Chapter 7. Life-Span Development of the Brain and Behavior

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Kayt Sukel Since its inception, the field of neuroscience has relied on animal models, from fruit flies to macaque monkeys, to better understand the behavior and inner workings of neurons. But while these models have led to remarkable insights about the brain in both health and in disease, they do have limitations. The very genetic differences that place us in different species also make the translation of neurobiological findings in animals to humans challenging—if not outright impossible. “We’ve now cured Alzheimer’s disease a dozen times over in mice, but we haven’t cured it in human patients,” said Matthew Blurton-James, Ph.D., a neurobiologist at the University of California, Irvine. “There’s clearly a big species difference in how this disease develops, which means our current animal models can’t get us the answers we’re searching for.” In the past few years, however, advances in technology have led to the development of innovative models to study the activity of human neurons—and how they communicate with one another. Such models, which include ex vivo tissue harvested from living human donors, organoids, and chimeric models (animal tissue modified with human genes or cells), are enabling scientists to investigate processes in ways that were previously unthinkable. “These new technologies, including those that use induced pluripotent stem cells (iPSCs), are really quite striking,” said Walter Koroshetz, M.D., director of the National Institute of Neurological Disorders and Stroke. “And the real advantage of these is that they offer us a new way to study human brain cells, particularly when it comes to developmental processes, that is incredibly valuable.” © 2020 The Dana Foundation

Keyword: Development of the Brain
Link ID: 26983 - Posted: 01.23.2020

By Gretchen Reynolds In a world that encourages inactivity, even our babies may be moving too little, according to an innovative new study of physical activity patterns during a child’s first year of life. The study, which used tiny activity trackers to monitor babies’ movements, found associations between infants’ squirming, kicking, crawling or stillness and the levels of fat around their middles, raising provocative questions about just how early any links between inactivity and obesity might begin. We already have considerable evidence, of course, that children in the Western world tend to be sedentary. According to recent estimates, most school-age children in the United States sit for more than eight hours a day, while children as young as 2 or 3 years of age can be sedentary for 90 percent or more of their waking hours. These statistics are concerning, because other studies suggest that inactive children face much higher risks of becoming overweight or obese than children who move more often. But little has been known about how much — or little — tiny babies move and if there might be correlations between their activities and their rotundity, and if such correlations matter. So, for the new study, which was published this month in Obesity, a group of researchers from Johns Hopkins University and other institutions decided to fit baby-size trackers to infants’ ankles and watch how they wiggled. They began by turning to new mothers already participating in a large, ongoing study of the health of mothers and newborns and asking if they could now track their babies’ activities. The researchers wound up recruiting 506 young boys and girls from various socioeconomic levels, more than half of them African-American. The researchers visited these infants in their homes when the babies were 3, 6, 9 and 12 months old, weighing and measuring the children, gently checking their body fat with calipers and fitting them with tiny accelerometers. © 2020 The New York Times Company

Keyword: Obesity; Development of the Brain
Link ID: 26978 - Posted: 01.22.2020

Edward Bullmore Unlikely as it may seem, #inflammation has become a hashtag. It seems to be everywhere suddenly, up to all sorts of tricks. Rather than simply being on our side, fighting infections and healing wounds, it turns out to have a dark side as well: the role it plays in causing us harm. It’s now clear that inflammation is part of the problem in many, if not all, diseases of the body. And targeting immune or inflammatory causes of disease has led to a series of breakthroughs, from new treatments for rheumatoid arthritis and other auto-immune diseases in the 1990s, through to the advent of immunotherapy for some cancers in the 2010s. Even more pervasively, low-grade inflammation, detectable only by blood tests, is increasingly considered to be part of the reason why common life experiences such as poverty, stress, obesity or ageing are bad for public health. Advertisement The brain is rapidly emerging as one of the new frontiers for inflammation. Doctors like myself, who went to medical school in the 20th century, were taught to think that there was an impermeable barrier between the brain and the immune system. In the 21st century, however, it has become clear that they are deeply interconnected and talk to each other all the time. Medical minds are now opening up to the idea that inflammation could be as widely and deeply implicated in brain and mind disorders as it is in bodily disorders. Advances in treatment of multiple sclerosis have shown the way. Many of the new medicines for MS were designed and proven to protect patients from brain damage caused by their own immune systems. The reasonably well-informed hope – and I emphasise those words at this stage – is that targeting brain inflammation could lead to breakthroughs in prevention and treatment of depression, dementia and psychosis on a par with the proven impact of immunological medicines for arthritis, cancer and MS. Indeed, a drug originally licensed for multiple sclerosis is already being tried as a possible immune treatment for schizophrenia. © 2020 Guardian News & Media Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 26975 - Posted: 01.21.2020

By Donna Jackson Nakazawa More than a decade ago, I was diagnosed with a string of autoimmune diseases, one after another, including a bone marrow disorder, thyroiditis, and then Guillain-Barré syndrome, which left me paralyzed while raising two young children. I recovered from Guillain-Barré only to relapse, becoming paralyzed again. My immune system was repeatedly and mistakenly attacking my body, causing the nerves in my arms, legs, and those I needed to swallow to stop communicating with my brain, leaving me confined to — and raising my children from — bed. As I slowly began to recover and learn to walk again, I noticed that along with residual physical losses I had experienced shifts in my mood and clarity of mind. Although I’d always been an optimistic person, I felt a bleak unshakable dread, which didn’t feel like the “old me.” I also noticed cognitive glitches. Names, words, and facts were hard to bring to mind. I can still recall cutting up slices of watermelon, putting them in a bowl, and staring down at them thinking, “What is this again?” I knew the word but couldn’t remember it. I covered my lapse by bringing the bowl to the table and waiting for my children to call out, “Yay! Watermelon!” And I thought, “Yes. Of course. Watermelon.” As a science journalist whose niche spans neuroscience, immunology, and human emotion, I knew at the time that it didn’t make scientific sense that inflammation in the body could be connected to — much less cause — illness in the brain. At that time, scientific dogma held that the brain was the only organ in the body not ruled by the immune system. The brain was considered to be “immune privileged.” © 2020 STAT

Keyword: Glia; Alzheimers
Link ID: 26971 - Posted: 01.20.2020

By Karen Weintraub Alzheimer's disease has long been characterized by the buildup of two distinct proteins in the brain: first beta-amyloid, which accumulates in clumps, or plaques, and then tau, which forms toxic tangles that lead to cell death. But how beta-amyloid leads to the devastation of tau has never been precisely clear. Now a new study at the University of Alabama at Birmingham appears to describe that missing mechanism. The study details a cascade of events. Buildup of beta-amyloid activates a receptor that responds to a brain chemical called norepinephrine, which is commonly known for mobilizing the brain and body for action. Activation of this receptor by both beta-amyloid and norepinephrine boosts the activity of an enzyme that activates tau and increases the vulnerability of brain cells to it, according to the study, published in Science Translational Medicine. Essentially, beta-amyloid hijacks the norepinephrine pathway to trigger a toxic buildup of tau, says Qin Wang, the study’s senior author and a professor of neuropharmacology in the department of cell, developmental and integrative biology at the University of Alabama at Birmingham. “We really show that this norepinephrine is a missing piece of this whole Alzheimer’s disease puzzle,” she says. This cascade explains why so many previous Alzheimer’s treatments have failed, Wang says. Most of the drugs developed in recent decades have targeted the elimination of beta-amyloid. But the new research suggests that norepinephrine amplifies the damage wrought by that protein. © 2020 Scientific American

Keyword: Alzheimers
Link ID: 26967 - Posted: 01.17.2020

Ashley Yeager About four years ago, pathologist Matthew Anderson was examining slices of postmortem brain tissue from an individual with autism under a microscope when he noticed something extremely odd: T cells swarming around a narrow space between blood vessels and neural tissue. The cells were somehow getting through the blood-brain barrier, a wall of cells that separates circulating blood from extracellular fluid, neurons, and other cell types in the central nervous system, explains Anderson, who works at Beth Israel Deaconess Medical Center in Boston. “I just have seen so many brains that I know that this is not normal.” He soon identified more T-cell swarms, called lymphocytic cuffs, in a few other postmortem brains of people who had been diagnosed with autism. Not long after that, he started to detect another oddity in the brain tissue—tiny bubbles, or blebs. “I’d never seen them in any other brain tissue that I’ve looked at for many, many different diseases,” he says. Anderson began to wonder whether the neurological features he was observing were specific to autism. To test the idea, he and his colleagues examined postmortem brain tissue samples from 25 people with autism spectrum disorder (ASD) and 30 developmentally normal controls. While the lymphocytic cuffs only sporadically turned up in the brains of neurotypical individuals, the cuffs were abundant in a majority of the brains from individuals who had had ASD. Those same samples also had blebs that appeared in the same spots as the cuffs. Staining the brain tissue revealed that the cuffs were filled with an array of different types of T cells, while the blebs contained fragments of astrocytes, non-neuronal cells that support the physical structure of the brain and help to maintain the blood-brain barrier. © 1986–2020 The Scientist

Keyword: Autism; Neuroimmunology
Link ID: 26966 - Posted: 01.17.2020

There are differences in the way English and Italian speakers are affected by dementia-related language problems, a small study suggests. While English speakers had trouble pronouncing words, Italian speakers came out with shorter, simpler sentences. The findings could help ensure accurate diagnoses for people from different cultures, the researchers said. Diagnostic criteria are often based on English-speaking patients. In the University of California study of 20 English-speaking patients and 18 Italian-speaking patients, all had primary progressive aphasia - a neuro-degenerative disease which affects areas of the brain linked to language. It is a feature of Alzheimer's disease and other dementia disorders. Brain scans and tests showed similar levels of cognitive function in people in both language groups. But when the researchers asked participants to complete a number of linguistic tests, they picked up obvious differences between the two groups in the challenges they faced. 'Easier to pronounce' "We think this is specifically because the consonant clusters that are so common in English pose a challenge for a degenerating speech-planning system," said study author Maria Luisa Gorno-Tempini, professor of neurology and psychiatry. "In contrast, Italian is easier to pronounce, but has much more complex grammar, and this is how Italian speakers with [primary progressive aphasia] tend to run into trouble." As a result, the English speakers tended to speak less while the Italian speakers had fewer pronunciation problems, but simplified what they did say. English is a Germanic language while Italian is a Romance language, derived from Latin along with French, Spanish and Portuguese. The researchers, writing in Neurology, are concerned that many non-native English speakers may not be getting the right diagnosis "because their symptoms don't match what is described in clinical manuals based on studies of native English speakers". The San Francisco research team says it now wants to repeat the research in larger groups of patients, and look for differences between speakers of other languages, such as Chinese and Arabic. © 2020 BBC

Keyword: Alzheimers; Language
Link ID: 26954 - Posted: 01.13.2020

By Daniel J. Levitin I’m 62 years old as I write this. Like many of my friends, I forget names that I used to be able to conjure up effortlessly. When packing my suitcase for a trip, I walk to the hall closet and by the time I get there, I don’t remember what I came for. And yet my long-term memories are fully intact. I remember the names of my third-grade classmates, the first record album I bought, my wedding day. This is widely understood to be a classic problem of aging. But as a neuroscientist, I know that the problem is not necessarily age-related. Short-term memory contains the contents of your thoughts right now, including what you intend to do in the next few seconds. It’s doing some mental arithmetic, thinking about what you’ll say next in a conversation or walking to the hall closet with the intention of getting a pair of gloves. Short-term memory is easily disturbed or disrupted. It depends on your actively paying attention to the items that are in the “next thing to do” file in your mind. You do this by thinking about them, perhaps repeating them over and over again (“I’m going to the closet to get gloves”). But any distraction — a new thought, someone asking you a question, the telephone ringing — can disrupt short-term memory. Our ability to automatically restore the contents of the short-term memory declines slightly with every decade after 30. But age is not the major factor so commonly assumed. I’ve been teaching undergraduates for my entire career and I can attest that even 20-year-olds make short-term memory errors — loads of them. They walk into the wrong classroom; they show up to exams without the requisite No. 2 pencil; they forget something I just said two minutes before. These are similar to the kinds of things 70-year-olds do. © 2020 The New York Times Company

Keyword: Learning & Memory; Alzheimers
Link ID: 26952 - Posted: 01.13.2020

By Elizabeth Brico The statistics are heartbreaking. Each year in the U.S., about 32,000 newborns are diagnosed with neonatal abstinence syndrome, a form of withdrawal that can result from in utero exposure to a number of drugs taken by the mother during pregnancy. Opioids — both prescribed and illegal — are among the most common culprits. These medications can be necessary, even life-saving, but that doesn’t make the resultant NAS any easier to watch: Newborns who suffer from the syndrome may exhibit tremors, irritability, hyperactive reflexes, high-pitched crying, and other symptoms. But drugs are not solely to blame for the prolonged suffering many of these infants experience. The way NAS cases are handled also has a profound impact on their severity, and often leads to negative outcomes. Health care providers and law enforcement authorities have historically separated these fragile babies from their mothers, doling out severe punishments to the latter. Although there is a growing awareness that change is needed, many hospitals still use outdated approaches — and child welfare agencies are particularly behind the times in this arena. Recent studies suggest that policies that place blame on mothers only heighten a newborn’s suffering by preventing infants from accessing potent care for reducing withdrawal symptoms: contact with mom. Misperceptions about opioid addiction, dependency, and NAS are woven into the very fabric of U.S. and state law. In order to receive federal funding for child abuse prevention, health care workers are required to report substance-affected newborns to Child Protective Services. Additionally, states can require health care providers to report or test for drug exposure during pregnancy. In many cases, mothers are reported even if the exposure is the result of prescribed methadone or buprenorphine — opioid-based drugs commonly used to treat addiction.

Keyword: Drug Abuse; Development of the Brain
Link ID: 26943 - Posted: 01.09.2020

By Perri Klass, M.D. In December, the American Academy of Pediatrics put out a new clinical report on autism, an extensive document with an enormous list of references, summarizing 12 years of intense research and clinical activity. During this time, the diagnostic categories changed — Asperger’s syndrome and pervasive developmental disorder, diagnostic categories that once included many children, are no longer used, and we now consider all these children (and adults) to have autism spectrum disorder, or A.S.D. The salient diagnostic characteristics of A.S.D. are persistent problems with social communication, including problems with conversation, with nonverbal communication and social cues, and with relationships, together with restricted repetitive behavior patterns, including repetitive movements, rigid routines, fixated interests and sensory differences. Dr. Susan Hyman, the lead author on the new report, who is the division chief of developmental and behavioral pediatrics at Golisano Children’s Hospital at the University of Rochester, said in an email that much has changed over the past 12 years. She pointed in particular to increased medical awareness and understanding of conditions that often occur together with A.S.D., and to a greater emphasis on planning — together with families — how to support children as they grow. Dr. Susan E. Levy, a co-author of the statement who is a developmental behavioral pediatrician at Children’s Hospital of Philadelphia, said that one key message of the report is the emphasis on early identification and referral for treatment, even if a diagnosis of autism is suspected but not yet confirmed. The outcomes are better when treatment starts as early as possible, she said. The average age of diagnosis is now around 4 years, but the goal is to get it well under 2, she said. And children who are at higher risk — for example, those whose siblings have A.S.D. — should receive especially close screening and attention. © 2020 The New York Times Company

Keyword: Autism
Link ID: 26940 - Posted: 01.07.2020

By James Gallagher Health and science correspondent An early life full of neglect, deprivation and adversity leads to people growing up with smaller brains, a study suggests. The researchers at King's College London were following adopted children who spent time in "hellhole" Romanian orphanages. They grew up with brains 8.6% smaller than other adoptees. The researchers said it was the "most compelling" evidence of the impact on the adult brain. The appalling care at the orphanages came to light after the fall of Romania's communist dictator Nicolae Ceausescu in 1989. "I remember TV pictures of those institutions, they were shocking," Prof Edmund Sonuga-Barke, who now leads the study following those children, told the BBC. He described the institutions as "hellholes" where children were "chained into their cots, rocking, filthy and emaciated". The children were physically and psychologically deprived with little social contact, no toys and often ravaged by disease. The children studied had spent between two weeks and nearly four years in such institutions. Previous studies on children who were later adopted by loving families in the UK showed they were still experiencing mental health problems in adulthood. Higher levels of traits including autism, attention deficit hyperactivity disorder (ADHD) and a lack of fear of strangers (disinhibited social engagement disorder) have all been documented. The latest study, published in Proceedings of the National Academy of Sciences, is the first to scan the brains for answers. There were 67 Romanian adoptees in the study and their brains were compared to 21 adoptees who did not suffer early life deprivation. "What we found is really quite striking," Prof Sonuga-Barke told the BBC. First the total brain volume - the size of the brain - was 8.6% smaller in the Romanian adoptees on average. And the longer they spent in the Romanian orphanages, the greater the reduction in brain size. © 2020 BBC.

Keyword: Development of the Brain; Stress
Link ID: 26935 - Posted: 01.07.2020

By Sharon Jayson AUSTIN, Texas — Retired state employees Vickey Benford, 63, and Joan Caldwell, 61, are Golden Rollers, a group of the over-50 set that gets out on assorted bikes — including trikes for adults they call “three wheels of awesome” — for an hour of trail riding and camaraderie. “I love to exercise, and I like to stay fit,” said Caldwell, who tried out a recumbent bike, a low-impact option that can be easier on the back. “It keeps me young.” Benford encouraged Caldwell to join the organized rides, which have attracted more than 225 riders at city rec centers and senior activity centers. The cyclists can choose from a small, donated fleet of recumbent bikes, tandem recumbents and tricycles. “With seniors, it’s less about transportation and more about access to the outdoors, social engagement and quality of life,” said Christopher Stanton, whose idea for Golden Rollers grew out of the Ghisallo Cycling Initiative, a youth biking nonprofit he founded in 2011. But that’s not all, according to brain scientists. They point to another important benefit: Exercising both body and brain can help people stay healthier longer. The new thinking about aging considers not just how long one lives, but how vibrant one stays later in life. “If you’re living, you want to be living well,” said Tim Peterson, an assistant professor of internal medicine at the Washington University School of Medicine in St. Louis. “Most people who were interested in life span and were studying genes — which control life span — switched to ‘healthspan.’” “Healthspan,” a coinage now gaining traction, refers to the years that a person can expect to live in generally good health — free of chronic illnesses and cognitive decline that can emerge near life’s end. Although there’s only so much a person can do to delay the onset of disease, there’s plenty that scientists are learning to improve your chances of a better healthspan. © 2020 Kaiser Family Foundation

Keyword: Development of the Brain
Link ID: 26932 - Posted: 01.04.2020

Jerold Chun, M.D., Ph.D. Alzheimer’s disease (AD) is the most common cause of dementia, currently affecting an estimated 5.8 million Americans. It has been over a century since AD was first described, but it is still not sufficiently well understood to enable development of drugs to treat it. As lifespan continues to rise and for myriad other reasons, the number of AD cases per state in the US is predicted to increase 12 to 43 percent over the next five years. The lack of disease-modifying treatments may reflect a feature of AD pathology that was first noted in its initial description: the vast heterogeneity of the hallmark “senile plaques” that are found in all AD brains. When Alois Alzheimer and Oskar Fischer described the first cases of AD, they noted plaque accumulations of a protein called amyloid that builds up in between brain cells and interrupts cell-to-cell communication; amyloid plaques vary in size, shape, abundance, and location within the brain. “Among the plaques in the cerebral cortex many were of an extraordinary size, such as I have never seen,” Alois Alzheimer stated. “Some evidently arose from the fusion of smaller ones since they contained several central cores, but others had one exceptionally big central core and uncommonly large halo.” Disease heterogeneity extends to behavior and includes varying age of onset, symptoms, and disease progression. Some variability may be explained by genetic heterogeneity, since more than 33 AD risk factor genes have been identified via a technique called “genome wide association studies” (GWAS), which broadly samples DNA from cells outside of the brain to identify mutations that are present in every cell of the body. None of these genes, however, are considered to cause AD. © 2020 The Dana Foundation

Keyword: Alzheimers; Genes & Behavior
Link ID: 26931 - Posted: 01.04.2020

Nicola Davis and Hannah Devlin Tangles of a protein found inside the brain cells of people with Alzheimer’s disease can be used to predict future brain shrinkage, research suggests. In healthy people, a protein called tau is important in supporting the internal structure of brain cells. However, in those with Alzheimer’s, chemical changes take place that cause the protein to form tangles that disrupt the cells. Such tangles have previously been linked to a loss of brain cells. Now scientists have used imaging techniques to track the extent of tau tangles in the brains of those with early signs of Alzheimer’s, revealing that levels of the protein predict not only how much brain shrinkage will subsequently occur, but where. “Our study supports the notion that tau pathology accumulates upstream of brain tissue loss and clinical symptoms,” said Prof Gil Rabinovici, a co-author of the research from the University of California, San Francisco. A number of drugs targeting tau tangles are currently in clinical trials, including some that aim to interfere with the production of tau in the brain or its spread between cells. Dr Renaud La Joie, another author of the research, said the findings suggested the imaging technique could prove valuable both in choosing which patients to enrol to test such drugs and in monitoring whether the drugs work. Dr Laura Phipps, of Alzheimer’s Research UK, said: “The ability to track tau in the brain will be critical for testing treatments designed to prevent the protein causing damage, and the scans used in this study could be an important tool for future clinical trials.” Writing in the journal Science Translational Medicine, La Joie and colleagues report how they used an imaging technique called PET to study the brains of 32 people aged between 49 and 83 who were in the early stages of showing Alzheimer’s symptoms. © 2020 Guardian News & Media Limited

Keyword: Alzheimers; Brain imaging
Link ID: 26928 - Posted: 01.02.2020

By Gretchen Reynolds What’s good for your muscles can also be good for your mind. A Single Workout Can Alter the Brain A single, moderate workout may immediately change how our brains function and how well we recognize common names and similar information, according to a promising new study of exercise, memory and aging. The study adds to growing evidence that exercise can have rapid effects on brain function and also that these effects could accumulate and lead to long-term improvements in how our brains operate and we remember. Until recently, scientists thought that by adulthood, human brains were relatively fixed in their structure and function, especially compared to malleable tissues, like muscle, that continually grow and shrivel in direct response to how we live our lives. But multiple, newer experiments have shown that adult brains, in fact, can be quite plastic, rewiring and reshaping themselves in various ways, depending on our lifestyles. A hormone that is released during exercise may improve brain health and lessen the damage and memory loss that occur during dementia, a new study finds. The study, which was published this month in Nature Medicine, involved mice, but its findings could help to explain how, at a molecular level, exercise protects our brains and possibly preserves memory and thinking skills, even in people whose pasts are fading. Considerable scientific evidence already demonstrates that exercise remodels brains and affects thinking. Researchers have shown in rats and mice that running ramps up the creation of new brain cells in the hippocampus, a portion of the brain devoted to memory formation and storage. Exercise also can improve the health and function of the synapses between neurons there, allowing brain cells to better communicate. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26925 - Posted: 12.30.2019

By Gina Kolata Not long ago, the only way to know if someone had Alzheimer’s disease was to examine the brain in an autopsy. That is changing — and fast — with brain scans and spinal taps that can detect beta amyloid, the telltale Alzheimer’s protein. There is a blood test on the horizon that can detect beta amyloid, and researchers are experimenting with scans to look for another protein, called tau, also characteristic of Alzheimer’s. As this sort of diagnostic testing becomes widespread, more people who fear their memories are slipping will face a difficult question: Would I really want to know if I were getting Alzheimer’s disease? “This is a new era, and we are just at the precipice,” said Dr. Gil Rabinovici, a neurologist at the University of California, San Francisco. A positive test could help you get your affairs in order and plan your future. And a drug company, Biogen, claims to have the first treatment that may slow the course of the disease if begun early enough. Health insurers are prohibited by law — for now, at least — from denying coverage if you have Alzheimer’s. But there is nothing that prevents long-term-care and life insurers from denying you. Will your friends stay with you? How about your spouse? What would it be like to live with the knowledge that you will eventually be unable to recognize your family, or even to speak? For some who have been given diagnostic tests, those questions are all too real. When Dr. Daniel Gibbs, 68, a neurologist in Portland, Ore., noticed his memory starting to slip, he wanted to know if it was Alzheimer’s. He had seen its damage all too often in his patients. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26909 - Posted: 12.21.2019

By Gina Kolata Robert D. Moir, a Harvard scientist whose radical theories of the brain plaques in Alzheimer’s defied conventional views of the disease, but whose research ultimately led to important proposals for how to treat it, died on Friday at a hospice in Milton, Mass. He was 58. His wife, Julie Alperen, said the cause was glioblastoma, a type of brain cancer. Dr. Moir, who grew up on a farm in Donnybrook, a small town in Western Australia, had a track record for confounding expectations. He did not learn to read or write until he was nearly 12; Ms. Alperen said he told her that the teacher at his one-room schoolhouse was “a demented nun.” Yet, she said, he also knew from age 7 that he wanted to be a scientist. He succeeded in becoming a researcher who was modest and careful, said his Ph.D. adviser, Dr. Colin Masters, a neuropathologist at the University of Melbourne. So Dr. Masters was surprised when Dr. Moir began publishing papers proposing an iconoclastic rethinking of the pathology of Alzheimer’s disease. Dr. Moir’s hypothesis “was and is a really novel and controversial idea that he alone developed,” Dr. Masters said. “I never expected this to come from this quiet achiever.” Dr. Moir’s theory involved the protein beta amyloid, which forms plaques in the brains of Alzheimer’s patients. Conventional wisdom held that beta amyloid accumulation was a central part of the disease, and that clearing the brain of beta amyloid would be a good thing for patients. Dr. Moir proposed instead that beta amyloid is there for a reason: It is the way the brain defends itself against infections. Beta amyloid, he said, forms a sticky web that can trap microbes. The problem is that sometimes the brain goes overboard producing it, and when that happens the brain is damaged. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26908 - Posted: 12.21.2019

By Andrea Petersen Anne Firmender, 74, was working with her psychologist to come up with a list of her positive attributes. “I cook for others,” said Ms. Firmender. “It’s giving,” encouraged the psychologist, Dimitris Kiosses. “Good kids,” continued Ms. Firmender, who has four grown children and four grandchildren. “And great mother,” added Dr. Kiosses. Ms. Firmender smiled. Dr. Kiosses typed up the list and handed a printout to Ms. Firmender to take home. “When you’re feeling down and hard on yourself, you can remind yourself of your strengths,” he told her. Ms. Firmender, who has a history of mental health problems, was in therapy for depression. But she also has mild cognitive impairment and can have trouble remembering what day it is. So Dr. Kiosses was treating her with a novel approach called Problem Adaptation Therapy, or PATH. The therapy, developed at Weill Cornell Medicine in New York City and White Plains, N.Y., focuses on solving tangible problems that fuel feelings of sadness and hopelessness. It incorporates tools, like checklists, calendars, signs and videos, to make it accessible for people with memory issues. A caregiver is often involved. The approach is one of several new psychotherapies to treat anxiety and depression in people with cognitive impairments, including early to moderate dementia. Another, the Peaceful Mind program, developed by researchers at Baylor College of Medicine and elsewhere for patients with anxiety and dementia, simplifies traditional cognitive behavioral therapy and focuses on scheduling pleasurable activities and skills, like deep breathing. Therapy sessions are short and take place in patients’ homes. A program designed by researchers at University College London gives cards to patients to take home to remind them of key strategies. One that says “Stop and Think” prompts them to pause when they have panicky and unhelpful thoughts to help keep those thoughts from spiraling and creating more anxiety. © 2019 The New York Times Company

Keyword: Alzheimers; Depression
Link ID: 26884 - Posted: 12.09.2019

By Laura Sanders Call it a comeback — maybe. After being shelved earlier this year for lackluster preliminary results, a drug designed to slow Alzheimer’s progression is showing new signs of life. A more in-depth look at the data from two clinical trials suggests that patients on the biggest doses of the drug, called aducanumab, may indeed benefit, the company reported December 5. People who took the highest amounts of the drug declined about 30 percent less, as measured by a commonly used Alzheimer’s scale, than people who took a placebo, Samantha Haeberlein of the biotechnology company Biogen reported at the Clinical Trials on Alzheimer’s Disease meeting in San Diego. With these encouraging results in hand, Biogen, based in Cambridge, Mass., plans to seek drug approval from the U.S. Food and Drug Administration in early 2020. The results are “exhilarating, not just to the scientific community but our patients as well,” Sharon Cohen, a behavioral neurologist at the Toronto Memory Program, said during a panel discussion at the meeting. Cohen participated in the clinical trials and has received funding from Biogen. The presentation marks “an important moment for the Alzheimer’s field,” says Rebecca Edelmayer, director of scientific engagement for the Alzheimer’s Association in Chicago. Alzheimer’s disease slowly kills cells in the brain, gradually erasing people’s abilities to remember, navigate and think clearly. Current Alzheimer’s medicines can hold off symptoms temporarily, but don’t fight the underlying brain destruction. A treatment that could actually slow or even stop the damage would have a “huge impact for patients and their caregivers,” she says. © Society for Science & the Public 2000–2019

Keyword: Alzheimers
Link ID: 26879 - Posted: 12.06.2019

By Kelly Servick When Samantha Budd Haeberlein, Biogen’s head of clinical development, took the stage in San Diego, California, before a room full of Alzheimer’s disease researchers and physicians this morning, she knew she had some explaining to do. In October, the pharmaceutical company, based in Cambridge, Massachusetts, unexpectedly revived an experimental Alzheimer’s drug that it had declared a failure 7 months earlier. Ever since, scientists and industry analysts have been hungry for more detail about two large clinical trials meant to prove that Biogen’s drug, an antibody called aducanumab, slows down cognitive decline in the early stages of disease. At the Clinical Trials on Alzheimer’s Disease congress today, Budd Haeberlein tried to clarify what has emboldened the company to apply to the U.S. Food and Drug Administration (FDA) for market approval for aducanumab early next year. After analyzing more patient data than were available at the time of a discouraging preliminary analysis, she explained, the company found evidence that the higher of two tested doses led to 22% less cognitive decline after 78 weeks than a placebo in one trial. However, the other trial failed to show any benefit, leaving some researchers with a grim outlook on the drug. “I surely don’t think that it should be given market approval on the basis of these data,” says Robert Howard, a psychiatrist at University College London who has run clinical trials of potential Alzheimer’s treatments. More positive results from a subset of patients that weren’t preselected at the trial’s launch are not convincing, he says. “[Biogen has] broken all the rules, really, about how you analyze data and report it.” © 2019 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 26878 - Posted: 12.06.2019