By Amber Dance Isabelle Lousada was in her early 30s when she collapsed at her Philadelphia wedding in 1995. A London architect, she had suffered a decade of mysterious symptoms: tingling fingers, swollen ankles, a belly distended by her enlarged liver. The doctors she first consulted suggested she had chronic fatigue syndrome or that she’d been partying and drinking too hard. But her new brother-in-law, a cardiologist, felt that something else must be going on. A fresh series of doctor’s visits led, finally, to the proper diagnosis: Malformed proteins had glommed together inside Lousada’s bloodstream and organs. Those giant protein globs are called amyloid, and the diagnosis was amyloidosis. Amyloid diseases that affect the brain, such as Alzheimer’s and Parkinson’s diseases, receive the lion’s share of attention from medical professionals and the press. In contrast, amyloid diseases that affect other body parts are less familiar and rarely diagnosed conditions, says Gareth Morgan, a biochemist at Boston University Chobanian & Avedisian School of Medicine. Physicians may struggle to recognize and distinguish them, especially in early stages. Treatment options have also been limited — Lousada, now CEO of the nonprofit Amyloidosis Research Consortium in Newton, Massachusetts, was fortunate to survive thanks to a stem cell transplant that is too grueling or unsuitable for many with amyloidosis. Several new medications have come out in the last five years — and these, Lousada says, “have been real game-changers.” But although these therapies can block the formation of new, damaging amyloid, they can’t dissolve the amyloid that’s already built up. The body has natural processes to do so, but these are often too slow to clear years’ worth of built-up amyloid, especially in older individuals. And so patients still deal with amyloid clogging their organs, and people still die of amyloidosis, even if they survive longer than they once did. © 2023 Annual Reviews

Keyword: Alzheimers; Parkinsons
Link ID: 28731 - Posted: 04.09.2023

Visual: Andrew Bret Wallis/The Image Bank via Getty Images By Lina Tran At 25, Dasha Kiper moved in with a 98-year-old man. She’d just left a graduate program in clinical psychology; Mr. Kessler was a Holocaust survivor in the early stages of Alzheimer’s disease, whose son had hired Kiper as a live-in caregiver. One day, Mr. Kessler clambers onto a chair to replace the battery in a smoke detector. When he ignores her instructions to come down, Kiper loses her cool. She shouts that he’s incapable of changing the battery and doing much of anything for himself. Later, Kiper is filled with remorse. She should have known better than to yell at a nonagenarian with dementia. This is the focus of Kiper’s “Travelers to Unimaginable Lands: Stories of Dementia, the Caregiver, and the Human Brain” — not the mind of the patient, but the caregiver. Often, the spouses, children, and loved ones of people living with dementia succumb to arguing or pleading with their patients, despite reason. “We want to reestablish a shared reality,” Kiper writes. “It’s not cruelty but desperation that drives us to confront them with the truth.” Caregivers aren’t mere observers to cognitive decline but the “invisible victims” of dementia disorders, Kiper writes. They traverse warped realities that operate under different rules of time and memory. One caregiver says, referring to a famous case study by neurologist and author Oliver Sacks, it’s “like being an anthropologist on Mars.” But a caregiver’s slip-up isn’t necessarily the result of character flaws or a lapse in compassion. Rather, Kiper shows the healthy brain is riddled with cognitive biases that impede the work of caring for a person with an impaired mind. This takes a heavy toll. “People always ask about the patient,” one exasperated woman tells Kiper, after recounting how her husband, who doesn’t recognize her, takes to locking her out of their apartment each night. She starts carrying a spare key to let herself in after he falls asleep. “Let me tell you something, the patient is fine; it’s the caregiver who’s going crazy.”

Keyword: Alzheimers; Stress
Link ID: 28728 - Posted: 04.09.2023

ByJennifer Couzin-Frankel A class of Alzheimer’s drugs that aims to slow cognitive decline, including the antibody lecanemab that was granted accelerated approval in the United States in January, can cause brain shrinkage, researchers report in a new analysis. Although scientists and drug developers have documented this loss of brain volume in clinical trial participants for years, the scientific review, published yesterday in Neurology, is the first to look at data across numerous studies. It also links the brain shrinkage to a better known side effect of the drugs, brain swelling, which often presents without symptoms. “We don’t fully know what these changes might imply,” says Jonathan Jackson, a cognitive neuroscientist at Massachusetts General Hospital. But, “These data are extremely concerning, and it’s likely these changes are detrimental.” The analysis, which found that trial participants taking these Alzheimer’s drugs often developed more brain shrinkage than when they were on a placebo, alarmed Scott Ayton, a neuroscientist at the Florey Institute of Neuroscience and Mental Health in Melbourne, Australia, who led the work. “We’re talking about the possibility of brain damage” from treatment, says Ayton, who was invited by Eisai to join an advisory board on lecanemab’s rollout in Australia if the drug is approved there. “I find it very peculiar that these data, which are very important, have been completely ignored by the field.” A spokesperson for Eisai suggested there are benign theories for the brain shrinkage, too. The company said that although participants in its pivotal trial did experience “greater cortical volume loss on lecanemab relative to placebo,” those reductions may be due to antibody clearing the protein beta amyloid from the brain, and reducing inflammation. © 2023 American Association for the Advancement of Science.

Keyword: Alzheimers; Brain imaging
Link ID: 28721 - Posted: 03.29.2023

By Emily Underwood Many of our defining traits — including the languages we speak and how we connect with others — can be traced back at least in part to our earliest experiences. Although our brains remain malleable throughout our lives, most neuroscientists agree that the changes that occur in the womb and in the first few years of life are among the most consequential, with an outsize effect on our risk of developmental and psychiatric conditions. “Early on in life, the brain is still forming itself,” says Claudia Lugo-Candelas, a clinical psychologist at Columbia University and coauthor of an overview of the prenatal origins of psychiatric illness in the Annual Review of Clinical Psychology. Starting from a tiny cluster of stem cells, the brain develops into a complex organ of roughly 100 billion neurons and trillions of connections in just nine months. Compared to the more subtle brain changes that occur later in life, Lugo-Candelas says, what happens in utero and shortly after birth “is like building the house, versus finishing the deck.” But just how this process unfolds, and why it sometimes goes awry, has been a hard mystery to crack, largely because so many of the key events are difficult to observe. The first magnetic resonance imaging (MRI) scans of baby and fetal brains were taken back in the early 1980s, and doctors seized on the tool to diagnose major malformations in brain structure. But neuroimaging tools that can capture the baby brain’s inner workings in detail and spy on fetal brain activity in pregnant moms are much newer developments. Today, this research, coupled with long-term studies that follow thousands of individual children for years, is giving scientists new insights into how the brain develops. These advances have propelled researchers to a different stage than they were in even five years ago, says Damien Fair, a neuroscientist at the University of Minnesota who studies developmental conditions like autism and attention deficit hyperactivity disorder (ADHD). © 2023 Annual Reviews

Keyword: Development of the Brain; ADHD
Link ID: 28718 - Posted: 03.25.2023

By Emily Anthes The prevalence of autism spectrum disorder in American children rose between 2018 and 2020, continuing a long-running trend, according to a study released by the Centers for Disease Control and Prevention on Thursday. In 2020, an estimated one in 36 8-year-olds had autism, up from one in 44 in 2018. The prevalence was roughly 4 percent in boys and 1 percent in girls. The rise does not necessarily mean that autism has become more common among children, and it could stem from other factors, such as increased awareness and screening. “I have a feeling that this is just more discovery,” said Catherine Lord, a professor of psychiatry at the University of California, Los Angeles medical school, who was not involved in the research. “The question is what’s happening next to these kids, and are they getting services?” The rise was especially sharp among Black, Hispanic, and Asian or Pacific Islander children. For the first time, autism was significantly more prevalent among 8-year-olds in these groups than in white children, who have traditionally been more likely to receive autism diagnoses. “These patterns might reflect improved screening, awareness and access to services among historically underserved groups,” the researchers wrote. But why the prevalence in these children has surpassed that in white children is an open question that requires more investigation, Dr. Lord said. An accompanying study, also published on Thursday, suggests that the pandemic may have disrupted or delayed the detection of autism in younger children. © 2023 The New York Times Company

Keyword: Autism
Link ID: 28717 - Posted: 03.25.2023

Jon Hamilton Mora Leeb places some pieces into a puzzle during a local puzzle tournament. The 15-year-old has grown up without the left side of her brain after it was removed when she was very young. Seth Leeb In most people, speech and language live in the brain's left hemisphere. Mora Leeb is not most people. When she was 9 months old, surgeons removed the left side of her brain. Yet at 15, Mora plays soccer, tells jokes, gets her nails done, and, in many ways, lives the life of a typical teenager. "I can be described as a glass-half-full girl," she says, pronouncing each word carefully and without inflection. Her slow, cadence-free speech is one sign of a brain that has had to reorganize its language circuits. Yet to a remarkable degree, Mora's right hemisphere has taken on jobs usually done on the left side. It's an extreme version of brain plasticity, the process that allows a brain to modify its connections to adapt to new circumstances. Brain plasticity is thought to underlie learning, memory, and early childhood development. It's also how the brain revises its circuitry to help recover from a brain injury — or, in Mora's case, the loss of an entire hemisphere. Scientists hope that by understanding the brains of people like Mora, they can find ways to help others recover from a stroke or traumatic brain injury. They also hope to gain a better understanding of why very young brains are so plastic. Sometime in the third trimester of Ann Leeb's pregnancy, the child she was carrying had a massive stroke on the left side of her brain. No one knew it at the time. © 2023 npr

Keyword: Development of the Brain; Epilepsy
Link ID: 28714 - Posted: 03.23.2023

Heidi Ledford A mouse’s brain (red and blue) hosts a human astrocyte (green) that arose from transplanted neural stem cells.Credit: Liu et al./Cell (2023) In a technical “tour de force”, researchers have analysed multiple traits of individual cells to pinpoint those that give rise to crucial components of the human brain. The analysis, published on 16 March in Cell1, uses a combination of protein and RNA analysis to painstakingly purify and classify individual stem cells and their close relatives isolated from human brains. Researchers then injected different types of cell into mice and monitored the cells as they divided and their progeny took on specialized roles in the brain. The hope is that this study, and others like it, will illuminate how such developmental programmes go awry in neurological diseases — and how they can be harnessed to create new therapies. “The census of stem and progenitor cells in the developing human brain is really just beginning,” says Arnold Kriegstein, a developmental neuroscientist at the University of California, San Francisco, who was not involved in the research. “This work offers a nice window into some of that complexity.” The brain is an intricate symphony of different cells, each of which performs essential functions. Star-shaped cells known as astrocytes, for example, are important for supporting metabolism in neurons, and loss of astrocyte function is linked to neurodegenerative conditions such as Alzheimer’s disease. Oligodendrocytes are cells that create a protective, insulating sheath around the connections between neurons. When they are damaged — as in diseases such as multiple sclerosis — communication between neurons slows or stops altogether. © 2023 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 28707 - Posted: 03.18.2023

By McKenzie Prillaman The wiring of one insect’s brain no longer contains much uncharted territory. All of the nerve cells — and virtually every connection between them — in a larval fruit fly brain have now been mapped, researchers report in the March 10 Science. It’s the most complex whole brain wiring diagram yet created. Previously, just three organisms — a sea squirt and two types of worm — had their brain circuitry fully diagrammed to this resolution. But the brains of those creatures have only a few hundred neurons. The scientists who conducted the new study wanted to understand much more complicated brains. Fruit flies (Drosophila melanogaster) share a wide range of behaviors with humans, including integrating sensory information and learning. Larvae perform nearly all the same actions as adult flies — except for some, like flying and mating — but have smaller brains, making data collection much faster (SN: 7/19/18). The idea for this project came 12 years ago, says neuroscientist Marta Zlatic of the MRC Laboratory of Molecular Biology in Cambridge, England. At that time, she and her colleagues captured electron microscope images of the entire larval fruit fly brain. They then stitched those images together in a computer and manually traced each neuron to create a 3-D rendering of the cells. Finally, the team found the connections where information gets passed between the cells, and even determined the sending and receiving ends. Neurons transmit information to one another in circuits. Exploring the neurons’ connectivity patterns — not just directly linked partners, but also the links of linked cells and so on — revealed 93 different types of neurons. The classes were consistent with preexisting groupings characterized by shape and function. And nearly 75 percent of the most well-connected neurons were tied to the brain’s learning center, indicating the importance of learning in animals. © Society for Science & the Public 2000–2023.

Keyword: Brain imaging; Development of the Brain
Link ID: 28697 - Posted: 03.11.2023

By Jacob Beck, Sam Clarke Imagine hosting a party. You arrange snacks, curate a playlist and place a variety of beers in the refrigerator. Your first guest shows up, adding a six-pack before taking one bottle for himself. You watch your next guest arrive and contribute a few more beers, minus one for herself. Ready for a drink, you open the fridge and are surprised to find only eight beers remaining. You haven't been consciously counting the beers, but you know there should be more, so you start poking around. Sure enough, in the crisper drawer, behind a rotting head of romaine, are several bottles. How did you know to look for the missing beer? It's not like you were standing guard at the refrigerator, tallying how many bottles went in and out. Rather you were using what cognitive scientists call your number sense, a part of the mind that unconsciously solves simple math problems. While you were immersed in conversation with guests, your number sense was keeping tabs on how many beers were in the fridge. For a long time scientists, mathematicians and philosophers have debated whether this number sense comes preinstalled or is learned over time. Plato was among the first in the Western tradition to propose that humans have innate mathematical abilities. In Plato's dialogue Meno, Socrates coaxes the Pythagorean theorem out of an uneducated boy by asking him a series of simple questions. Socrates's takeaway is that the boy had innate knowledge of the Pythagorean theorem all along; the questioning just helped him express it. In the 17th century John Locke rejected this idea, insisting that the human mind begins as a tabula rasa, or blank slate, with almost all knowledge acquired through experience. This view, known as empiricism, in contrast to Plato's nativism, was later further developed by John Stuart Mill, who argued that we learn two plus three is five by seeing many examples where it holds true: two apples and three apples make five apples, two beers and three beers make five beers, and so on.

Keyword: Development of the Brain; Learning & Memory
Link ID: 28693 - Posted: 03.08.2023

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