By Erica Goode Authors don’t get to choose what’s going on in the world when their books are published. More than a few luckless writers ended up with a publication date of Sept. 11, 2001, or perhaps Nov. 8, 2016, the day Donald Trump was elected. But Charan Ranganath, the author of “Why We Remember: Unlocking Memory’s Power to Hold on to What Matters,”was more fortunate. His book went on sale last month, not long after the Department of Justice released a report describing President Joe Biden as an “elderly man with a poor memory” who, in interviews, was “struggling to remember events,” including the year that his son Beau died. BOOK REVIEW — “Why We Remember: Unlocking Memory’s Power to Hold on to What Matters,” by Charan Ranganath (Doubleday, 304 pages). The special counsel’s report immediately became a topic of intense discussion — disputed by the White House, seized on by many Republicans, analyzed by media commentators, and satirized by late-night television hosts. But for Ranganath, a psychologist and neuroscientist at the University of California, Davis, who for decades has been studying the workings of memory, the report’s release was a stroke of luck. His book, which dispels many widespread but wrongheaded assumptions about memory — including some to which that special counsel Robert K. Hur appears to subscribe — could easily have been written as a corrective response. If Ranganath has a central message, it is that we are far too concerned about forgetting. Memory does not work like a recording device, preserving everything we have heard, seen, said, and done. Not remembering names or exact dates; having no recollection of the details of a conversation; being unable to recall where you left your glasses or your keys; or watching movies you saw in the past as if you are seeing them for the first time — these are not the symptoms of a failing brain.

Keyword: Learning & Memory
Link ID: 29172 - Posted: 03.02.2024

By Pam Belluck Long Covid may lead to measurable cognitive decline, especially in the ability to remember, reason and plan, a large new study suggests. Cognitive testing of nearly 113,000 people in England found that those with persistent post-Covid symptoms scored the equivalent of 6 I.Q. points lower than people who had never been infected with the coronavirus, according to the study, published Wednesday in The New England Journal of Medicine. People who had been infected and no longer had symptoms also scored slightly lower than people who had never been infected, by the equivalent of 3 I.Q. points, even if they were ill for only a short time. The differences in cognitive scores were relatively small, and neurological experts cautioned that the results did not imply that being infected with the coronavirus or developing long Covid caused profound deficits in thinking and function. But the experts said the findings are important because they provide numerical evidence for the brain fog, focus and memory problems that afflict many people with long Covid. “These emerging and coalescing findings are generally highlighting that yes, there is cognitive impairment in long Covid survivors — it’s a real phenomenon,” said James C. Jackson, a neuropsychologist at Vanderbilt Medical Center, who was not involved in the study. He and other experts noted that the results were consistent with smaller studies that have found signals of cognitive impairment. The new study also found reasons for optimism, suggesting that if people’s long Covid symptoms ease, the related cognitive impairment might, too: People who had experienced long Covid symptoms for months and eventually recovered had cognitive scores similar to those who had experienced a quick recovery, the study found. © 2024 The New York Times Company

Keyword: Attention; Learning & Memory
Link ID: 29171 - Posted: 02.29.2024

Terry Gross When cognitive neuroscientist Charan Ranganath meets someone for the first time, he's often asked, "Why am I so forgetful?" But Ranganath says he's more interested in what we remember, rather than the things we forget. "We're not designed to carry tons and tons of junk with us. I don't know that anyone would want to remember every temporary password that they've ever had," he says. "I think what [the human brain is] designed for is to carry what we need and to deploy it rapidly when we need it." Ranganath directs the Dynamic Memory Lab at the University of California, Davis, where he's a professor of psychology and neuroscience. In the new book, Why We Remember, he writes about the fundamental mechanisms of memory — and why memories often change over time. Sponsor Message Ranganath recently wrote an op-ed for The New York Times in which he reflected on President Biden's memory gaffes — and the role that memory plays in the current election cycle. "I'm just not in the position to say anything about the specifics of [either Biden or Trump's] memory problems," he says. "This is really more of an issue of people understanding what happens with aging. And, one of the nice things about writing this editorial is I got a lot of feedback from people who felt personally relieved by this because they're worried about their own memories." I think it would be a good idea to have a comprehensive physical and mental health evaluation that's fairly transparent. We certainly have transparency or seek transparency about other things like a candidate's finances, for instance. And obviously health is a very important factor. And I think at the end of the day, we'll still be in a position of saying, "OK, what's enough? What's the line between healthy and unhealthy?" But I think it's important to do because yes, as we get older we do have memory problems. ... © 2024 npr

Keyword: Learning & Memory; Development of the Brain
Link ID: 29166 - Posted: 02.27.2024

Fen-Biao Gao Around 55 million people worldwide suffer from dementia such as Alzheimer’s disease. On Feb. 22, 2024, it was revealed that former talk show host Wendy Williams had been diagnosed with frontotemporal dementia, or FTD, a rare type of dementia that typically affects people ages 45 to 64. Bruce Willis is another celebrity who was diagnosed with the syndrome, according to his family. In contrast to Alzheimer’s, in which the major initial symptom is memory loss, FTD typically involves changes in behavior. The initial symptoms of FTD may include changes in personality, behavior and language production. For instance, some FTD patients exhibit inappropriate social behavior, impulsivity and loss of empathy. Others struggle to find words and to express themselves. This insidious disease can be especially hard for families and loved ones to deal with. There is no cure for FTD, and there are no effective treatments. Up to 40% of FTD cases have some family history, which means a genetic cause may run in the family. Since researchers identified the first genetic mutations that cause FTD in 1998, more than a dozen genes have been linked to the disease. These discoveries provide an entry point to determine the mechanisms that underlie the dysfunction of neurons and neural circuits in the brain and to use that knowledge to explore potential approaches to treatment. I am a researcher who studies the development of FTD and related disorders, including the motor neuron disease amyotrophic lateral sclerosis, or ALS. ALS, also known as Lou Gehrig’s disease, results in progressive muscle weakness and death. Uncovering the similarities in pathology and genetics between FTD and ALS could lead to new ways to treat both diseases. Genes contain the instructions cells use to make the proteins that carry out functions essential to life. Mutated genes can result in mutated proteins that lose their normal function or become toxic. © 2010–2024, The Conversation US, Inc.

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 29161 - Posted: 02.25.2024

David Robson Scientific discoveries can emerge from the strangest places. In early 1900s France, the doctor Albert Calmette and the veterinarian Camille Guérin aimed to discover how bovine tuberculosis was transmitted. To do so, they first had to find a way of cultivating the bacteria. Sliced potatoes – cooked with ox bile and glycerine – proved to be the perfect medium. As the bacteria grew, however, Calmette and Guérin were surprised to find that each generation lost some of its virulence. Animals infected with the microbe (grown through many generations of their culture) no longer became sick but were protected from wild TB. In 1921, the pair tested this potential vaccine on their first human patient – a baby whose mother had just died of the disease. It worked, and the result was the Bacille Calmette-Guérin (BCG) vaccine that has saved millions of lives. A black and white image pf Camille Guérin and physician Albert Calmette side by side. French veterinarian Camille Guérin and physician Albert Calmette developed the BCG jab in 1921 using sliced potatoes cooked with ox bile and glycerine. Photograph: Musée Pasteur Calmette and Guérin could have never imagined that their research would inspire scientists investigating an entirely different kind of disease more than a century later. Yet that is exactly what is happening, with a string of intriguing studies suggesting that BCG can protect people from developing Alzheimer’s disease. If these preliminary results bear out in clinical trials, it could be one of the cheapest and most effective weapons in our fight against dementia. According to the World Health Organization, 55 million people now have dementia, with about 10 million new cases each year. Alzheimer’s disease is by far the most common form, accounting for about 60%-70% of cases. It is characterised by clumps of a protein called amyloid beta that accumulate within the brain, killing neurons and destroying the synaptic connections between the cells. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 29160 - Posted: 02.25.2024

By Tina Hesman Saey One particular retrovirus — embedded in the DNA of jawed vertebrates — helps turn on production of a protein needed to insulate nerve fibers, researchers report February 15 in Cell. Such insulation, called myelin, may have helped make speedy thoughts and complex brains possible. The retrovirus trick was so handy, in fact, that it showed up many times in the evolution of vertebrates with jaws, the team found. Retroviruses — also known as jumping genes or retrotransposons — are RNA viruses that make DNA copies of themselves to embed in a host’s DNA. Scientists once thought of remnants of ancient viruses as genetic garbage, but that impression is changing, says neuroscientist Jason Shepherd, who was not involved in the study. “We’re finding more and more that these retrotransposons and retroviruses have influenced the evolution of life on the planet,” says Shepherd, of the University of Utah Spencer Fox Eccles School of Medicine in Salt Lake City. Remains of retroviruses were already known to have aided the evolution of the placenta, the immune system and other important milestones in human evolution (SN: 5/16/17). Now, they’re implicated in helping to produce myelin. Myelin is a coating of fat and protein that encases long nerve fibers known as axons. The coating works a bit like the insulation around an electrical wire: Nerves sheathed in myelin can send electrical signals faster than uninsulated nerves can. © Society for Science & the Public 2000–2024.

Keyword: Glia; Evolution
Link ID: 29154 - Posted: 02.20.2024

By Matt Richtel Growing numbers of children and adolescents are being prescribed multiple psychiatric drugs to take simultaneously, according to a new study by researchers at the University of Maryland. The phenomenon is increasing despite warnings that psychotropic drug combinations in young people have not been tested for safety or studied for their impact on the developing brain. The study, published Friday in JAMA Open Network, looked at the prescribing patterns among patients 17 or younger enrolled in Medicaid from 2015 to 2020 in a single U.S. state that the researchers declined to name. In this group, there was a 9.5 percent increase in the prevalence of “polypharmacy,” which the study defined as taking three or more different classes of psychiatric medications, including antidepressants, mood-stabilizing anticonvulsants, sedatives and drugs for A.D.H.D. and anxiety drugs. The study looked at only one state, but state data have been used in the past to explore this issue, in part because of the relative ease of gathering data from Medicaid, the health insurance program administered by states. At the same time, some research using nationally weighted samples have revealed the increasing prevalence of polypharmacy among young people. One recent paper drew data from the National Ambulatory Medical Care Survey and found that in 2015, 40.7 percent of people aged 2 to 24 in the United States who took a medication for A.D.H.D. also took a second psychiatric drug. That figure had risen from 26 percent in 2006. The latest data from the University of Maryland researchers show that, at least in one state, the practice continues to grow and “was significantly more likely among youths who were disabled or in foster care,” the new study noted. Mental health experts said that psychotropic medications can prove very helpful and that doctors have discretion to prescribe what they see fit. A concern among some experts is that many drugs used in frequently prescribed cocktails have not been approved for use in young people. And it is unclear how the simultaneous use of multiple psychotropic medications affects brain development long-term. © 2024 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 29152 - Posted: 02.20.2024

Nancy S. Jecker & Andrew Ko Putting a computer inside someone’s brain used to feel like the edge of science fiction. Today, it’s a reality. Academic and commercial groups are testing “brain-computer interface” devices to enable people with disabilities to function more independently. Yet Elon Musk’s company, Neuralink, has put this technology front and center in debates about safety, ethics and neuroscience. In January 2024, Musk announced that Neuralink implanted its first chip in a human subject’s brain. The Conversation reached out to two scholars at the University of Washington School of Medicine – Nancy Jecker, a bioethicst, and Andrew Ko, a neurosurgeon who implants brain chip devices – for their thoughts on the ethics of this new horizon in neuroscience. How does a brain chip work? Neuralink’s coin-size device, called N1, is designed to enable patients to carry out actions just by concentrating on them, without moving their bodies. Subjects in the company’s PRIME study – short for Precise Robotically Implanted Brain-Computer Interface – undergo surgery to place the device in a part of the brain that controls movement. The chip records and processes the brain’s electrical activity, then transmits this data to an external device, such as a phone or computer. The external device “decodes” the patient’s brain activity, learning to associate certain patterns with the patient’s goal: moving a computer cursor up a screen, for example. Over time, the software can recognize a pattern of neural firing that consistently occurs while the participant is imagining that task, and then execute the task for the person. © 2010–2024, The Conversation US, Inc.

Keyword: Robotics; Learning & Memory
Link ID: 29151 - Posted: 02.20.2024

By Miryam Naddaf An analysis of around 1,500 blood proteins has identified biomarkers that can be used to predict the risk of developing dementia up to 15 years before diagnosis. The findings, reported today in Nature Aging1, are a step towards a tool that scientists have been in search of for decades: blood tests that can detect Alzheimer’s disease and other forms of dementia at a very early, pre-symptomatic stage. Researchers screened blood samples from more than 50,000 healthy adults in the UK Biobank, 1,417 of whom developed dementia in a 14-year period. They found that high blood levels of four proteins — GFAP, NEFL, GDF15 and LTBP2 — were strongly associated with dementia. “Studies such as this are required if we are to intervene with disease-modifying therapies at the very earliest stage of dementia,” said Amanda Heslegrave, a neuroscientist at University College London, in a statement to the Science Media Centre in London. According to the World Health Organization, more than 55 million people worldwide currently live with dementia. People are often diagnosed only when they notice memory problems or other symptoms. At that point, the disease might have been progressing for years. “Once we diagnose it, it’s almost too late,” says study co-author Jian-Feng Feng, a computational biologist at Fudan University in Shanghai, China. “And it’s impossible to reverse it.” By screening 1,463 proteins in blood samples from 52,645 people, the authors found that increased levels of GFAP, NEFL, GDF15 and LTBP2 were associated with dementia and Alzheimer’s disease. For some participants who developed dementia, blood levels of these proteins were outside normal ranges more than ten years before symptom onset. © 2024 Springer Nature Limited

Keyword: Alzheimers
Link ID: 29146 - Posted: 02.13.2024

By Claudia López Lloreda By squirting cells from a 3D printer, researchers have created tissue that looks—and acts—like a chunk of brain. In recent years, scientists have learned how to load up 3D printers with cells and other scaffolding ingredients to create living tissues, but making realistic brainlike constructs has been a challenge. Now, one team has shown that, by modifying its printing techniques, it can print and combine multiple subtypes of cells that better mimic signaling in the human brain. “It’s remarkable that [the researchers] can replicate” how brain cells work, says Riccardo Levato, a regenerative medicine researcher at Utrecht University who was not involved with the study. “It’s the first demonstration that, with some simple organization [of cells], you can start getting some interesting functional [responses].” The new technology, described last week in Cell Stem Cell, could offer advantages over existing techniques that neuroscientists use to create 3D brain tissues in the lab. One common approach involves using stem cells to grow miniature brainlike blobs called organoids. But researchers can’t control the types of cells or their precise location in these constructs. Each organoid “is unique,” making it difficult to reproduce research results, says neuroscientist Su-Chun Zhang of the University of Wisconsin–Madison, an author of the new study. With the right kind of 3D printing, however, “you can control where different cell types are placed,” says developmental biologist Francis Szele of the University of Oxford. Past studies have used 3D printers to construct brain tissues that allowed researchers to study how the cells matured and made connections, and even integrate printed tissue into mouse brains. But those constructs had limited functionality. And efforts that produced more functional printed tissue used rat cells, not human cells. © 2024 American Association for the Advancement of Science.

Keyword: Development of the Brain; Robotics
Link ID: 29145 - Posted: 02.10.2024

Ian Sample Science editor After a decades-long and largely fruitless hunt for drugs to combat Alzheimer’s disease, an unlikely candidate has raised its head: the erectile dysfunction pill Viagra. Researchers found that men who were prescribed Viagra and similar medications were 18% less likely to develop the most common form of dementia years later than those who went without the drugs. The effect was strongest in men with the most prescriptions, with scientists finding a 44% lower risk of Alzheimer’s in those who received 21 to 50 prescriptions of the erectile dysfunction pills over the course of their study. While the findings are striking, the observational study cannot determine whether Viagra and similar pills protect against Alzheimer’s or whether men who are already less prone to the condition are simply more likely to use the tablets. “We can’t say that the drugs are responsible, but this does give us food for thought on how we move into the future,” said the lead author Dr Ruth Brauer at University College London. “We now need a proper clinical trial to look at the effects of these drugs on Alzheimer’s in women as well as men.” Brauer and her colleagues analysed medical records for more than 260,000 men who were diagnosed with erectile dysfunction but had no evidence of memory or thinking problems. Just over half were taking PDE5 inhibitor drugs, including sildenafil (sold as Viagra), avanafil, vardenafil and tadalafil. The men were followed for an average of five years to record any new cases of Alzheimer’s. © 2024 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29138 - Posted: 02.08.2024

By David Marchese Our memories form the bedrock of who we are. Those recollections, in turn, are built on one very simple assumption: This happened. But things are not quite so simple. “We update our memories through the act of remembering,” says Charan Ranganath, a professor of psychology and neuroscience at the University of California, Davis, and the author of the illuminating new book “Why We Remember.” “So it creates all these weird biases and infiltrates our decision making. It affects our sense of who we are.” Rather than being photo-accurate repositories of past experience, Ranganath argues, our memories function more like active interpreters, working to help us navigate the present and future. The implication is that who we are, and the memories we draw on to determine that, are far less fixed than you might think. “Our identities,” Ranganath says, “are built on shifting sand.” What is the most common misconception about memory? People believe that memory should be effortless, but their expectations for how much they should remember are totally out of whack with how much they’re capable of remembering.1 Another misconception is that memory is supposed to be an archive of the past. We expect that we should be able to replay the past like a movie in our heads. The problem with that assumption is that we don’t replay the past as it happened; we do it through a lens of interpretation and imagination. Semantic memory is the term for the memory of facts and knowledge about the world. standpoint? It’s exceptionally hard to answer the question of how much we can remember. What I’ll say is that we can remember an extraordinary amount of detail that would make you feel at times as if you have a photographic memory. We’re capable of these extraordinary feats. I would argue that we’re all everyday-memory experts, because we have this exceptional semantic memory, which is the scaffold for episodic memory. I know it sounds squirmy to say, “Well, I can’t answer the question of how much we remember,” but I don’t want readers to walk away thinking memory is all made up. © 2024 The New York Times Company

Keyword: Learning & Memory
Link ID: 29134 - Posted: 02.06.2024

By Sabrina Malhi Researchers have found a possible link between the common hormone disorder PCOS and cognitive decline later in life. PCOS, which stands for polycystic ovary syndrome, is the most common endocrine disorder among women ages 15 to 44. However, it is often underdiagnosed because many of its symptoms, including abnormal menstrual cycles and excess hair, can be attributed to other causes. The syndrome was first described in 1935 by American gynecologists Irving F. Stein and Michael L. Leventhal. They published a paper documenting a group of women with lack of periods, excess body hair and enlarged ovaries with multiple cysts. Their work helped identify and characterize PCOS as it is known today. Health experts hypothesize that genetic factors could contribute to the development of the condition, but the exact causes are still unknown. Here’s what to know about PCOS and its potential link to cognitive health. PCOS is a chronic hormonal disorder characterized by overproduction of androgens, which are typically considered male hormones. High androgen levels can lead to irregular menstrual cycles and fertility issues when excessively produced in women. In the United States, 6 to 12 percent of people assigned female at birth who are of reproductive age are affected by PCOS, according to data from the Centers for Disease Control and Prevention. The condition is associated with an increased risk of obesity, high blood pressure, high cholesterol and endometrial cancer. PCOS is also often linked to insulin resistance, which can result in elevated blood sugar levels and an escalated risk of Type 2 diabetes. The condition can contribute to various metabolic issues, including high blood pressure, excess abdominal fat, and abnormal cholesterol or triglyceride levels. People with PCOS face an elevated risk of developing cardiovascular problems, such as high blood pressure, high cholesterol levels and an increased risk of heart disease. A recent study in the journal Neurology found that people with PCOS performed lower than normal on a suite of cognitive tests.

Keyword: Hormones & Behavior; Learning & Memory
Link ID: 29132 - Posted: 02.06.2024

By Laura Sanders Under extremely rare circumstances, it appears that Alzheimer’s disease can be transmitted between people. Five people who received contaminated injections of a growth hormone as children went on to develop Alzheimer’s unusually early, researchers report January 29 in Nature Medicine. The findings represent “the first time iatrogenic Alzheimer’s disease has been described,” neurologist John Collinge said January 25 in a news briefing, referring to a disease caused by a medical procedure. That sounds alarming, but researchers are quick to emphasize that Alzheimer’s disease is not contagious in everyday life, including caretaking and most medical settings. Support Science Today. Thank you for being a subscriber to Science News! Interested in more ways to support STEM? Consider making a gift to our nonprofit publisher, Society for Science, an organization dedicated to expanding scientific literacy and ensuring that every young person can strive to become an engineer or scientist. Donate Now “We are not suggesting for a moment that you can catch Alzheimer’s disease,” said Collinge, of the University College London’s Institute of Prion Diseases. “This is not transmissible in the sense of a viral or bacterial infection.” The reassurance is echoed by Carlo Condello, a neurobiologist at the University of California, San Francisco who wasn’t involved in the study. “In no way do we believe sporadic Alzheimer’s disease is a communicable disease,” he says. “Only under incredibly artificial, now out-of-date, medical practices is this appearing. It’s no longer an issue.” © Society for Science & the Public 2000–202

Keyword: Alzheimers
Link ID: 29126 - Posted: 01.31.2024

By Ben Guarino Billionaire technologist Elon Musk announced this week that his company Neuralink has implanted its brain-computer interface into a human for the first time. The recipient was “recovering well,” Musk wrote on his social media platform X (formerly Twitter) on Monday evening, adding that initial results showed “promising neuron spike detection”—a reference to brain cells’ electrical activity. Each wireless Neuralink device contains a chip and electrode arrays of more than 1,000 superthin, flexible conductors that a surgical robot threads into the cerebral cortex. There the electrodes are designed to register thoughts related to motion. In Musk’s vision, an app will eventually translate these signals to move a cursor or produce text—in short, it will enable computer control by thinking. “Imagine if Stephen Hawking could communicate faster than a speed typist or auctioneer. That is the goal,” Musk wrote of the first Neuralink product, which he said is named Telepathy. The U.S. Food and Drug Administration had approved human clinical trials for Neuralink in May 2023. And last September the company announced it was opening enrollment in its first study to people with quadriplegia. Monday’s announcement did not take neuroscientists by surprise. Musk, the world’s richest man, “said he was going to do it,” says John Donoghue, an expert in brain-computer interfaces at Brown University. “He had done the preliminary work, built on the shoulders of others, including what we did starting in the early 2000s.” Neuralink’s original ambitions, which Musk outlined when he founded the company in 2016, included meshing human brains with artificial intelligence. Its more immediate aims seem in line with the neural keyboards and other devices that people with paralysis already use to operate computers. The methods and speed with which Neuralink pursued those goals, however, have resulted in federal investigations into dead study animals and the transportation of hazardous material. © 2024 SCIENTIFIC AMERICAN

Keyword: Robotics
Link ID: 29124 - Posted: 01.31.2024

By Ben Guarino Billionaire technologist Elon Musk announced this week that his company Neuralink has implanted its brain-computer interface into a human for the first time. The recipient was “recovering well,” Musk wrote on his social media platform X (formerly Twitter) on Monday evening, adding that initial results showed “promising neuron spike detection”—a reference to brain cells’ electrical activity. Each wireless Neuralink device contains a chip and electrode arrays of more than 1,000 superthin, flexible conductors that a surgical robot threads into the cerebral cortex. There the electrodes are designed to register thoughts related to motion. In Musk’s vision, an app will eventually translate these signals to move a cursor or produce text—in short, it will enable computer control by thinking. “Imagine if Stephen Hawking could communicate faster than a speed typist or auctioneer. That is the goal,” Musk wrote of the first Neuralink product, which he said is named Telepathy. The U.S. Food and Drug Administration had approved human clinical trials for Neuralink in May 2023. And last September the company announced it was opening enrollment in its first study to people with quadriplegia. Monday’s announcement did not take neuroscientists by surprise. Musk, the world’s richest man, “said he was going to do it,” says John Donoghue, an expert in brain-computer interfaces at Brown University. “He had done the preliminary work, built on the shoulders of others, including what we did starting in the early 2000s.” Neuralink’s original ambitions, which Musk outlined when he founded the company in 2016, included meshing human brains with artificial intelligence. Its more immediate aims seem in line with the neural keyboards and other devices that people with paralysis already use to operate computers. The methods and speed with which Neuralink pursued those goals, however, have resulted in federal investigations into dead study animals and the transportation of hazardous material. © 2024 SCIENTIFIC AMERICAN

Keyword: Robotics
Link ID: 29123 - Posted: 01.31.2024

By Laurie McGinley ABINGTON, Pa. — Wrapped in a purple blanket, Robert Williford settles into a quiet corner of a bustling neurology clinic, an IV line delivering a colorless liquid into his left arm. The 67-year-old, who has early Alzheimer’s disease, is getting his initial dose of Leqembi. The drug is the first to clearly slow the fatal neurodegenerative ailment that afflicts 6.7 million older Americans, though the benefits may be modest. The retired social worker, one of the first African Americans to receive the treatment, hopes it will ease his forgetfulness so “I drive my wife less crazy.” But as Williford and his doctors embark on this treatment, they are doing so with scant scientific data about how the medication might work in people of color. In the pivotal clinical trial for the drug, Black patients globally accounted for only 47 of the 1,795 participants — about 2.6 percent. For U.S. trial sites, the percentage was 4.5 percent. The proportion of Black enrollees was similarly low for Eli Lilly Alzheimer’s drug, called donanemab, expected to be cleared by the Food and Drug Administration in coming months. Black people make up more than 13 percent of the U.S. population. The paltry data for the new class of groundbreaking drugs, which strip a sticky substance called amyloid beta from the brain, has ignited an intense debate among researchers and clinicians. Will the medications — the first glimmer of hope after years of failure — be as beneficial for African Americans as for White patients? “Are these drugs going to work in non-Whites? And particularly in Blacks? We just don’t have enough data, I don’t think,” said Suzanne E. Schindler, a clinical neurologist and dementia specialist at Washington University in St. Louis.

Keyword: Alzheimers
Link ID: 29122 - Posted: 01.31.2024

Karla Kaun Many people are wired to seek and respond to rewards. Your brain interprets food as rewarding when you are hungry and water as rewarding when you are thirsty. But addictive substances like alcohol and drugs of abuse can overwhelm the natural reward pathways in your brain, resulting in intolerable cravings and reduced impulse control. A popular misconception is that addiction is a result of low willpower. But an explosion of knowledge and technology in the field of molecular genetics has changed our basic understanding of addiction drastically over the past decade. The general consensus among scientists and health care professionals is that there is a strong neurobiological and genetic basis for addiction. As a behavioral neurogeneticist leading a team investigating the molecular mechanisms of addiction, I combine neuroscience with genetics to understand how alcohol and drugs influence the brain. In the past decade, I have seen changes in our understanding of the molecular mechanisms of addiction, largely due to a better understanding of how genes are dynamically regulated in the brain. New ways of thinking about how addictions form have the potential to change how we approach treatment. Each of your brain cells has your genetic code stored in long strands of DNA. For all that DNA to fit into a cell, it needs to be packed tightly. This is achieved by winding the DNA around “spools” of protein called histones. Areas where DNA is unwound contain active genes coding for proteins that serve important functions within the cell. When gene activity changes, the proteins your cells produce also change. Such changes can range from a single neuronal connection in your brain to how you behave. This genetic choreography suggests that while your genes affect how your brain develops, which genes are turned on or off when you are learning new things is dynamic and adapts to suit your daily needs. © 2010–2024, The Conversation US, Inc.

Keyword: Drug Abuse; Epigenetics
Link ID: 29108 - Posted: 01.23.2024

By Mark Johnson There had been early clues, but it was a family game of dominoes around Christmas 2021 that convinced Susan Stewart that something was wrong with her husband. Charlie Stewart, then 75 and retired, struggled to match the dots on different domino tiles. Susan assumed it was a vision problem. Charlie’s memory was fine, and he had no family history of dementia. But months later the Marin County, Calif., couple were shocked to learn that his domino confusion was a sign he had a lesser-known variant of Alzheimer’s disease. For patients with this variant, called posterior cortical atrophy, the disease begins with problems affecting vision rather than memory. The unusual early symptoms mean that thousands of people may go years before receiving the correct diagnosis, experts said. That may change with the first large-scale international study of the condition, published Monday in the journal Lancet Neurology. An international team led by researchers at the University of California at San Francisco studied records of 1,092 PCA patients from 16 countries and found that, on average, the syndrome begins affecting patients at age 59 ― about five to six years earlier than most patients with the more common form of Alzheimer’s. Although the number of patients with PCA has not been established, researchers say that the variant may account for as many as 10 percent of all Alzheimer’s cases; that would put the number of Americans with the condition close to 700,000. “We have a lot of work to do to raise awareness about the syndrome,” said Gil D. Rabinovici, one of the study’s authors and director of the UCSF Alzheimer’s Disease Research Center. “One thing that we found in our large study is that by the time people are diagnosed, they’ve had [the disease] for quite a few years.” The study authors said they hope greater awareness of the syndrome will help doctors diagnose it earlier and will encourage researchers to include patients with PCA in future Alzheimer’s clinical trials. Unusual symptoms delay diagnosis

Keyword: Alzheimers; Vision
Link ID: 29107 - Posted: 01.23.2024

By Holly Barker Sensory issues associated with autism may be caused by fluctuating neuronal noise — the background hum of electrical activity in the brain — according to a new mouse study. Up to 90 percent of autistic people report sensory problems, including heightened sensitivity to sounds or an aversion to certain smells. Yet others barely register sensory cues and may seek out sensations by making loud noises or rocking back and forth. But thinking in terms of hyper- or hyposensitivity may be an oversimplification, says Andreas Frick, lead investigator and research director at INSERM. “It’s becoming clear now that things are a lot more nuanced.” For instance, the brain’s response to visual patterns — measured using electroencephalography (EEG) recordings — varies more between viewings in autistic people than in those without the condition, one study found. And functional MRI has detected similar variability among autistic people, suggesting sensory problems may arise from inconsistent brain responses. In the new study, Frick and his colleagues found variability in the activity of individual neurons in a mouse model of fragile X syndrome, one of the leading causes of autism. That variability in neuronal response maps to fluctuations in the levels of noise in the brain, the study found. Noise within the brain isn’t necessarily a bad thing. In fact, an optimum amount is ideal: a little can give neurons the ‘push’ they might need to fire an action potential, while too much can make it difficult for the brain to distinguish between different stimuli. But in animals modeling fragile X syndrome, noise fluctuates such that they process sensory information less reliably, Frick says. © 2023 Simons Foundation.

Keyword: Autism
Link ID: 29105 - Posted: 01.18.2024