by Laura Dattaro Neurons deep in the prefrontal cortex of fragile X model mice have trouble generating the electrical spikes needed to transmit information, according to a new study. The difficulty originates from faulty sodium channels. Fragile X syndrome, one of the leading genetic causes of autism, results from mutations in the gene FMR1. People with the condition often have difficulty with executive-function skills, such as working memory and planning. The new study may explain why, says Randi Hagerman, medical director of the MIND Institute at the University of California, Davis: The disruption to signals propagating through the prefrontal cortex may impede the region’s role in coordinating communication among other parts of the brain. Some drugs that regulate sodium channels, such as the diabetes drug metformin, are already approved for use in people. “This is a great animal model to look at the effects of medication,” says Hagerman, who was not involved in the new work. Mutations in the autism-linked gene SCN2A, which encodes a protein for the sodium channel Nav1.2, also suppress dendritic spikes, researchers previously showed in mice. The cellular mechanism for channel disruption is different between the models, but it’s possible that multiple genetic causes of autism “coalesce around sodium channel disfunction,” says Darrin Brager, research associate professor of neuroscience at the University of Texas at Austin and lead investigator on the FMR1 study. “The same channel is altered, and that’s changing the way the cells are able to integrate information and transmit it.” © 2023 Simons Foundation

Keyword: Development of the Brain; Genes & Behavior
Link ID: 28677 - Posted: 02.22.2023

By Dani Blum The family of Bruce Willis announced that the actor has frontotemporal dementia, known as FTD, a form of dementia that occurs most commonly when nerve cells in the frontal and temporal lobes of the brain decrease in number. Mr. Willis, 67, was previously diagnosed with aphasia, which prompted him to retire from acting. “FTD is a cruel disease that many of us have never heard of and can strike anyone,” the family wrote in a statement. There are two main variants of FTD: primary progressive aphasia, which hampers a patient’s ability to communicate, and behavioral variant frontotemporal dementia, which manifests as personality and behavioral changes. “It hits the parts of the brain that make us the most human,” said Dr. Bruce Miller, a professor of neurology at the University of California, San Francisco. FTD is the most common cause of dementia for people under the age of 60, said Susan Dickinson, the chief executive of the Association for Frontotemporal Degeneration. There are roughly 50,000 people in the United States with a diagnosis of FTD, she added, although many experts consider that number to be a vast undercount, because of how challenging it can be to diagnose. There is no blood test or single biomarker to diagnose the condition — doctors instead identify it based on symptoms and neuroimaging. On average, it takes patients more than three years to get an accurate diagnosis, Ms. Dickinson said. People with primary progressive aphasia may struggle to speak in full sentences or have difficulty comprehending conversations. They may have a hard time writing or reading. Those with the behavioral variant of FTD may act out of character, said Dr. Ian Grant, an assistant professor of neurology at the Northwestern University Feinberg School of Medicine. Families will say that patients “seem like they’ve lost a little bit of their filter,” he said. Someone who is typically quiet and reserved may start spewing profanities, for example, or loudly comment on a stranger’s appearance. The person may act apathetic, Dr. Miller said, losing motivation. Some may also display a lack of empathy for those around them. © 2023 The New York Times Company

Keyword: Alzheimers; Language
Link ID: 28675 - Posted: 02.18.2023

By Allison Whitten The neocortex stands out as a stunning achievement of biological evolution. All mammals have this swath of tissue covering their brain, and the six layers of densely packed neurons within it handle the sophisticated computations and associations that produce cognitive prowess. Since no animals other than mammals have a neocortex, scientists have wondered how such a complex brain region evolved. The brains of reptiles seemed to offer a clue. Not only are reptiles the closest living relatives of mammals, but their brains have a three-layered structure called a dorsal ventricular ridge, or DVR, with functional similarities to the neocortex. For more than 50 years, some evolutionary neuroscientists have argued that the neocortex and the DVR were both derived from a more primitive feature in an ancestor shared by mammals and reptiles. Now, however, by analyzing molecular details invisible to the human eye, scientists have refuted that view. By looking at patterns of gene expression in individual brain cells, researchers at Columbia University showed that despite the anatomical similarities, the neocortex in mammals and the DVR in reptiles are unrelated. Instead, mammals seem to have evolved the neocortex as an entirely new brain region, one built without a trace of what came before it. The neocortex is composed of new types of neurons that seem to have no precedent in ancestral animals. The paper describing this work, which was led by the evolutionary and developmental biologist Maria Antonietta Tosches, was published last September in Science. This process of evolutionary innovation in the brain isn’t limited to the creation of new parts. Other work by Tosches and her colleagues in the same issue of Science showed that even seemingly ancient brain regions are continuing to evolve by getting rewired with new types of cells. The discovery that gene expression can reveal these kinds of important distinctions between neurons is also prompting researchers to rethink how they define some brain regions and to reassess whether some animals might have more complex brains than they thought. All Rights Reserved © 2023

Keyword: Development of the Brain; Evolution
Link ID: 28668 - Posted: 02.15.2023

ByRachel Zamzow A long-smoldering debate among scientists studying autism has erupted. At issue is language—for example, whether researchers should describe autism as a “disorder,” “disability,” or “difference,” and whether its associated features should be called “symptoms” or simply “traits.” In scientific papers and commentaries published in recent months, some have decried ableist language among their colleagues whereas others have defended traditional terminology—with both sides saying they have the best interests of autistic people in mind. The vitriol is harming the field and silencing researchers, some fear, but others see it as a long-overdue reckoning. Since autism’s earliest descriptions in the academic literature as a condition affecting social interaction and communication, researchers and clinicians have framed it as a medical disorder, with a set of symptoms to be treated. Historically, autistic children have been institutionalized and subjected to treatments involving physical punishment, food restriction, and electric shocks. Even today, the most widely used autism therapy—applied behavior analysis—is seen by some as a harmful tool of normalization. Many autistic people and their families have instead embraced the view that their difficulties lie not with their autism, but with a society that isn’t built to support them. But according to some autism researchers, the field still too often defaults to terms with negative connotations. For example, in addition to “symptom” and “disorder,” many scientists use the term “comorbid” rather than the more neutral “co-occurring” to describe conditions that tend to accompany autism. Similarly, some argue the oft-used phrase “people with autism,” as opposed to “autistic person,” can imply that autism is necessarily an unwanted harmful condition. In a recent survey of 195 autism researchers, 60% of responses included views about autistic people the study authors deemed dehumanizing, objectifying, or stigmatizing. Some responses described autistic people as “shut down from the outside world” or “completely inexpressive and apparently without emotions,” according to the November 2022 Frontiers in Psychology study. “What is worse than I thought was how blatant a lot of the content was, which shows that, for [a] large proportion of participants, they did not consider the things they were saying to be problematic at all,” says lead author Monique Botha, a psychologist at the University of Stirling.

Keyword: Autism
Link ID: 28660 - Posted: 02.08.2023

by Peter Hess An autism-linked mutation in the gene CHD8 yields wildly different physical and behavioral traits in mice depending on their genetic backgrounds, according to a study of 33 mouse strains. The findings were published today in Neuron. The results serve as a stark reminder that traits associated with an autism-linked mutation reflect more than just that mutation, says senior investigator Pat Levitt, chair of developmental neurogenetics at Children’s Hospital Los Angeles in California. Differences in genetic background could also explain why some findings from autism model mice have failed to replicate across labs, he adds. People with CHD8 mutations often have autism, intellectual disability, gastrointestinal issues and macrocephaly — larger-than-average head size — but not all of them have all of these traits. This variability may stem from interactions between the mutations and other variants across the genome, says study investigator Manal Tabbaa, a postdoctoral research fellow in Levitt’s lab. The new work does not reveal how the same CHD8 mutation can affect different mice — or people — differently. But researchers could use the genetically diverse rodents to answer this question, and to better understand and model autism’s heterogeneity, Tabbaa and Levitt say. “This is such a comprehensive approach to understand a really clinically relevant question, and it’s almost unbelievable that just three people could do this amount of work, considering how much it looks like was done,” says Joseph Gleeson, professor of neurosciences at the University of California, San Diego, who was not involved in the study. “They are just scratching the surface of what could be really fantastic future efforts.” © 2023 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28657 - Posted: 02.08.2023

By Dana G. Smith Do you: Cut the tags out of your clothes? Relive (and regret) past conversations? Have episodes of burnout and fatigue? Zone out while someone is talking? Become hyper-focused while working on a project? Take on dozens of hobbies? Daydream? Forget things? According to TikTok, you might have attention deficit hyperactivity disorder. Videos about the psychiatric condition are all over the social media app, with the #adhd hashtag receiving more than 17 billion views to date. Many feature young people describing their specific (and sometimes surprising) symptoms, like sensitivity to small sensory annoyances (such as clothing tags) or A.D.H.D. paralysis, a type of extreme procrastination. After viewing these videos, many people who were not diagnosed with A.D.H.D. as children may question whether they would qualify as adults. As with most psychiatric conditions, A.D.H.D. symptoms can range in type and severity. And many of them “are behaviors everyone experiences at some point or another,” said Joel Nigg, a professor of psychiatry at Oregon Health & Science University. The key to diagnosing the condition, however, requires “determining that it’s serious, it’s extreme” and it’s interfering with people’s lives, he said. It’s also critical that the symptoms have been present since childhood. Those nuances can be lost on social media, experts say. In fact, one study published earlier this year found that more than half of the A.D.H.D. videos on TikTok were misleading. If a video (or article) has you thinking you may have undiagnosed A.D.H.D., here’s what to consider. Approximately 4 percent of adults in the United States have enough symptoms to qualify for A.D.H.D., but only an estimated one in 10 of them is diagnosed and treated. For comparison, roughly 9 percent of children in the United States have been diagnosed with the condition, and three-quarters have received medication or behavioral therapy for it. One reason for the lack of diagnoses in adults is that when people think of A.D.H.D., they often imagine a boy who can’t sit still and is disruptive in class, said Dr. Deepti Anbarasan, a clinical associate professor of psychiatry at the NYU Grossman School of Medicine. But those stereotypical hyperactive symptoms are present in just 5 percent of adult cases, she said. © 2023 The New York Times Company

Keyword: ADHD
Link ID: 28646 - Posted: 01.27.2023

By Annabelle Timsit A new study of more than 29,000 older adults has identified six habits — from eating a variety of foods to regularly reading or playing cards — that are linked with a lower risk of dementia and a slower rate of memory decline. Eating a balanced diet, exercising the mind and body regularly, having regular contact with others, and not drinking or smoking — these six “healthy lifestyle factors” were associated with better cognitive outcomes in older adults, in a large Chinese study conducted over a decade and published in the BMJ on Wednesday. While researchers have long known that there is a link between dementia and factors such as social isolation and obesity, the size and scope of the new study adds substantial evidence to a global body of research that suggests a healthy lifestyle may help brains age better. It also suggests that the effects of a healthy lifestyle are beneficial even for people who are genetically more susceptible to memory decline — a “very hope-giving” finding for the millions of individuals around the world who carry the APOEε4 gene, a major risk factor for Alzheimer’s disease, said Eef Hogervorst, chair of biological psychology at Loughborough University, who was not involved in the study. Memory naturally declines gradually as people age. Some older people may develop dementia, an umbrella term that can include Alzheimer’s, and generally describes a deterioration in cognitive function that goes beyond the normal effects of aging. But for many, “memory loss can merely be senescent forgetfulness,” write the authors of the BMJ study — like forgetting the name of that TV program you used to love, or that pesky fact you wanted to look up. Memory loss is no less damaging for being gradual, and age-related memory decline can in some cases be an early symptom of dementia. But the good news, the researchers say, is that it “can be reversed or become stable rather than progress to a pathological state.” How do you live to be 100? Good genes, getting outside and friends.

Keyword: Alzheimers
Link ID: 28644 - Posted: 01.27.2023

ByMeredith Wadman A massive data mining study has found numerous associations between common viruses like the flu and devastating neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease). The findings expand on previous research linking individual viruses to neurological diseases. But experts caution that the study, which relied on electronic medical records rather than biological samples, merely describes correlations and doesn’t prove causation. Still, it’s “really exciting,” says Kristen Funk, a neuroimmunologist who studies Alzheimer’s at the University of North Carolina, Charlotte. Rather than homing in on, say, the relationship between herpes simplex infections and Alzheimer’s—a recent focus in her own field—“this research broadens that scope to look at different viruses and more neurodegenerative diseases.” Scientists have found connections between viruses and neurodegenerative diseases before. Previous studies uncovered ties between the influenza virus and Parkinson’s, for example, and between genital warts (caused by human papillomavirus) and dementia. A landmark project published in Science last year cemented another connection: Epidemiologists who analyzed 2 decades of data from the blood tests of 10 million U.S. soldiers reported that it’s nearly impossible to develop multiple sclerosis without first being infected with the Epstein-Barr virus—a ubiquitous pathogen long suspected of causing MS. Inspired by that paper, National Institutes of Health (NIH) researchers wondered whether they could mine other large databases to tease out more associations. They focused on viral links to six neurodegenerative diseases: Alzheimer’s, Parkinson’s, dementia, ALS, MS, and vascular dementia. (Some scientists dispute that MS and vascular dementia are neurodegenerative diseases.)

Keyword: Alzheimers; Parkinsons
Link ID: 28638 - Posted: 01.25.2023

Kaitlyn Radde Socially isolated older adults have a 27% higher chance of developing dementia than older adults who aren't, a new study by Johns Hopkins researchers found. "Social connections matter for our cognitive health, and it is potentially easily modifiable for older adults without the use of medication," Dr. Thomas Cudjoe, an assistant professor of medicine at Johns Hopkins and a senior author of the study, said in a news release. Published in the Journal of the American Geriatrics Society, the study tracked 5,022 dementia-free U.S. adults who were 65 or older – with an average age of 76 – and not living in a residential care facility. About 23% of participants were socially isolated. Social isolation is defined as having few relationships and few people to interact with regularly. The study measured this based on whether or not participants lived alone, talked about "important matters" with two or more people in the past year, attended religious services or participated in social events. Participants were assigned one point for each item, and those who scored a zero or one were classified as socially isolated. Over the course of nine years, researchers periodically administered cognitive tests. Overall, about 21% of the study participants developed dementia. But among those were who were socially isolated, about 26% developed dementia – compared to slightly less than 20% for those who were not socially isolated. The study did not find significant differences by race or ethnicity. However, more than 70% of the participants in the study were white – with particularly small sample sizes of Hispanic, Asian and Native participants – and the authors call for further research on the topic. © 2023 npr

Keyword: Alzheimers
Link ID: 28631 - Posted: 01.18.2023

By Elizabeth Pennisi Biologists have long known that new protein-coding genes can arise through the duplication and modification of existing ones. But some protein genes can also arise from stretches of the genome that once encoded aimless strands of RNA instead. How new protein genes surface this way has been a mystery, however. Now, a study identifies mutations that transform seemingly useless DNA sequences into potential genes by endowing their encoded RNA with the skill to escape the cell nucleus—a critical step toward becoming translated into a protein. The study’s authors highlight 74 human protein genes that appear to have arisen in this de novo way—more than half of which emerged after the human lineage branched off from chimpanzees. Some of these newcomer genes may have played a role in the evolution of our relatively large and complex brains. When added to mice, one made the rodent brains grow bigger and more humanlike, the authors report this week in Nature Ecology & Evolution. “This work is a big advance,” says Anne-Ruxandra Carvunis, an evolutionary biologist at the University of Pittsburgh, who was not involved with the research. It “suggests that de novo gene birth may have played a role in human brain evolution.” Although some genes encode RNAs that have structural or regulatory purposes themselves, those that encode proteins instead create an intermediary RNA. Made in the nucleus like other RNAs, these messenger RNAs (mRNAs) exit into the cytoplasm and travel to organelles called ribosomes to tell them how to build the gene’s proteins. A decade ago, Chuan-Yun Li, an evolutionary biologist at Peking University, and colleagues discovered that some human protein genes bore a striking resemblance to DNA sequences in rhesus monkeys that got transcribed into long noncoding RNAs (lncRNAs), which didn’t make proteins or have any other apparent purpose. Li couldn’t figure out what it had taken for those stretches of monkey DNA to become true protein-coding genes in humans. © 2023 American Association for the Advancement of Science.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 28624 - Posted: 01.07.2023

by Giorgia Guglielmi About five years ago, Catarina Seabra made a discovery that led her into uncharted scientific territory. Seabra, then a graduate student in Michael Talkowski’s lab at Harvard University, found that disrupting the autism-linked gene MBD5 affects the expression of other genes in the brains of mice and in human neurons. Among those genes, several are involved in the formation and function of primary cilia — hair-like protrusions on the cell’s surface that sense its external environment. “This got me intrigued, because up to that point, I had never heard of primary cilia in neurons,” Seabra says. She wondered if other researchers had linked cilia defects to autism-related conditions, but the scientific literature offered only sparse evidence, mostly in mice. Seabra, now a postdoctoral researcher in the lab of João Peça at the Center for Neuroscience and Cell Biology at the University of Coimbra in Portugal, is spearheading an effort to look for a connection in people: The Peça lab established a biobank of dental stem cells obtained from baby teeth of 50 children with autism or other neurodevelopmental conditions. And the team plans to look at neurons and brain organoids made from those cells to see if their cilia show any defects in structure or function. Other neuroscientists, too, are working to understand the role of cilia during neurodevelopment. Last September, for example, researchers working with tissue samples from mice discovered that cilia on the surface of neurons can form junctions, or synapses, with other neurons — which means cilia defects could, at least in theory, hinder the development of neural circuitry and activity. Other teams have connected several additional autism-related genes, beyond MBD5, to the tiny cell antennae. © 2023 Simons Foundation

Keyword: Autism
Link ID: 28623 - Posted: 01.07.2023

By Laurie McGinley The Food and Drug Administration on Friday approved an Alzheimer’s drug that slowed cognitive decline in a major study, offering patients desperately needed hope — even as doctors sharply debated the safety of the drug and whether it provides a significant benefit. The FDA said the drug, called lecanemab, is for patients with mild cognitive impairment or early dementia because of Alzheimer’s. The accelerated approval was based on a mid-stage trial that showed the treatment effectively removed a sticky protein called amyloid beta — considered a hallmark of the illness — from the brain. A larger trial, conducted more recently, found the drug, which will be sold under the brand name Leqembi, slowed the progression of Alzheimer’s disease by 27 percent. “This treatment option is the latest therapy to target and affect the underlying disease process of Alzheimer’s, instead of only treating the symptoms of the disease,” Billy Dunn, director of the FDA’s Office of Neuroscience, said in a statement. The approval followed a barrage of criticism endured by the FDA for its 2021 approval of Aduhelm, another amyloid-targeting drug that had been panned by the agency’s outside experts. Lecanemab is getting a warmer reception but disagreements remain. Many neurologists and advocates hailed lecanemab, given intravenously twice a month, as an important advance — one that follows years of failure involving Alzheimer’s drugs. They said the treatment will allow patients to stay longer in the milder stages of the fatal, neurodegenerative disorder, which afflicts more than 6 million people in the United States.

Keyword: Alzheimers
Link ID: 28622 - Posted: 01.07.2023

By Freda Kreier Living through the COVID-19 pandemic may have matured teens’ brains beyond their years. From online schooling and social isolation to economic hardship and a mounting death count, the last few years have been rough on young people. For teens, the pandemic and its many side effects came during a crucial window in brain development. Now, a small study comparing brain scans of young people from before and after 2020 reveals that the brains of teens who lived through the pandemic look about three years older than expected, scientists say. This research, published December 1 in Biological Psychiatry: Global Open Science, is the first to look at the impact of the pandemic on brain aging. The finding reveals that “the pandemic hasn’t been bad just in terms of mental health for adolescents,” says Ian Gotlib, a clinical neuroscientist at Stanford University. “It seems to have altered their brains as well.” The study can’t link those brain changes to poor mental health during the pandemic. But “we know there is a relationship between adversity and the brain as it tries to adapt to what it’s been given,” says Beatriz Luna, a developmental cognitive neuroscientist at the University of Pittsburgh, who wasn’t involved in the research. “I think this is a very important study that sets the ball rolling for us to look at this.” The roots of this study date back to nearly a decade ago, when Gotlib and his colleagues launched a project in California’s Bay Area to study depression in adolescents. The researchers were collecting information on the mental health of the kids in the study, and did MRI scans of their brains. © Society for Science & the Public 2000–2023.

Keyword: Development of the Brain; Stress
Link ID: 28620 - Posted: 01.04.2023

By Ellen Barry The effect of social media use on children is a fraught area of research, as parents and policymakers try to ascertain the results of a vast experiment already in full swing. Successive studies have added pieces to the puzzle, fleshing out the implications of a nearly constant stream of virtual interactions beginning in childhood. A new study by neuroscientists at the University of North Carolina tries something new, conducting successive brain scans of middle schoolers between the ages of 12 and 15, a period of especially rapid brain development. The researchers found that children who habitually checked their social media feeds at around age 12 showed a distinct trajectory, with their sensitivity to social rewards from peers heightening over time. Teenagers with less engagement in social media followed the opposite path, with a declining interest in social rewards. The study, published on Tuesday in JAMA Pediatrics, is among the first attempts to capture changes to brain function correlated with social media use over a period of years. The study has important limitations, the authors acknowledge. Because adolescence is a period of expanding social relationships, the brain differences could reflect a natural pivot toward peers, which could be driving more frequent social media use. “We can’t make causal claims that social media is changing the brain,” said Eva H. Telzer, an associate professor of psychology and neuroscience at the University of North Carolina, Chapel Hill, and one of the authors of the study. But, she added, “teens who are habitually checking their social media are showing these pretty dramatic changes in the way their brains are responding, which could potentially have long-term consequences well into adulthood, sort of setting the stage for brain development over time.” © 2023 The New York Times Company

Keyword: Development of the Brain; Stress
Link ID: 28619 - Posted: 01.04.2023

Linda Geddes Science correspondent Scientists have developed a blood test to diagnose Alzheimer’s disease without the need for expensive brain imaging or a painful lumbar puncture, where a sample of cerebrospinal fluid (CSF) is drawn from the lower back. If validated, the test could enable faster diagnosis of the disease, meaning therapies could be initiated earlier. Alzheimer’s is the most common form of dementia, but diagnosis remains challenging – particularly during the earlier stages of the disease. Current guidelines recommend detection of three distinct markers: abnormal accumulations of amyloid and tau proteins, as well as neurodegeneration – the slow and progressive loss of neuronal cells in specified regions of the brain. This can be done through a combination of brain imaging and CSF analysis. However, a lumbar puncture can be painful and people may experience headaches or back pain after the procedure, while brain imaging is expensive and takes a long time to schedule. Prof Thomas Karikari at the University of Pittsburgh, in Pennsylvania, US, who was involved in the study, said: “A lot of patients, even in the US, don’t have access to MRI and PET scanners. Accessibility is a major issue.” The development of a reliable blood test would be an important step forwards. “A blood test is cheaper, safer and easier to administer, and it can improve clinical confidence in diagnosing Alzheimer’s and selecting participants for clinical trial and disease monitoring,” Karikari said. Although current blood tests can accurately detect abnormalities in amyloid and tau proteins, detecting markers of nerve cell damage that are specific to the brain has been harder. Karikari and his colleagues around the world focused on developing an antibody-based blood test that would detect a particular form of tau protein called brain-derived tau, which is specific to Alzheimer’s disease. © 2022 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 28616 - Posted: 12.28.2022

By Deborah Blum Back in the year 2000, sitting in his small home office in California’s Mill Valley, surrounded by stacks of spreadsheets, Jay Rosner hit one of those dizzying moments of dismay. An attorney and the executive director of The Princeton Review Foundation, the philanthropic arm of the private test-preparation and tutoring company, The Princeton Review, Rosner was scheduled to give testimony in a highly charged affirmative action lawsuit against the University of Michigan. He knew the case, Grutter v. Bollinger, was eventually headed to the U.S. Supreme Court, but as he reviewed the paperwork, he discovered a daunting gap in his argument.  Rosner had been asked to explore potential racial and cultural biases baked into standardized testing. He believed such biases, which critics had been surfacing for years prior, were real, but in that moment, he felt himself coming up short. “I suddenly realized that I would be deposed on this issue,” he recalled, “and I had no data to support my hypothesis, only deductive reasoning.”   The punch of that realization still resonates. Rosner is the kind of guy who really likes data to stand behind his points, and he recalls an anxiety-infused hunt for some solid facts. Rosner was testifying about an entrance exam for law school, the LSAT, for which he could find no particulars. But he knew that a colleague had data on how students of different racial backgrounds answered specific questions on another powerful standardized test, the SAT, long used to help decide undergraduate admission to colleges — given in New York state. He decided he could use that information to make a case by analogy. The two scholars agreed to crunch some numbers.  Based on past history of test results, he knew that White students would overall have higher scores than Black students. Still, Rosner expected Black students to perform better on some questions. To his shock, he found no trace of such balance. The results were “incredibly uniform,” he said, skewing almost entirely in favor of White students. “Every single question except one in the New York state data on four SATs favored Whites over Blacks,” Rosner recalled.

Keyword: Intelligence; Genes & Behavior
Link ID: 28611 - Posted: 12.24.2022

By Anthea Rowan To many, the word “hobby” signifies something lightweight or trivial. Yet taking on a new hobby as one ages might provide an important defense against dementia, some experts say. About 5.8 million adults over 65 in the United States live with Alzheimer’s disease or other dementia disorders, according to the Centers for Disease Control and Prevention. One in 9 Americans over 65 has Alzheimer’s, according to the Alzheimer’s Association. And although the rate of dementia may be falling thanks to lifestyle changes, more of us are living longer, which means the societal burden of dementia is rising. David Merrill, an adult and geriatric psychiatrist and director of the Pacific Brain Health Center in Santa Monica, Calif., suggests we use the word “pursuit” instead of “hobby,” as it elevates the concept of an activity to something demanding, something requiring concentration or collaboration. Something we ought to chase down. Activities that demand focus and industry are the whetstone to keeping cognition sharp, Merrill says. Our brains, he continues, are like any other part of our body. “‘Use it or lose it’ is not just a hypothesis, it’s a basic biologic fact that holds as true for our brains as our muscles or our bones.” While there is as yet no surefire way to prevent dementia or cure it, the Lancet in 2020 identified 12 potentially modifiable risk factors for the condition; they include physiological (blood pressure, diabetes, hearing loss), lifestyle choices (smoking, drinking, physical inactivity), environmental (air pollution) depression, social isolation and a lower level of education. The Alzheimer Society of Canada is also clear about what we can do to help minimize our dementia risk: keep cognitively engaged, learn new things, meet new people, keep a diary, remain curious and engage in conversations.

Keyword: Alzheimers; Learning & Memory
Link ID: 28605 - Posted: 12.21.2022

Patrick Barkham Three species of cetacean stranded off the coast of Scotland, including a bottlenose dolphin and a long-finned pilot whale, have been found to have the classic markers of Alzheimer’s disease, according to a study. Although types of dementia have been fairly widely detected in other animals, Alzheimer’s disease has not been found to occur naturally in species other than humans. But researchers from the University of Glasgow, the universities of St Andrews and Edinburgh and the Moredun Research Institute in Scotland were surprised to find that postmortem tests of 22 toothed whales, or odontocetes, detected three key brain changes associated with human Alzheimer’s disease in three animals. Scientists do not know the cause of this brain degeneration but it could support one theory about why some groups or pods of whales and dolphins run aground in shallow water. Some mass strandings have been linked to increasing anthropogenic noise in the oceans, but Alzheimer’s-like signs in the brain could support a “sick leader” theory, whereby mostly healthy cetaceans are stranded because they follow a group leader that has become confused or lost. The researchers found signs of Alzheimer’s in three of 22 stranded odontocetes: a white-beaked dolphin, a bottlenose dolphin and a long-finned pilot whale, also a member of the dolphin family.

Keyword: Alzheimers
Link ID: 28604 - Posted: 12.21.2022

By Sandra G. Boodman The 23-year-old patient arrived in the back of a police car and was in four point restraints — hands and feet strapped to a gurney — when emergency physician Elizabeth Mitchell saw her at a Los Angeles hospital early on March 17. Chloe R. Kral was being held on a 5150, shorthand in California for an emergency psychiatric order that allows people deemed dangerous to themselves or others to be involuntarily confined for 72 hours. She had spent the previous six months at a private treatment center receiving care for bipolar disorder and depression. Chloe had improved and was set to move to transitional housing when she suddenly became combative and threatened to harm staff and kill herself. Police had taken her to the emergency room at Cedars-Sinai Marina del Rey Hospital before a planned transfer to a mental hospital. Chloe, Mitchell recalled, was “mumbling about Rosa Parks” when they met. She managed to tell the doctor that she hadn’t used drugs or alcohol, but was otherwise incoherent. “We get a lot of psychiatric patients, and they’re just waiting for placement,” Mitchell said. But something indefinable — Mitchell characterized it as “maybe gut instinct” honed by nearly two decades of practice — prompted her to order a CT scan of Chloe’s head to better assess her mental status. When she pulled up the image, Mitchell gasped. “I had never seen anything like it,” she said. She rounded up her colleagues and “made everyone in the whole ER come look.” “I was speechless,” she said. “All I could think was ‘How did no one figure this out?’ ”

Keyword: Depression; Schizophrenia
Link ID: 28603 - Posted: 12.21.2022

By Yasemin Saplakoglu It’s often subtle at first. A lost phone. A forgotten word. A missed appointment. By the time a person walks into a doctor’s office, worried about signs of forgetfulness or failing cognition, the changes to their brain have been long underway — changes that we don’t yet know how to stop or reverse. Alzheimer’s disease, the most common form of dementia, has no cure. “There’s not much you can do. There are no effective treatments. There’s no medicine,” said Riddhi Patira, a behavioral neurologist in Pennsylvania who specializes in neurodegenerative diseases. That’s not how the story was supposed to go. Three decades ago, scientists thought they had cracked the medical mystery of what causes Alzheimer’s disease with an idea known as the amyloid cascade hypothesis. It accused a protein called amyloid-beta of forming sticky, toxic plaques between neurons, killing them and triggering a series of events that made the brain waste away. The amyloid cascade hypothesis was simple and “seductively compelling,” said Scott Small, the director of the Alzheimer’s Disease Research Center at Columbia University. And the idea of aiming drugs at the amyloid plaques to stop or prevent the progression of the disease took the field by storm. Decades of work and billions of dollars went into funding clinical trials of dozens of drug compounds that targeted amyloid plaques. Yet almost none of the trials showed meaningful benefits to patients with the disease. That is, until September, when the pharmaceutical giants Biogen and Eisai announced that in a phase 3 clinical trial, patients taking the anti-amyloid drug lecanemab showed 27% less decline in their cognitive health than patients taking a placebo did. Last week, the companies revealed the data, now published in the New England Journal of Medicine, to an excited audience at a meeting in San Francisco. Simons Foundation © 2022

Keyword: Alzheimers
Link ID: 28595 - Posted: 12.15.2022