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By NICHOLAS BAKALAR A new study links diet soft drinks to an increased risk for stroke and dementia. Researchers studied more than 4,000 people over 45 who had filled out food-frequency questionnaires and had periodic health examinations between 1991 and 2001. The scientists tracked their health over the next 10 years and found 97 cases of stroke and 81 cases of dementia. The study, in the journal Stroke, found that compared with those who did not drink diet soda, people who drank one to six artificially sweetened drinks a week had twice the risk of stroke. There were similar, although weaker, associations for dementia risk. The reasons for the link remain unknown. The study adjusted for age, sex, education, physical activity, diabetes, smoking and many other characteristics that might affect the risks. But the senior author, Dr. Sudha Seshadri, a professor of neurology at Boston University School of Medicine, said that there were additional variables the study could not address. For example, she said, people might have switched to diet soda because they already had cardiovascular problems. Still, she added, there are health benefits associated with some drinks, like tea or coffee, “but not with soda of any kind, either diet or not.” © 2017 The New York Times Company

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: 23542 - Posted: 04.27.2017

Doing moderate exercise several times a week is the best way to keep the mind sharp if you're over 50, research suggests. Thinking and memory skills were most improved when people exercised the heart and muscles on a regular basis, a review of 39 studies found. This remained true in those who already showed signs of cognitive decline. Taking up exercise at any age was worthwhile for the mind and body, the Australian researchers said. Exercises such as T'ai Chi were recommended for people over the age of 50 who couldn't manage other more challenging forms of exercise, the study in the British Journal of Sports Medicine said. Physical activity has long been known to reduce the risk of a number of diseases, including type-2 diabetes and some cancers, and it is thought to play a role in warding off the brain's natural decline as we enter middle age. The theory is that through exercise the brain receives a greater supply of blood, oxygen and nutrients that boost its health as well as a growth hormone that helps the formation of new neurons and connections. In this analysis of previous studies, researchers from the University of Canberra looked at the effects of at least four weeks of structured physical exercise on the brain function of adults. In a variety of brain tests, they found evidence of aerobic exercise improving cognitive abilities, such as thinking, reading, learning and reasoning, while muscle training - for example, using weights - had a significant effect on memory and the brain's ability to plan and organise, the so-called executive functions. Joe Northey, study author and researcher from the Research Institute for Sport and Exercise at Canberra, said the findings were convincing enough to enable both types of exercise to be prescribed to improve brain health in the over-50s. © 2017 BBC.

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: 23532 - Posted: 04.25.2017

By James Gallagher Health and science reporter, Scientists hope they have found a drug to stop all neurodegenerative brain diseases, including dementia. In 2013, a UK Medical Research Council team stopped brain cells dying in an animal for the first time, creating headline news around the world. But the compound used was unsuitable for people, as it caused organ damage. Now two drugs have been found that should have the same protective effect on the brain and are already safely used in people. "It's really exciting," said Prof Giovanna Mallucci, from the MRC Toxicology Unit in Leicester. She wants to start human clinical trials on dementia patients soon and expects to know whether the drugs work within two to three years. Why might they work? The novel approach is focused on the natural defence mechanisms built into brain cells. When a virus hijacks a brain cell it leads to a build-up of viral proteins. Cells respond by shutting down nearly all protein production in order to halt the virus's spread. Many neurodegenerative diseases involve the production of faulty proteins that activate the same defences, but with more severe consequences. The brain cells shut down production for so long that they eventually starve themselves to death. This process, repeated in neurons throughout the brain, can destroy movement, memory or even kill, depending on the disease. It is thought to take place in many forms of neurodegeneration, so safely disrupting it could treat a wide range of diseases. In the initial study, the researchers used a compound that prevented the defence mechanism kicking in. © 2017 BBC.

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: 23512 - Posted: 04.20.2017

By Grace Rubenstein, North Dakota’s sparse geography has long made it a natural frontier: Pioneers here pushed the boundaries of westward expansion, then agriculture, and recently domestic oil drilling. Now the state finds itself on the leading edge of a new boom that it never would have chosen: Alzheimer’s disease. Cases are rocketing up across the United States, and especially in North Dakota, which has the country’s second highest death rate from the disease. While Alzheimer’s is the sixth leading cause of death nationally, it already ranks third here. “Everybody knows somebody” affected by the disease, said Kendra Binger, a program manager with the Alzheimer’s Association of Minnesota and North Dakota. As public awareness rises along with the numbers of cases, “it’s hard to ignore anymore.” This makes the state an ideal laboratory to glimpse at the future of Alzheimer’s in America, and to identify strategies that could help the rest of the country cope. The devastating disease has strained families and the state budget. So North Dakota — a place that prides itself on personal independence and financial parsimony — has found new ways to support its residents and a new consensus to spend money on prevention. The state’s primary strategy is to assist family caregivers — the estimated 30,000 North Dakota spouses, siblings, sons, and daughters looking after loved ones with dementia. A half-dozen consultants roam the state to evaluate families’ needs, train caregivers, connect them to services, and offer advice. Studies show the program has helped families keep their loved ones out of nursing homes and save the state money. © 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: 23508 - Posted: 04.19.2017

by Emilie Reas Alzheimer’s disease (AD) has been characterized as a “complete loss of self.” Early on when memory begins to fade, the victim has difficulty recalling names, their grocery list or where they put their keys. As the disease progresses, they have trouble staying focused, planning and performing basic daily activities. From the exterior, dementia appears to ravage one’s intellect and personality; yet as mere observers, it’s impossible to ascertain how consciousness of the self and environment is transformed by dementia. The celebrated late neurologist Oliver Sacks once suggested that, “Style, neurologically, is the deepest part of one’s being and may be preserved, almost to the last, in dementia.” Is this remaining neurological “style” sufficient to preserve consciousness? Is the AD patient aware of their deteriorating cognition, retaining a sense of identity or morality, or can they still connect with friends and loved ones? Emerging advances in neuroscience have enabled researchers to more precisely probe the AD brain, suggesting that although some aspects of consciousness are compromised by dementia, others are remarkably spared. Scientists are beginning to piece together how the selective loss of some functions, but the preservation of others, alters consciousness in AD. A recent study found that the severity of cognitive impairment strongly relates to “meta-cognition” (reflecting on one’s own condition), moral judgments and thinking about the future, whereas basic personal identity and body awareness remain. Perhaps the most widely observed deficit in consciousness is “anosognosia,” impaired awareness of one’s own illness; whereas individuals with mild cognitive impairment (MCI; considered a precursor to full AD) are aware of their declining memory, AD patients may be unaware of their impairments. These behavioral signs suggest that only some aspects of consciousness and self-awareness are truly lost in AD.

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: 23444 - Posted: 04.04.2017

By Linda Searing The precise cause, or causes, of dementias such as Alzheimer’s disease remain unclear, but one theory points to molecules called free radicals that can damage nerve cells. This damage, called oxidative stress, may lead to changes in the brain over time that result in dementia. Might antioxidant supplements prevent this? The study involved 7,540 men 60 and older (average age, 67) with no indications of dementia and no history of serious head injury, substance abuse or neurological conditions that affect cognition. They were randomly assigned to take vitamin E (an antioxidant, 400 International Units daily), selenium (also an antioxidant, 200 micrograms daily), both vitamin E and selenium or a placebo. The men also had their memory assessed periodically. In just over five years, 325 of the men (about 4 percent) developed dementia, with essentially no difference in the rate of occurrence between those who took one or both supplements and those who took the placebo. The researchers concluded that the antioxidant supplements “did not forestall dementia and are not recommended as preventive agents.” Who may be affected? Older men. The risk for dementia increases with advanced age and is most common among the very elderly. Memory loss is the most well-known symptom, but people with dementia may also have problems thinking, speaking, controlling emotions and doing daily activities such as getting dressed and eating. Alzheimer’s disease is the most common type of dementia, affecting more than 5.5 million Americans, including more than 10 percent of those 65 and older and more women than men. Caveats Participants took the supplements for a relatively short time. Whether the findings would apply to women was not tested. The study did not prove that the dementia developed by the study participants was caused by oxidative stress. © 1996-2017 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: 23403 - Posted: 03.25.2017

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