Richard Luscombe Federal health authorities on Tuesday gave approval to an experimental new drug that has shown to delay the onset of Alzheimer’s disease in trials. Donanemab, manufactured by Eli Lilly, is the second medication that has won the blessing of the Food and Drug Administration (FDA) to treat patients showing early symptoms of the disease, most prominently cognitive impairment. Last year, authorities cleared the drug lecanemab, marketed under the brand name Leqembi, after it demonstrated a similar decline in the progression of Alzheimer’s in a control group. The treatments are not a cure, but the first to physically alter the course of the disease rather than just addressing its symptoms, the FDA said. The video player is currently playing an ad. Indianapolis-based Eli Lilly reported the success of its trial a year ago, and subsequently applied for the FDA authorization that was announced today. Experts at the time said it “could be the beginning of the end of Alzheimer’s disease”, which affects almost 7 million people, mostly older Americans, according to the Alzheimer’s Association. “Kisunla demonstrated very meaningful results for people with early symptomatic Alzheimer’s disease, who urgently need effective treatment options,” Anne White, executive vice-president of Eli Lilly said on Tuesday, referring to donanemab by the brand name it will be sold under. © 2024 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29374 - Posted: 07.03.2024

By Charles Q. Choi The largest-yet single-cell genomics analysis reveals new details of the molecular pathways and cell types that are altered in the cortex in people with autism. The work, published last month in Science, also hints at how genes linked to the condition contribute to these brain differences. The findings are part of a package of 14 new papers from PsychENCODE, a multi-institution consortium launched in 2015 to study the molecular basis of neuropsychiatric conditions. The initiative’s latest phase of research analyzed human brains at the single-cell level instead of relying on bulk tissue samples as in previous efforts. “Single-cell analysis gives you the ability to really understand a condition in terms of cell-cell interactions, and how a condition might affect different cell types in very different ways,” says PsychENCODE chair Daniel Geschwind, professor of human genetics, neurology and psychiatry at the University of California, Los Angeles, who led the new autism study. Past work by Geschwind and others identified a “molecular signature” in tissue samples of autism brains, characterized by increased expression of immune signaling genes, decreased activity of synaptic and neuronal genes, and a reduction in the regional gene-expression patterns typically seen across the cortex. The first single-cell analysis—involving cells from 15 autistic and 16 non-autistic people, and published in 2019—hinted at a role for microglia and excitatory neurons in layer 2/3 of the cortex. The new study confirms these previous findings and expands autism’s molecular signature to include a subtype of interneurons and layer 5/6 excitatory neurons, which project to other cortical areas. It also adds gene-expression changes, such as heightened immune responses in oligodendrocytes, cells that help produce the myelin sheath insulating the central nervous system. “That suggests there may be something going on broadly with connectivity in autism,” Geschwind says. © 2024 Simons Foundation

Keyword: Autism; Epigenetics
Link ID: 29371 - Posted: 06.26.2024

By Gina Kolata and Pam Belluck A committee of independent advisers to the Food and Drug Administration voted unanimously on Monday that the benefits outweigh the risks of the newest experimental drug for Alzheimer’s disease. Alzheimer’s afflicts more than six million Americans. It has no cure, and there is no treatment or lifestyle modification that can restore memory loss or reverse cognitive decline. The drug, made by Eli Lilly, is donanemab. It modestly slowed cognitive decline in patients in the early stages of the disease but also had significant safety risks, including swelling and bleeding in the brain. The committee concluded, though, that the consequences of Alzheimer’s are so dire that even a modest benefit can be worthwhile. The F.D.A. usually follows the advice of the agency’s advisory committees but not always. The drug is based on a long-held hypothesis that Alzheimer’s disease begins when rough hard balls of amyloid, a protein, pile up in patients’ brains, followed by a cascade of reactions leading to the death of neurons. The idea is to treat Alzheimer’s by attacking amyloid, clearing it from the brain. Two similar amyloid-fighting drugs were approved recently: Leqembi, made by Eisai and Biogen, was approved last year. That drug’s risks and modest benefits are similar to those of donanemab. Aduhelm, made by Biogen, is the other drug and was approved in 2021 but was discontinued because there was insufficient evidence that it could benefit patients. Donanemab was expected to be approved earlier this year, but in March, the F.D.A. decided that, instead, it would require donanemab to undergo the scrutiny of an independent advisory committee, a surprise to Eli Lilly. © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29354 - Posted: 06.11.2024

Hannah Devlin Science correspondent A 10-minute brain scan could detect dementia several years before people develop noticeable symptoms, a study suggests. Scientists used a scan of “resting” brain activity to identify whether people would go on to develop dementia, with an estimated 80% accuracy up to nine years before people received a diagnosis. If the findings were confirmed in a larger cohort, the scan could become a routine procedure in memory clinics, scientists said. “We’ve known for a long time that the function of the brain starts to change many years before you get dementia symptoms,” said Prof Charles Marshall, who led the work at Queen Mary University of London. “This could help us to be more precise at identifying those changes using an MRI scan that you could do on any NHS scanner.” The research comes as a new generation of Alzheimer’s drugs are on the horizon. The UK’s Medicines and Healthcare products Regulatory Agency (MHRA) is assessing lecanemab, made by Eisai and Biogen, and donanemab, made by Eli Lilly, and both drugs are widely expected to be licensed this year. “Predicting who is going to get dementia in the future will be vital for developing treatments that can prevent the irreversible loss of brain cells that causes the symptoms of dementia,” Marshall said. The researchers used functional MRI (fMRI) scans from 1,100 UK Biobank volunteers to detect changes in the brain’s “default mode network” (DMN). The scan measures correlations in brain activity between different regions while the volunteer lies still, not doing any particular task. The network, which reflects how effectively different regions are communicating with each other, is known to be particularly vulnerable to Alzheimer’s disease. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Brain imaging
Link ID: 29349 - Posted: 06.08.2024

By Elissa Welle The traditional story of Alzheimer’s disease casts two key proteins in starring roles—each with clear stage directions: Plaques of sticky amyloid beta protein accumulate outside neurons as the condition unfolds, and tangles of tau protein gum up the insides of the cells. But it may be time for a rewrite. Amyloid beta, too, coalesces inside neurons and seems to mark them for early death, according to research posted on a preprint server last November. In brain slices from people with Alzheimer’s, but not in those from age-matched controls, cells containing intracellular amyloid beta decreased in number as the disease progressed. At first, the result appeared to be a mistake, says study investigator Alessia Caramello, a postdoctoral researcher in the UK Dementia Research Institute. Intracellular amyloid beta is “nowhere to be found” in most discussions of Alzheimer’s disease, she says. “It’s never mentioned. Never ever.” Instead, the field has long focused on the buildup of amyloid beta outside the cell. But even before those plaques form, there seems to be another pathological event, she says—namely intracellular amyloid—“Why not look at it?” The work from Caramello and her colleagues is not the first to suggest that amyloid beta, or Abeta for short, wreaks havoc inside neurons, not just in the extracellular space between them. This “inside-out” hypothesis, as it has been called, has implications for how scientists understand Alzheimer’s disease. In particular, it could help to account for some big mysteries around the condition—such as why the extent of amyloid beta plaques in the brain doesn’t always correlate with symptoms, why neurons die and why treatments to lessen plaques marginally slow down, but do not halt, the disease. “It just puts a totally different spin on how you need to address this,” says Gunnar Gouras, professor of experimental neurology at Lund University and a proponent of the inside-out hypothesis. “It’s really a cell biological, neurobiological issue that is a bit more complex. And we need to also study this instead of just saying, ‘Abeta is bad; we’ve got to get rid of it.’” © 2024 Simons Foundation

Keyword: Alzheimers
Link ID: 29335 - Posted: 06.02.2024

By Ben Casselman Long before people develop dementia, they often begin falling behind on mortgage payments, credit card bills and other financial obligations, new research shows. A team of economists and medical experts at the Federal Reserve Bank of New York and Georgetown University combined Medicare records with data from Equifax, the credit bureau, to study how people’s borrowing behavior changed in the years before and after a diagnosis of Alzheimer’s or a similar disorder. What they found was striking: Credit scores among people who later develop dementia begin falling sharply long before their disease is formally identified. A year before diagnosis, these people were 17.2 percent more likely to be delinquent on their mortgage payments than before the onset of the disease, and 34.3 percent more likely to be delinquent on their credit card bills. The issues start even earlier: The study finds evidence of people falling behind on their debts five years before diagnosis. “The results are striking in both their clarity and their consistency,” said Carole Roan Gresenz, a Georgetown University economist who was one of the study’s authors. Credit scores and delinquencies, she said, “consistently worsen over time as diagnosis approaches, and so it literally mirrors the changes in cognitive decline that we’re observing.” The research adds to a growing body of work documenting what many Alzheimer’s patients and their families already know: Decision-making, including on financial matters, can begin to deteriorate long before a diagnosis is made or even suspected. People who are starting to experience cognitive decline may miss payments, make impulsive purchases or put money into risky investments they would not have considered before the disease. “There’s not just getting forgetful, but our risk tolerance changes,” said Lauren Hersch Nicholas, a professor at the University of Colorado School of Medicine who has studied dementia’s impact on people’s finances. “It might seem suddenly like a good move to move a diversified financial portfolio into some stock that someone recommended.” © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29334 - Posted: 06.02.2024

By Elie Dolgin The COVID-19 pandemic didn’t just reshape how children learn and see the world. It transformed the shape of their eyeballs. As real-life classrooms and playgrounds gave way to virtual meetings and digital devices, the time that children spent focusing on screens and other nearby objects surged — and the time they spent outdoors dropped precipitously. This shift led to a notable change in children’s anatomy: their eyeballs lengthened to better accommodate short-vision tasks. Study after study, in regions ranging from Europe to Asia, documented this change. One analysis from Hong Kong even reported a near doubling in the incidence of pathologically stretched eyeballs among six-year-olds compared with pre-pandemic levels1. This elongation improves the clarity of close-up images on the retina, the light-sensitive layer at the back of the eye. But it also makes far-away objects appear blurry, leading to a condition known as myopia, or short-sightedness. And although corrective eyewear can usually address the issue — allowing children to, for example, see a blackboard or read from a distance — severe myopia can lead to more-serious complications, such as retinal detachment, macular degeneration, glaucoma and even permanent blindness. Rates of myopia were booming well before the COVID-19 pandemic. Widely cited projections in the mid-2010s suggested that myopia would affect half of the world’s population by mid-century (see ‘Rising prevalence’), which would effectively double the incidence rate in less than four decades2 (see ‘Affecting every age’). Now, those alarming predictions seem much too modest, says Neelam Pawar, a paediatric ophthalmologist at the Aravind Eye Hospital in Tirunelveli, India. “I don’t think it will double,” she says. “It will triple.” © 2024 Springer Nature Limited

Keyword: Vision; Development of the Brain
Link ID: 29329 - Posted: 05.29.2024

By Laura Sanders It’s a bit like seeing a world in a grain of sand. Except the view, in this case, is the exquisite detail inside a bit of human brain about half the size of a grain of rice. Held in that minuscule object is a complex collective of cells, blood vessels, intricate patterns and biological puzzles. Scientists had hints of these mysteries in earlier peeks at this bit of brain (SN: 6/29/21). But now, those details have been brought into new focus by mapping the full landscape of some 57,000 cells, 150 million synapses and their accompanying 23 centimeters of blood vessels, researchers report in the May 10 Science. The full results, the scientists hope, may lead to greater insights into how the human brain works. “We’re going in and looking at every individual connection attached to every cell — a very high level of detail,” says Viren Jain, a computational neuroscientist at Google Research in Mountain View, Calif. The big-picture goal of brain mapping efforts, he says, is “to understand how human brains work and what goes wrong in various kinds of brain diseases.” The newly mapped brain sample was removed during a woman’s surgery for epilepsy, so that doctors could reach a deeper part of the brain. The bit, donated with the woman’s consent, was from the temporal lobe of the cortex, the outer part of the brain involved in complex mental feats like thinking, remembering and perceiving. This digital drawing of a person's head shows the brain inside. An arrow points to the bottom left side of the brain. After being fixed in a preservative, the brain bit was sliced into almost impossibly thin wisps, and then each slice was imaged with a high-powered microscope. Once these views were collected, researchers used computers to digitally reconstruct the three-dimensional objects embedded in the piece of brain. © Society for Science & the Public 2000–2024

Keyword: Brain imaging; Development of the Brain
Link ID: 29324 - Posted: 05.25.2024

By Angie Voyles Askham Some questions about neurons, such as how they give rise to behavior, are tricky to answer when those cells are embedded within their natural milieu. “Is residence in a nervous system sufficient to allow synapses to form?” says Kristin Baldwin, professor of genetics and development at Columbia University. “Are synapses that we can see sufficient to allow communication? And is synaptic communication sufficient to actually endow an animal with a set of behaviors that would be appropriate for it?” The best way to answer those questions is to put the cells in a new environment where their extrinsic and intrinsic influences can be teased apart, says Xin Jin, assistant professor of neuroscience at the Scripps Research Institute. For a long time, Jin says, that new environment was the unnatural setting of a petri dish. But two new studies that make use of chimeric mice—animals with both mouse and rat cells in their brain—point to another option: One demonstrates how rat stem cells can restore a mouse’s ability to smell, whereas the other shows how rat stem cells can give rise to a forebrain in mice that would otherwise lack one. The studies were published last month in Cell. Because rat brains are larger than mouse brains and develop at a different rate, the chimeras enable researchers to probe the competing forces of a cell’s intrinsic programming and its external environment. The work opens up doors for new research and the ability to explore the origins of species-specific cellular behaviors, says Jin, who was not involved in either study. “It’s sort of a fundamental ‘nature versus nurture,’” says Baldwin, who led one of the new studies. © 2024 Simons Foundation

Keyword: Development of the Brain
Link ID: 29312 - Posted: 05.18.2024

By Carissa Wong Researchers have mapped a tiny piece of the human brain in astonishing detail. The resulting cell atlas, which was described today in Science1 and is available online, reveals new patterns of connections between brain cells called neurons, as well as cells that wrap around themselves to form knots, and pairs of neurons that are almost mirror images of each other. The 3D map covers a volume of about one cubic millimetre, one-millionth of a whole brain, and contains roughly 57,000 cells and 150 million synapses — the connections between neurons. It incorporates a colossal 1.4 petabytes of data. “It’s a little bit humbling,” says Viren Jain, a neuroscientist at Google in Mountain View, California, and a co-author of the paper. “How are we ever going to really come to terms with all this complexity?” The brain fragment was taken from a 45-year-old woman when she underwent surgery to treat her epilepsy. It came from the cortex, a part of the brain involved in learning, problem-solving and processing sensory signals. The sample was immersed in preservatives and stained with heavy metals to make the cells easier to see. Neuroscientist Jeff Lichtman at Harvard University in Cambridge, Massachusetts, and his colleagues then cut the sample into around 5,000 slices — each just 34 nanometres thick — that could be imaged using electron microscopes. Jain’s team then built artificial-intelligence models that were able to stitch the microscope images together to reconstruct the whole sample in 3D. “I remember this moment, going into the map and looking at one individual synapse from this woman’s brain, and then zooming out into these other millions of pixels,” says Jain. “It felt sort of spiritual.” When examining the model in detail, the researchers discovered unconventional neurons, including some that made up to 50 connections with each other. “In general, you would find a couple of connections at most between two neurons,” says Jain. Elsewhere, the model showed neurons with tendrils that formed knots around themselves. “Nobody had seen anything like this before,” Jain adds. © 2024 Springer Nature Limited

Keyword: Brain imaging; Development of the Brain
Link ID: 29304 - Posted: 05.14.2024

Nicola Davis Science correspondent Having two copies of a gene variant known to predispose people to Alzheimer’s could in fact represent a distinct genetic form of the disease, researchers have said. The variant, known as ApoE4, has long been known to increase the risk of developing Alzheimer’s, with two copies conferring greater risk than one. Now research has revealed almost everyone with two copies of the variant goes on to develop Alzheimer’s disease (AD), suggesting it is not only a risk factor but a cause. “Over 95% of the individuals [with two copies of ApoE4], have AD pathology either in the brain or in the biomarkers that we analysed,” said Dr Juan Fortea, the co-author of the research from the Sant Pau hospital in Barcelona. The video player is currently playing an ad. His team said the predicability of the age at which symptoms began was similar to other genetic forms of the disease such as autosomal-dominant Alzheimer’s disease (ADAD) and Alzheimer’s disease in Down syndrome (DSAD). Dr Victor Montal, a co-author from Barcelona Supercomputing Center, said the research had catalysed a paradigm shift in the understanding of the disease. “Whereas previously, the etiology of dementia was known in less than 1% of cases, our work has now enabled the identification of causative factors in over 15% of instances,” he said. However, the study did not shed light on the risk of developing dementia itself for people with two copies of ApoE4. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 29292 - Posted: 05.07.2024

By Dana G. Smith When it comes to aging, we tend to assume that cognition gets worse as we get older. Our thoughts may slow down or become confused, or we may start to forget things, like the name of our high school English teacher or what we meant to buy at the grocery store. But that’s not the case for everyone. For a little over a decade, scientists have been studying a subset of people they call “super-agers.” These individuals are age 80 and up, but they have the memory ability of a person 20 to 30 years younger. Most research on aging and memory focuses on the other side of the equation — people who develop dementia in their later years. But, “if we’re constantly talking about what’s going wrong in aging, it’s not capturing the full spectrum of what’s happening in the older adult population,” said Emily Rogalski, a professor of neurology at the University of Chicago, who published one of the first studies on super-agers in 2012. A paper published Monday in the Journal of Neuroscience helps shed light on what’s so special about the brains of super-agers. The biggest takeaway, in combination with a companion study that came out last year on the same group of individuals, is that their brains have less atrophy than their peers’ do. The research was conducted on 119 octogenarians from Spain: 64 super-agers and 55 older adults with normal memory abilities for their age. The participants completed multiple tests assessing their memory, motor and verbal skills; underwent brain scans and blood draws; and answered questions about their lifestyle and behaviors. The scientists found that the super-agers had more volume in areas of the brain important for memory, most notably the hippocampus and entorhinal cortex. They also had better preserved connectivity between regions in the front of the brain that are involved in cognition. Both the super-agers and the control group showed minimal signs of Alzheimer’s disease in their brains. © 2024 The New York Times Company

Keyword: Learning & Memory; Development of the Brain
Link ID: 29280 - Posted: 04.30.2024

Jon Hamilton Scientists have found a way to restore brain cells impaired by a rare and life-threatening genetic disorder called Timothy syndrome. A type of drug known as an antisense oligonucleotide allowed clusters of human neurons to develop normally even though they carried the mutation responsible for Timothy syndrome, a team reports in the journal Nature. The approach may help researchers develop treatments for other genetic conditions, including some that cause schizophrenia, epilepsy, ADHD, and autism spectrum disorder. "It's immensely exciting because we now have the tools," says Dr. Sergiu Pasca, a professor of psychiatry and behavioral sciences at Stanford University and the study's senior author. "It's the beginning of a new era for many of these diseases that we first thought were untreatable," says Dr. Huda Zoghbi, a professor at Baylor College of Medicine who was not involved in the research. But most of these conditions involve multiple genes, not just one — and scientists don't yet know enough about these multiple gene disorders to effectively treat them with antisense oligonucleotides, Zoghbi says. Timothy Syndrome has been diagnosed in fewer than 100 people worldwide. Children born with it often have heart problems, autism, epilepsy, developmental delay, and intellectual disability. But because Timothy syndrome is caused by a mutation in a single gene, it offers scientists a way to study changes that affect brain development. "Rare syndromes that are very clearly defined genetically are sort of like windows, or Rosetta Stones, into understanding other, more common conditions," Pasca says. © 2024 npr

Keyword: Autism; Genes & Behavior
Link ID: 29277 - Posted: 04.30.2024

By Laura Sanders What does it feel like to be a rat? We will never know, but some very unusual mice may now have an inkling. In a series of new experiments, bits of rat brain grew inside the brains of mice. Donor stem cells from rats formed elaborate — and functional — neural structures in mice’s brains, despite being from a completely different species, researchers report in two papers published April 25 in Cell. The findings are “remarkable,” says Afsaneh Gaillard, a neuroscientist at INSERM and the University of Poitiers in France. “The ability to generate specific neuronal cells that can successfully integrate into the brain may provide a solution for treating a variety of brain diseases associated with neuronal loss.” These chimeric mice are helping to reveal just how flexible brain development can be (SN: 3/29/23). And while no one is suggesting that human brains could be grown in another animal, the results may help clarify biological details relevant to interspecies organ transplants, the researchers say. The success of these rat-mouse hybrids depended on timing: The rat and mouse cells had to grow into brains together from a very young stage. Stem cells from rats that had the potential to mature into several different cell types were injected into mouse embryos. From there, these rat cells developed alongside mice cells in the growing brain, though researchers couldn’t control exactly where the rat cells ended up. In one set of experiments, researchers first cleared the way for these rat cells to develop in the young mouse brains. Stem cell biologist Jun Wu and colleagues used a form of the genetic tool CRISPR to inactivate a mouse gene that instructs their brain cells to build a forebrain, a large region involved in learning, remembering and sensing the world. This left the mice without forebrains — normally, a lethal problem. © Society for Science & the Public 2000–2024.

Keyword: Development of the Brain; Neurogenesis
Link ID: 29274 - Posted: 04.26.2024

Sofia Quaglia Noise pollution from traffic stunts growth in baby birds, even while inside the egg, research has found. Unhatched birds and hatchlings that are exposed to noise from city traffic experience long-term negative effects on their health, growth and reproduction, the study found. “Sound has a much stronger and more direct impact on bird development than we knew before,” said Dr Mylene Mariette, a bird communication expert at Deakin University in Australia and a co-author of the study, published in the journal Science. “It would be wise to work more to reduce noise pollution.” A growing body of research has suggested that noise pollution causes stress to birds and makes communication harder for them. But whether birds are already distressed at a young age because they are affected by noise, or by how noise disrupts their environment and parental care, was still unclear. Mariette’s team routinely exposed zebra finch eggs for five days to either silence, soothing playbacks of zebra finch songs, or recordings of city traffic noises such as revving motors and cars driving past. They did the same with newborn chicks for about four hours a night for up to 13 nights, without exposing the birds’ parents to the sounds. They noticed that the bird eggs were almost 20% less likely to hatch if exposed to traffic noise. The chicks that did hatch were more than 10% smaller and almost 15% lighter than the other hatchlings. When the team ran analyses on their red blood cells and their telomeres – a piece of DNA that shortens with stress and age – they were more eroded and shorter than their counterparts’. The effects continued even after the chicks were no longer exposed to noise pollution, and carried over into their reproductive age four years later. The birds disturbed by noise during the early stages of their lives produced fewer than half as many offspring as their counterparts. © 2024 Guardian News & Media Limited

Keyword: Hearing; Development of the Brain
Link ID: 29273 - Posted: 04.26.2024

By Sara Reardon Researchers have hailed organoids — 3D clusters of cells that mimic aspects of human organs — as a potential way to test drugs and even eliminate some forms of animal experimentation. Now, in two studies published on 24 April in Nature1,2, biologists have developed gut and brain organoids that could improve understanding of colon cancer and help to develop treatments for a rare neurological disorder. “In the last ten years, people spent a lot of time to develop and understand how to make organoids,” says Shuibing Chen, a chemical biologist at Weill Cornell Medical College in New York City. “But this is the time now to think more about how to use” the models. Organoids — particularly those made from human stem cells — sometimes reveal things that animal models can’t, says Sergiu Pașca, a neuroscientist at Stanford University in California and a co-author of one of the studies1. Pașca’s group studies Timothy syndrome: a genetic disorder involving autism, neurological problems and heart conditions that affects only a few dozen people in the world. Timothy syndrome is caused by a single mutation in a gene called CACNA1C, which encodes a channel through which calcium ions enter cells including neurons. Pașca says that there are no good animal models for Timothy syndrome because the underlying mutation doesn’t always cause the same symptoms in rodents. “It became very clear to us we’d need to find a way of testing in vivo,” he says. © 2024 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 29271 - Posted: 04.26.2024

By Diana Kwon Overall, people in U.S. live longer than they did a hundred years ago. The growing number of people reaching old age has meant an increased proportion are at risk of developing dementia or Alzheimer’s disease, illnesses that typically strike later in life. However, researchers have found that, in the U.S. and elsewhere, dementia risk may actually be decreasing, at least in a subset of the population. A new study provides a potential explanation for this trend: Human brains may be getting larger—and thus more resilient to degeneration—over time. Several large population studies in countries including the U.S. and Great Britain have found that, in recent decades, the number of new cases, or incidence, of dementia has declined. Among these is the Framingham Heart Study, which has been collecting data from individuals living in Framingham, Massachusetts since 1948. Now accommodating a third generation of participants, the study includes data from more than 15,000 people. In 2016, Sudha Seshadri, a neurologist at UT Health San Antonio and her colleagues published findings revealing that while the prevalence—the total number of people with dementia—had increased, the incidence had declined since the late 1970s. “That was a piece of hopeful news,” Seshadri says. “It suggested that over 30 years, the average age at which somebody became symptomatic had gone up.” These findings left the team wondering: What was the cause of this reduced dementia risk? While the cardiovascular health of the Framingham residents and their descendants—which can influence the chances of developing dementia—had also improved over the decades, this alone could not fully explain the decline. On top of that, the effect only appeared in people who had obtained a high school diploma, which, according to Seshadri, pointed to the possibility that greater resilience against dementia may result from changes that occur in early life. © 2024 SCIENTIFIC AMERICAN,

Keyword: Development of the Brain; Learning & Memory
Link ID: 29265 - Posted: 04.20.2024

By Saima S. Iqbal Before becoming a researcher, Aimee Grant worked as a caregiver for six years in Cornwall, England, supporting autistic adults in group homes. But only more than a decade later, after befriending an autistic colleague at a sociology conference, did she realize she was autistic herself. The stereotypical view of autism as a brain impairment more commonly found in men made it difficult for Grant to make sense of her internal world. From an early age, she struggled to pick up on important social cues and found the sounds and scents in her environment distractingly painful. But like many children in her generation, she says, she grew accustomed to either dismissing or disguising her discomfort. It was by listening to some of the stories of her female peers that Grant saw that the label could fit. Receiving a diagnosis in 2019 prompted her to “reframe [my] entire life,” she says. She began working with her mind rather than against it. She no longer felt the same pressure to seem as nonautistic as possible with friends and family members, and she began to make use of accommodations at work, such as a light filter for her computer monitor. Today, as a public health researcher at Swansea University in Wales, Grant aims to uncover the lived experience of autistic people. Many scientists and clinicians see autism as a developmental disorder that hinders a person’s ability to understand and communicate with others. Grant believes that their work often obscures the heterogeneity of autism. And because many studies view autism as a disease, they overlook the reality that autistic people can feel more disabled by widespread misunderstanding and a lack of accommodations than by autistic traits themselves. © Society for Science & the Public 2000–2024.

Keyword: Autism
Link ID: 29261 - Posted: 04.20.2024

By Joanne Silberner In March, the sons of Gabriel García Márquez, the Nobel Prize-winning Colombian writer, published a posthumous novel against the specific wishes their father expressed before he died in 2014 at the age of 87. García Márquez had struggled through several versions of the book as dementia set in, and, perhaps stung by uncharacteristic negative reviews from his previous novel, didn’t want the new one published. “Until August,” the story of a woman who travels to her mother’s grave once a year and takes a new lover on each visit, got mixed reviews. Some were outright harsh. In The New York Times, Michael Greenberg wrote “It would be hard to imagine a more unsatisfying goodbye.” García Márquez’s decline, he continued, “seems to have been steep enough to prevent him from holding together the kind of imagined world that the writing of fiction demands.” Wendy Mitchell, who was an administrator with England’s National Health Service until her diagnosis of early-onset Alzheimer’s disease in 2014, recalled the moment she learned of the publication plans last year. “I type every day for fear of dementia snatching away that creative skill, which I see as my escape from dementia,” she wrote last October in The Guardian. “Maybe Márquez thought the same?” The novel’s publication raises some vital questions about living with an aging and perhaps ailing brain. What do mild cognitive impairment and dementia do to our creativity? How do these conditions affect our ability to use words, formulate sentences, and craft stories? Neuroscientists have been exploring these questions for several decades. First, a few definitions. People with mild cognitive impairment have lost more of their cognitive functioning than others their age, and often struggle to remember things. But they’re capable of managing daily activities like dressing, eating, bathing, and finding their way around. In dementia, cognitive difficulties have increased enough to interfere with daily life, and personality changes are more likely.

Keyword: Alzheimers
Link ID: 29254 - Posted: 04.13.2024

By Helen Bradshaw Walk into a gas station in the United States, and you may see more than just boxes of cigarettes lining the back wall. Colorful containers containing delta-8, a form of the substance THC, are sold in gas stations and shops across the country, and teens are buying them. A recent survey of more than 2,000 U.S. high school seniors found that more than 11 percent of them had used delta-8 in the past year, researchers report March 12 in JAMA. This is the first year the Monitoring the Future study, one of the leading nationally representative surveys of drug use trends among adolescents in the United States, looked at delta-8 use. Because more than 1 in 10 senior students said they used the drug, the survey team plans to monitor delta-8 use every year going forward. “We don’t really want to see any kids being exposed to cannabis, because it potentially increases their risk for developmental harms … and some psychiatric reactions” such as suicidal thoughts, says Alyssa Harlow, a researcher on the survey and an epidemiologist at the University of Southern California Keck School of Medicine in Los Angeles. Despite its prevalence, especially in the South and the Midwest, delta-8 is still new to consumers and research. Science News talked with Harlow and addiction researcher Jessica Kruger of the University of Buffalo in New York to help explain the delta-8 craze and its effects on kids. What is delta-8-THC? Cannabis plants contain over 100 compounds known as cannabinoids. Delta-8 is one of them. The most well-known is delta-9-tetrahydrocannabinol, or delta-9-THC. © Society for Science & the Public 2000–2024.

Keyword: Drug Abuse
Link ID: 29248 - Posted: 04.11.2024