1999 and 2012, the study’s findings add to mounting evidence that chronic inflammation – a common feature of many autoimmune disorders – may be a trigger of dementia and Alzheimer’s disease. Previous studies have found that if infections or chronic inflammatory diseases – including diabetes – have pushed a person’s immune system into overdrive, this can lead to immune cells attacking healthy brain tissue. Varying effect According to the analysis, people with multiple sclerosis are among those with autoimmune disorders who are most likely to develop dementia. This finding isn’t very surprising, as the disorder is caused by the immune system attacking the central nervous system. The study, led by Michael Goldacre at the University of Oxford, found that people with the condition have double the risk of developing dementia. But other autoimmune disorders were also associated with rises in dementia risk. The skin condition psoriasis was linked to a 29 per cent increase, while the risk of developing dementia was 46 per cent higher in people who have lupus erythematosus, a disorder that involves rashes and fatigue. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: 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: 23300 - Posted: 03.02.2017

By Edward G. Barrett It’s no secret that fewer than 10 percent of investigational drugs achieve regulatory approval and reach the marketplace. But the chances of success for drugs developed to treat Alzheimer’s disease are even more grim. Despite researchers’ valiant efforts to stall, slow, or even beat this devastating neurodegenerative condition, there are still no effective drugs available to the estimated 5.4 million Americans with the disease. The scientific community has watched in dismay, time and again, as potential Alzheimer’s drugs that produced promising data in rodent models failed to work as expected in humans. For the most part, these drugs have pursued the promising “amyloid hypothesis,” which states that the disease may be caused by accumulation of beta-amyloid peptide in brain tissue resulting in neuron-killing plaques. But so far, no drug candidates targeting the beta-amyloid pathway have prevailed through late-stage clinical trials. Earlier this year, for example, Merck halted a Phase 2/3 trial of verubecestat, a small molecule inhibitor of a protein implicated in the buildup of beta-amyloid, called beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), due to a lack of efficacy. Another high-profile example occurred late last year, when Eli Lilly’s solanezumab, a monoclonal antibody active against the beta-amyloid peptide, failed to prevent cognitive decline in a Phase 3 trial. These accumulating failures call into question the promise of targeting the formation and occurrence of amyloid plaques as a viable approach for treating Alzheimer’s. So how do we break the chain? Are there other approaches we could be taking that could give us valuable insight before investing in human studies? © 1986-2017 The Scientist

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: 23295 - Posted: 03.01.2017

By GRETCHEN REYNOLDS For some people with early-stage Alzheimer’s disease, frequent, brisk walks may help to bolster physical abilities and slow memory loss, according to one of the first studies of physical activity as an experimental treatment for dementia. But the study’s results, while encouraging, showed that improvements were modest and not universal, raising questions about just how and why exercise helps some people with dementia and not others. Alzheimer’s disease affects more than five million people in the United States and more than 35 million worldwide, a number that is expected to double within 20 years. There are currently no reliable treatments for the disease. But past studies of healthy elderly people have found relationships between regular exercise and improved memories. Physically active older people are, for instance, significantly less likely than those who are sedentary to develop mild cognitive impairment, a frequent precursor to Alzheimer’s disease. Physically fit older people also tend to have more volume in their brain’s hippocampus than do sedentary people of the same age, brain scans show. The hippocampus is the portion of the brain most intimately linked with memory function. But most of this research has examined whether exercise might prevent Alzheimer’s disease. Little has been known about whether it might change the trajectory of the disease in people who already have the condition. So for the new study, published in February in PLoS One, researchers at the University of Kansas decided to work directly with people who had previously been given a diagnosis of Alzheimer’s disease. Because the disease can affect coordination as it progresses, the researchers focused on men and women in its early stages, who were still living at home and could safely walk by themselves or perform other types of light exercise. © 2017 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: 23294 - Posted: 03.01.2017

Laurel Hamers Clusters of a toxic bacterial protein have a surprising structure, differing from similar clumps associated with Alzheimer’s and Parkinson’s in humans, scientists report in the Feb. 24 Science. These clusters, called amyloids, are defined in part by their structure: straight regions of protein chains called beta strands, folded accordion-style into flat beta sheets, which then stack up to form a fiber. That definition might now need to be broadened. “All the amyloids that have been structurally looked at so far have certain characteristics,” says Matthew Chapman, a biologist at the University of Michigan in Ann Arbor who wasn’t part of the work. “This is the odd amyloid out right now.” In the human brain, misfolded proteins can form amyloids that trigger neurodegenerative diseases. But amyloids aren’t always a sign of something gone wrong — some bacteria make amyloids to help defend their turf. In Staphylococcus aureus, for example, the PSMα3 protein assembles into amyloids that help the bacteria kill other cells. Previous research suggested that PSMα3 clusters were like any other amyloid. But researchers using X-ray crystallography found that instead of straight beta strands, the PSMα3 fiber was made up of curly structures called alpha helices that resemble an old-fashioned phone cord. The helices still formed a familiar fiber shape just like the beta strands did, but the sheets making up that fiber were rippled instead of flat. |© Society for Science & the Public 2000 - 2017.

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: 23274 - Posted: 02.24.2017

By RONI CARYN RABIN Older adults who started sleeping more than nine hours a night — but had not previously slept so much — were at more than double the risk of developing dementia a decade later than those who slept nine hours or less, researchers report. The increased risk was not seen in people who had always slept more than nine hours. “We’re not suggesting you go wake up Grandpa. We think this might be a marker for the risk of dementia, not a cause” of the illness, said Dr. Sudha Seshadri, a professor of neurology at Boston University School of Medicine and the senior author of the study, in Neurology. Using data from 2,457 people, average age 72, who were part of a study in Framingham, Mass., the researchers found that those with a new habit of excessive slumber were at a greater risk of all forms of dementia, including Alzheimer’s, which is characterized by a buildup of beta amyloid, a toxic protein fragment that forms plaques in the brain. “My suspicion is that this is a compensatory mechanism: that at a time when amyloid is building up in the brain, people may be sleeping longer as the body is reacting and trying to remove it from the brain,” Dr. Seshadri added. © 2017 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: 23270 - Posted: 02.24.2017

Hannah Devlin Rambling and long-winded anecdotes could be an early sign of Alzheimer’s disease, according to research that suggests subtle changes in speech style occur years before the more serious mental decline takes hold. The scientists behind the work said it may be possible to detect these changes and predict if someone is at risk more than a decade before meeting the threshold for an Alzheimer’s diagnosis. Janet Cohen Sherman, clinical director of the Psychology Assessment Center at Massachusetts General Hospital, said: “One of the greatest challenges right now in terms of Alzheimer’s disease is to detect changes very early on when they are still very subtle and to distinguish them from changes we know occur with normal ageing.” Speaking at the American Association for the Advancement of Science in Boston, Sherman outlined new findings that revealed distinctive language deficits in people with mild cognitive impairment (MCI), a precursor to dementia. “Many of the studies to date have looked at changes in memory, but we also know changes occur in language,” she said. “I’d hope in the next five years we’d have a new linguistic test.” Sherman cites studies of the vocabulary in Iris Murdoch’s later works, which showed signs of Alzheimer’s years before her diagnosis, and the increasingly repetitive and vague phrasing in Agatha Christie’s final novels – although the crime writer was never diagnosed with dementia. Another study, based on White House press conference transcripts, found striking changes in Ronald Reagan’s speech over the course of his presidency, while George HW Bush, who was a similar age when president, showed no such decline.

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: Brain Asymmetry, Spatial Cognition, and Language
Link ID: 23259 - Posted: 02.21.2017

Bret Stetka In a series of recent interviews, President Donald Trump's longtime personal physician Dr. Harold N. Bornstein told The New York Times that our new commander in chief has what amounts to a pretty unremarkable medical chart. Like about a quarter of American adults, Trump is on a statin for high cholesterol. He also takes a daily baby aspirin for heart health, an occasional antibiotic for rosacea, a skin condition, and Propecia, a pill to promote hair growth. Bornstein also told the Times that should he be appointed White House doctor, he probably wouldn't test the president for baseline dementia risk, something many doctors have argued should be mandatory. At 70, Trump is the oldest American president to ever take office. Couple his age with a family history of dementia — his father Fred developed Alzheimer's disease in his 80s — and one could argue that the question of baseline cognitive testing for the U.S. head of state has taken on new relevance. An assortment of fairly simple tests exist that can establish a reference point for cognitive capacity and detect early symptoms of mental decline. One of the most common such screens is the Mini-Mental Status Examination, a series of questions that gauges attention, orientation and short-term memory. It takes about five to 10 minutes to complete. Yet admitting vulnerability of any kind isn't something politicians have been keen to do. The true health of politicians has likely been cloaked in secrecy since the days of Mesopotamian kings, but definitely since the Wilson administration. © 2017 npr

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: 23243 - Posted: 02.17.2017

By John Carroll, Scratch yet another Phase III Alzheimer’s drug hopeful. Merck announced late Tuesday that it is shuttering its EPOCH trial for the BACE inhibitor verubecestat in mild-to-moderate Alzheimer’s after the external data monitoring committee concluded that the drug was a bust, with “virtually” no chance of success. A separate Phase III study in prodromal patients, set to read out in two years, will continue as investigators found no signs of safety issues. This is one of Merck’s top late-stage drugs, and news of the failure drove down the pharma giant’s shares in after-market trading by 2.45%. BACE drugs essentially seek to interfere in the process that creates amyloid beta, a toxic protein often found in the brains of Alzheimer’s patients. As the top amyloid beta drugs like bapineuzumab and solanezumab — which sought to extract existing amyloid beta loads — ground their way to repeated failures, developers in the field turned increasingly to BACE therapies as an alternative mechanism that could provide the key to slowing this disease down. Merck’s effort was the most advanced in the pipeline, but Eli Lilly and others are still in hot pursuit with their own persistent BACE efforts. Teams from Biogen/Eisai and Novartis/Amgen are also beavering away on BACE. “Alzheimer’s disease is one of the most pressing and daunting medical issues of our time, with inherent, substantial challenges to developing an effective disease-modifying therapy for people with mild-to-moderate disease. Studies such as EPOCH are critical, and we are indebted to the patients in this study and their caregivers,” said Dr. Roger M. Perlmutter, president, Merck Research Laboratories. © 2017 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: 23238 - Posted: 02.16.2017

In a study of mice and monkeys, National Institutes of Health funded researchers showed that they could prevent and reverse some of the brain injury caused by the toxic form of a protein called tau. The results, published in Science Translational Medicine, suggest that the study of compounds, called tau antisense oligonucleotides, that are genetically engineered to block a cell’s assembly line production of tau, might be pursued as an effective treatment for a variety of disorders. Cells throughout the body normally manufacture tau proteins. In several disorders, toxic forms of tau clump together inside dying brain cells and form neurofibrillary tangles, including Alzheimer’s disease, tau-associated frontotemporal dementia, chronic traumatic encephalopathy and progressive supranuclear palsy. Currently there are no effective treatments for combating toxic tau. "This compound may literally help untangle the brain damage caused by tau,” said Timothy Miller, M.D., Ph.D., the David Clayson Professor of Neurology at Washington University, St. Louis, and the study's senior author. Antisense oligonucleotides are short sequences of DNA or RNA programmed to turn genes on or off. Led by Sarah L. DeVos, a graduate student in Dr. Miller’s lab, the researchers tested sequences designed to turn tau genes off in mice that are genetically engineered to produce abnormally high levels of a mutant form of the human protein. Tau clusters begin to appear in the brains of 6-month-old mice and accumulate with age. The mice develop neurologic problems and die earlier than control mice.

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: 23205 - Posted: 02.09.2017

By Emily Underwood LOS ANGELES, CALIFORNIA—In a barbed wire–enclosed parking lot 100 meters downwind of the Route 110 freeway, an aluminum hose sticks out of a white trailer, its nozzle aimed at an overpass. Every minute, the hose sucks up hundreds of liters of air mixed with exhaust from the roughly 300,000 cars and diesel-burning freight trucks that rumble by each day. Crouched inside the trailer, a young chemical engineer named Arian Saffari lifts the lid off a sooty cylinder attached to the hose, part of a sophisticated filtration system that captures and sorts pollutants by size. Inside is a scientific payload: particles of sulfate, nitrate, ammonium, black carbon, and heavy metal at least 200 times smaller than the width of a human hair. The particles are too fine for many air pollution sensors to accurately measure, says Saffari, who works in a lab led by Constantinos Sioutas at the University of Southern California (USC) here. Typically smaller than 0.2 µm in diameter, these “ultrafine” particles fall within a broader class of air pollutants commonly referred to as PM2.5 because of their size, 2.5 µm or less. When it comes to toxicity, size matters: The smaller the particles that cells are exposed to, Saffari says, the higher their levels of oxidative stress, marked by the production of chemically reactive molecules such as peroxides, which can damage DNA and other cellular structures. © 2017 American Association for the Advancement of Science.

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: 23158 - Posted: 01.27.2017

By Andy Coghlan NEW drug will finally cure Alzheimer’s! Sound familiar? Seemingly every other week, the results of one preliminary trial or another promise that a game-changing drug for Alzheimer’s disease is just around the corner. Check back a few months later, though, and all mention of the drug has vanished, save perhaps for a terse story about a failed trial. Almost all clinical trials of new drugs to combat Alzheimer’s fail. No drug has bucked the trend in 20 years, but you wouldn’t know it from the constant promises of a breakthrough. Last November, after the failure of a particularly high-profile trial, for some the jig was up. “There are no treatments that can slow or reverse this devastating condition,” says Bryce Vissel at the University of Technology in Sydney, Australia. “There is no question that we have to look at Alzheimer’s in a different way.” So are we heading in the right direction, or do we need to rip up all the textbooks and start over? Alzheimer’s is the most common cause of dementia, and by some metrics its prevalence is rising. Alzheimer’s Disease International estimates that in 2015, 46.8 million people worldwide had dementia, a number that is set to double every 20 years, mostly because of an increasing number of older people in developing countries like India and China, leading to a global healthcare crisis. © Copyright Reed Business Information Ltd.

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: 23149 - Posted: 01.26.2017

Sarah DeVos Targeting tangles of tau protein in mice with Alzheimer’s-like symptoms has reversed their brain damage, halting memory loss and extending their lives. Clumps of two types of sticky protein build up in the brains of people with Alzheimer’s disease: beta-amyloid plaques, and tangles of tau. While many attempts to develop drugs to treat Alzheimer’s have targeted beta-amyloid, tau protein tangles have long been suspected to play a role in memory loss. “Tau is what correlates with memory problems, so one hypothesis is that lowering tau could be beneficial,” says Tim Miller of Washington University in St Louis, Missouri. Now Miller’s team has purged tau tangles from the brains of Alzheimer’s-like mice for the first time. They used fragments of RNA called antisense oligonucleotides to sabotage the gene that makes tau, preventing it from being fully translated into protein. Once a day for four weeks, the team injected the antisense treatment, named Tau-ASO12, into the fluid at the base of each mouse’s spine. The mice had been genetically engineered to make a rogue form of tau similar to what is seen in people with Alzheimer’s, predisposing the mice to developing tau-related brain problems. The drug successfully spread throughout the brain, and was linked to a reduction in levels of tau that was made. It also seemed to destroy existing tau tangles, and prevent tau from spreading around the brain in older mice. © Copyright Reed Business Information Ltd.

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: 23148 - Posted: 01.26.2017

By Joshua A. Krisch At the core of Alzheimer’s disease are amyloid-beta (Aβ) peptides, which self-assemble into protein fibrils that form telltale plaques in the brain. Now, the results of a study published today (January 4) in Nature suggest that certain fibril formations are more likely to appear in cases of rapidly progressive Alzheimer’s disease, as opposed to less-severe subtypes. The findings increase scientists’ understanding of the structure of these fibrils, and may eventually contribute to new tests and treatments for Alzheimer’s disease. “It is generally believed that some form of the aggregated Aβ peptide leads to Alzheimer’s disease, and it’s conceivable that different fibril structures could lead to neurodegeneration with different degrees of aggressiveness,” said coauthor Robert Tycko, a principal investigator at the National Institute of Diabetes and Digestive Kidney Disease. “But the mechanism by which this happens is uncertain. Some structures may be more inert and benign. Others may be more inherently toxic or prone to spread throughout the brain tissue.” Prior research has demonstrated that Aβ fibrils with various molecular structures exhibit different levels of toxicity in neuronal cell cultures, a finding confirmed in subsequent mouse trials. One study even demonstrated that Aβ fibrils cultured from patients with rapidly progressive Alzheimer’s disease are different in size and resistance to chemical denaturation than those isolated from patients with more slowly progressing disease. Building on these observations, Tycko and colleagues set out to better characterize the structures of these fibrils and get a better handle on the potential correlations between structure and disease subtype. © 1986-2017 The Scientist

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: 23066 - Posted: 01.07.2017

By Gary Stix The last six months have witnessed the failure of two drugs in late-stage clinical trials for which the research community had high hopes. In truth, these new reports should not have come as too much of a surprise. Drug after drug continues to show little or no effect in helping the more than 5 million patients in the U.S. diagnosed with Alzheimer’s. Scientists who study neurodegenerative diseases have started to call for new approaches that go beyond targeting the amyloid in plaques and the tau in tangles, proteins that have been thought to be culprits in killing brain cells. One organization—The Alzheimer’s Drug Discovery Foundation (ADDF)—has for years provided funding to move untried ideas into clinical trials. Howard Fillit, the organization’s executive director, recently gave Scientific American his surprisingly optimistic view of where research and drug development for Alzheimer’s is headed. There have been recent failures of late-stage clinical trials and a figure often cited is that more than 99 percent of Alzheimer's drugs fail. Given all that, what level of confidence do you have for the field moving forward? There's a lot of reason for hope. There are over 130 different clinical trials going on now. I remember the days when there were none. We have had many failures. But I think one of the big advances that is creating hope is that we know how to do clinical trials better now. In a study that is being conducted by Biogen, everyone who was recruited into that study actually had Alzheimer's disease, for the first time. © 2017 Scientific American

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: 23062 - Posted: 01.06.2017

Hannah Devlin Science correspondent People living near a busy road have an increased risk of dementia, according to research that adds to concerns about the impact of air pollution on human health. Roughly one in 10 cases of Alzheimer’s in urban areas could be associated with living amid heavy traffic, the study estimated – although the research stopped short of showing that exposure to exhaust fumes causes neurodegeneration. Hong Chen, the scientist who led the work at Public Health Ontario, said: “Increasing population growth and urbanisation has placed many people close to heavy traffic, and with widespread exposure to traffic and growing rates of dementia, even a modest effect from near-road exposure could pose a large public health burden.” Previously, scientists have linked air pollution and traffic noise to reduced density of white matter (the brain’s connective tissue) and lower cognition. A recent study suggested that magnetic nano-particles from air pollution can make their way into brain tissue. The latest study, published in The Lancet, found that those who live closest to major traffic arteries were up to 12% more likely to be diagnosed with dementia – a small but significant increase in risk. The study, which tracked roughly 6.6 million people for more than a decade, could not determine whether pollution is directly harmful to the brain. The increased dementia risk could also be a knock-on effect of respiratory and cardiac problems caused by traffic fumes or due to other unhealthy life-style factors associated with living in built-up urban environments. © 2017 Guardian News and Media Limited

Related chapters from BP7e: 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: 23058 - Posted: 01.05.2017

By LISA FELDMAN BARRETT Think about the people in your life who are 65 or older. Some of them are experiencing the usual mental difficulties of old age, like forgetfulness or a dwindling attention span. Yet others somehow manage to remain mentally sharp. My father-in-law, a retired doctor, is 83 and he still edits books and runs several medical websites. Why do some older people remain mentally nimble while others decline? “Superagers” (a term coined by the neurologist Marsel Mesulam) are those whose memory and attention isn’t merely above average for their age, but is actually on par with healthy, active 25-year-olds. My colleagues and I at Massachusetts General Hospital recently studied superagers to understand what made them tick. Our lab used functional magnetic resonance imaging to scan and compare the brains of 17 superagers with those of other people of similar age. We succeeded in identifying a set of brain regions that distinguished the two groups. These regions were thinner for regular agers, a result of age-related atrophy, but in superagers they were indistinguishable from those of young adults, seemingly untouched by the ravages of time. What are these crucial brain regions? If you asked most scientists to guess, they might nominate regions that are thought of as “cognitive” or dedicated to thinking, such as the lateral prefrontal cortex. However, that’s not what we found. Nearly all the action was in “emotional” regions, such as the midcingulate cortex and the anterior insula. My lab was not surprised by this discovery, because we’ve seen modern neuroscience debunk the notion that there is a distinction between “cognitive” and “emotional” brain regions. © 2017 The New York Times Company

Related chapters from BP7e: 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: 23045 - Posted: 01.02.2017