By Betsy Mason Despite weighing less than half an ounce, mountain chickadees are able to survive harsh winters complete with subzero temperatures, howling winds and heavy snowfall. How do they do it? By spending the fall hiding as many as 80,000 individual seeds, which they then retrieve — by memory — during the winter. Their astounding ability to keep track of that many locations puts their memory among the most impressive in the animal kingdom. It also makes chickadees an intriguing subject for animal behavior researchers. Cognitive ecologist Vladimir Pravosudov of the University of Nevada, Reno, has dedicated his career to studying this tough little bird’s amazing memory. Writing in 2013 on the cognitive ecology of food caching in the Annual Review of Ecology, Evolution, and Systematics, he and coauthor Timothy Roth argued that answers to big questions about the evolution of cognition may lie in the brains of these little birds. In July, at a meeting of the Animal Behavior Society in Chicago, Pravosudov presented his group’s latest research on the wild chickadees that live in the Sierra Nevada mountains. He and his graduate students were able to show for the first time that an individual bird’s spatial memory has a direct impact on its survival. The team did this by building an experimental contraption that uses radio-frequency identification (RFID) technology and electronic leg bands to test individual birds’ memory in the wild and then track their longevity. The researchers found that the birds with the best memory were most likely to survive the winter. What are some of the big ideas driving your work on chickadees? If some species are smart, or not smart, the question is: Why? Cognitive ecologists like me are specifically trying to figure out which ecological factors may have shaped the evolution of these differences in cognition. In other words, the idea is to understand the ecological and evolutionary reasons for variation in cognition. © 2020 Annual Reviews, Inc

Keyword: Learning & Memory
Link ID: 26968 - Posted: 01.17.2020

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 Matthew Hutson When you are stuck on a problem, sometimes it is best to stop thinking about it—consciously, anyway. Research has shown that taking a break or a nap can help the brain create pathways to a solution. Now a new study expands on the effect of this so-called incubation by using sound cues to focus the sleeping mind on a targeted problem. When humans sleep, parts of the brain replay certain memories, strengthening and transforming them. About a decade ago researchers developed a technique, called targeted memory reactivation (TMR), aimed at further reinforcing selected memories: when a sound becomes associated with a memory and is later played during sleep, that memory gets reactivated. In a study published last November in Psychological Science, scientists tested whether revisiting the memory of a puzzle during sleep might also improve problem-solving. About 60 participants visited the laboratory before and after a night of sleep. In an evening session, they attempted spatial, verbal and conceptual puzzles, with a distinct music clip repeating in the background for each, until they had worked on six puzzles they could not solve. Overnight they wore electrodes to detect slow-wave sleep—slumber's deepest phase, which may be important for memory consolidation—and a device played the sounds assigned to three of the six unsolved puzzles. The next day, back at the lab, the participants attempted the six puzzles again. (Each repeated the experiment with a different set of puzzles the following night.) All told, the subjects solved 32 percent of the sound-prompted puzzles versus 21 percent of the untargeted puzzles—a boost of more than 50 percent. © 2020 Scientific American

Keyword: Sleep; Learning & Memory
Link ID: 26938 - Posted: 01.07.2020

Natalie C Tronson Ph.D. We all have a strong intuitive sense of what memory is: it’s the conscious recollection of events, people, and places from our past. And it’s something we often wish we were better at so we didn’t continuously lose our keys, forget where our car was parked, and we could remember more facts for exams, remember people’s birthdays, or what I came all the way upstairs to grab. But memory is so much more. Memory is also how I can find my way around the town I live in now—and how I can still find my way around the town I grew up in, despite the many changes over the 25 years since I left. It’s how I know how to drive the car, and how I can sing four verses of Mary Had a Little Lamb to my child sitting in the back seat demanding that I sing. It’s why I know to stop at the red light, go at the green, and avoid the stretch of road that has been under construction for the past six months. It’s also one reason why I feel anxious when pedestrians run across the street randomly, and why our cats come running home when they hear the front door of our house open. That’s a lot of different types of memory just for a quick drive home: memory for spatial learning, verbal memory for songs, motor learning for driving, and episodic memory, among others, are in there too. Not only are there a lot of different types of memory, but there is also a lot of real estate and energy in our brains (and in the brains of many other species) taken up for learning and memory processes. © 2020 Sussex Publishers, LLC

Keyword: Learning & Memory
Link ID: 26937 - 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

Ryan F. Mandelbaum Scientists have uncovered a new kind of electrical process in the human brain that could play a key role in the unique way our brains compute. Our brains are computers that work using a system of connected brain cells, called neurons, that exchange information using chemical and electric signals called action potentials. Researchers have discovered that certain cells in the human cortex, the outer layer of the brain, transmit signals in a way not seen in corresponding rodent cells. This process might be important to better understanding our unique brains and to improving programs that are based on a model of the human brain. “Human neurons may be more powerful computational devices than previously thought,” study corresponding author Matthew Larkum at Humboldt University of Berlin told Gizmodo in an email. Human brains have a thick cortex, especially the second and third layers (L2/3) from the surface. These layers contain brain cells with lots of branches, called dendrites, that connect them to and exchange information with other brain cells. The researchers acquired and analyzed slices of L2/3 tissue from patients with epilepsy and tumors, focusing specifically on these dendrites. Larkum explained via email that epilepsy surgeries provided a sufficient amount of available cortex tissue, while the tumor patient tissue was used to ensure that the observations weren’t unique to people with epilepsy. The team hooked the tissues to a patch clamp—essentially a system that constructs an electrical circuit from the cells and a measurement instrument—and used fluorescing microscope to observe the action of these L2/3 cells. The team noticed that inputted electrical currents ignited more action potentials than they would in rodent cells and that a chemical that should have blocked the dendrites’ activity did not completely do so. © 2020 G/O Media Inc.

Keyword: Learning & Memory
Link ID: 26934 - Posted: 01.04.2020

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 Nayef Al-Rodhan Facebook recently announced it had acquired CTRL-Labs, a U.S. start-up working on wearable tech that allows people to control digital devices with their brain. The social media company is only the latest in a long string of firms investing in what has come to be termed “neurotechnology.” Earlier this year Neuralink, a company backed by Elon Musk, announced that it hopes to begin human trials for computerized brain implants. These projects may seem like science fiction, but this drive to get more out of our brains is nothing new—from tea, caffeine and nicotine, to amphetamines and the narcolepsy drug Modafinil, drugs have long been used as rudimentary attempts at cognitive enhancement. And in our tech-driven world, the drive to cognitively enhance is stronger than ever—and is leading us to explore new and untested methods. In today’s hypercompetitive world, everyone is looking for an edge. Improving memory, focus or just the ability to work longer hours are all key to getting ahead, and a drug exists to improve each of them. In 2017, 30 percent of Americans said they had used “smart drug” supplements, known as nootropics, at least once that year, even if studies repeatedly demonstrate that they have a negligible effect on intellect. Advertisement For some, however, nootropics are not enough, and so they turn to medical-grade stimulants. The most famous of these is Adderall, which boosts focus and productivity far more than commercial nootropics. A well-established black market thrives on university campuses and in financial centers, supplying these drugs to people desperate to gain a competitive edge. © 2019 Scientific American

Keyword: Learning & Memory; Drug Abuse
Link ID: 26886 - Posted: 12.10.2019

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