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

Jon Hamilton Sam and John Fetters, 19, are identical twins at opposite ends of the autism spectrum. Sam is a sophomore at Amherst College who plans to double major in history and political science. In his free time, he runs marathons. John attends a special school, struggles to form sentences, and likes to watch "Teletubbies" and "Sesame Street." Two brothers. Same genes. Different flavors of autism. To scientists, twins like Sam and John pose an important question: How can a disorder that is known to be highly genetic look so different in siblings who share the same genome? "That is one of the greatest mysteries right now in research on autism," says Dr. Stephanie Morris, a pediatric neurologist at the Kennedy Krieger Institute in Baltimore. Solving that mystery could help explain autism's odd mix of nature and nurture, Morris says. It also might help "modify the trajectory" of autistic children experiencing speech and language delays, or difficulty with social communication. Identical twins on separate paths Sam and John are spending the weekend with their mom, Kim Leaird, at the family's apartment in West Tisbury, a small town on Martha's Vineyard. The twins are crowded together on a couch. Even seated, they look tall. Standing, Sam is 6 feet five inches, his brother just an inch shorter. John lets Sam do most of the talking. He frequently touches his brother, who sometimes takes his hand. John has "a truly tremendous amount of empathy," Sam says. "He's able to be very supportive." © 2024 npr

Keyword: Autism; Genes & Behavior
Link ID: 29239 - Posted: 04.04.2024

by Alex Blasdel Patient One was 24 years old and pregnant with her third child when she was taken off life support. It was 2014. A couple of years earlier, she had been diagnosed with a disorder that caused an irregular heartbeat, and during her two previous pregnancies she had suffered seizures and faintings. Four weeks into her third pregnancy, she collapsed on the floor of her home. Her mother, who was with her, called 911. By the time an ambulance arrived, Patient One had been unconscious for more than 10 minutes. Paramedics found that her heart had stopped. After being driven to a hospital where she couldn’t be treated, Patient One was taken to the emergency department at the University of Michigan. There, medical staff had to shock her chest three times with a defibrillator before they could restart her heart. She was placed on an external ventilator and pacemaker, and transferred to the neurointensive care unit, where doctors monitored her brain activity. She was unresponsive to external stimuli, and had a massive swelling in her brain. After she lay in a deep coma for three days, her family decided it was best to take her off life support. It was at that point – after her oxygen was turned off and nurses pulled the breathing tube from her throat – that Patient One became one of the most intriguing scientific subjects in recent history. For several years, Jimo Borjigin, a professor of neurology at the University of Michigan, had been troubled by the question of what happens to us when we die. She had read about the near-death experiences of certain cardiac-arrest survivors who had undergone extraordinary psychic journeys before being resuscitated. Sometimes, these people reported travelling outside of their bodies towards overwhelming sources of light where they were greeted by dead relatives. Others spoke of coming to a new understanding of their lives, or encountering beings of profound goodness. Borjigin didn’t believe the content of those stories was true – she didn’t think the souls of dying people actually travelled to an afterworld – but she suspected something very real was happening in those patients’ brains. In her own laboratory, she had discovered that rats undergo a dramatic storm of many neurotransmitters, including serotonin and dopamine, after their hearts stop and their brains lose oxygen. She wondered if humans’ near-death experiences might spring from a similar phenomenon, and if it was occurring even in people who couldn’t be revived. © 2024 Guardian News & Media Limited

Keyword: Consciousness; Attention
Link ID: 29236 - Posted: 04.02.2024

By Paula Span The phone awakened Doug Nordman at 3 a.m. A surgeon was calling from a hospital in Grand Junction, Colo., where Mr. Nordman’s father had arrived at the emergency room, incoherent and in pain, and then lost consciousness. At first, the staff had thought he was suffering a heart attack, but a CT scan found that part of his small intestine had been perforated. A surgical team repaired the hole, saving his life, but the surgeon had some questions. “Was your father an alcoholic?” he asked. The doctors had found Dean Nordman malnourished, his peritoneal cavity “awash with alcohol.” The younger Mr. Nordman, a military personal finance author living in Oahu, Hawaii, explained that his 77-year-old dad had long been a classic social drinker: a Scotch and water with his wife before dinner, which got topped off during dinner, then another after dinner, and perhaps a nightcap. Having three to four drinks daily exceeds current dietary guidelines, which define moderate consumption as two drinks a day for men and one for women, or less. But “that was the normal drinking culture of the time,” said Doug Nordman, now 63. At the time of his 2011 hospitalization, though, Dean Nordman, a retired electrical engineer, was widowed, living alone and developing symptoms of dementia. He got lost while driving, struggled with household chores and complained of a “slipping memory.” He had waved off his two sons’ offers of help, saying he was fine. During that hospitalization, however, Doug Nordman found hardly any food in his father’s apartment. Worse, reviewing his father’s credit card statements, “I saw recurring charges from the Liquor Barn and realized he was drinking a pint of Scotch a day,” he said. Public health officials are increasingly alarmed by older Americans’ drinking. The annual number of alcohol-related deaths from 2020 through 2021 exceeded 178,000, according to recently released data from the Centers for Disease Control and Prevention: more deaths than from all drug overdoses combined. © 2024 The New York Times Company

Keyword: Drug Abuse; Alzheimers
Link ID: 29234 - Posted: 04.02.2024

By Saugat Bolakhe For desert ants, Earth’s magnetic field isn’t just a compass: It may also sculpt their brains. Stepping outside their nest for the first time, young ants need to learn how to forage. The ants train partly by walking a loop near their nests for the first three days. During this stroll, they repeatedly pause and then pirouette to gaze back at the nest entrance, learning how to find their way back home. But when the magnetic field around the nest entrance was disturbed, ant apprentices couldn’t figure out where to look, often gazing in random directions, researchers report in the Feb. 20 Proceedings of the National Academy of Sciences. What’s more, the altered magnetic field seemed to affect connections between neurons in the learning and memory centers in the young ants’ brains. The finding “may make it easier to better understand how magnetic fields are sensed [in animals]” as scientists now know one way that magnetic fields can influence brain development, says Robin Grob, a biologist at the Norwegian University of Science and Technology in Trondheim. For years, scientists have known that some species of birds, fishes, turtles, moths and butterflies rely on Earth’s magnetic field to navigate (SN: 4/3/18). In 2018, Grob and other scientists added desert ants to that list. Young ants first appeared to use the magnetic field as a reference while learning how to use landmarks and the sun as guides to orient themselves in the right direction to gaze back toward the nest with its small, hard-to-see entrance. However, knowing where in the brain magnetic cues are processed has proved challenging. © Society for Science & the Public 2000–2024.

Keyword: Animal Migration; Development of the Brain
Link ID: 29227 - Posted: 03.30.2024

By Catherine Offord Bone marrow transplants between mice can transmit symptoms and pathology associated with Alzheimer’s disease, according to a controversial study published today in Stem Cell Reports. Its authors found that healthy mice injected with marrow from a mouse strain carrying an extremely rare, Alzheimer’s-linked genetic mutation later developed cognitive problems and abnormal clumping of proteins in the brain. In claims that other scientists in the field have criticized as overstated, the team says its findings demonstrate “Alzheimer’s disease transmission” and support screening of human bone marrow, organ, and blood donors for mutations related to neurodegeneration. “The findings are not by any means conclusive,” says Lary Walker, a neuroscientist at Emory University. Although the team’s approach offers an interesting way to study potential causes of neurodegeneration, he says, “the mice do not have Alzheimer’s disease,” only certain symptoms that mimic those of the disorder and require further study. He and other scientists stress that the new findings should not deter people who medically need bone marrow or other transplants. Alzheimer’s is partly characterized by so-called plaques of beta amyloid, a fragment of a larger protein called APP, around cells in the brain. Although there are rare, early-onset versions of the disease driven by specific mutations in the gene coding for APP or related proteins, most cases arise in people over age 65 and don’t have a single known cause. Some research hints that in very unusual scenarios, Alzheimer’s could be transmitted via human tissue or medical equipment contaminated with disease-causing proteins. Earlier this year, for example, U.K. scientists described dementia and beta amyloid buildup in several people who had received injections of growth hormone from the brains of deceased donors. (The procedure was once a medical treatment for certain childhood disorders but was abandoned in the 1980s.)

Keyword: Alzheimers; Hormones & Behavior
Link ID: 29225 - Posted: 03.30.2024

By Frances Vinall More than two-thirds of young children in Chicago could be exposed to lead-contaminated water, according to an estimate by the Johns Hopkins Bloomberg School of Public Health and the Stanford University School of Medicine. The research, published Monday in the journal JAMA Pediatrics, estimated that 68 percent of children under the age of 6 in Chicago are exposed to lead-contaminated drinking water. Of that group, 19 percent primarily use unfiltered tap water, which was associated with a greater increase in blood lead levels. “The extent of lead contamination of tap water in Chicago is disheartening — it’s not something we should be seeing in 2024,” lead author Benjamin Huynh, assistant professor of environmental health and engineering at the Johns Hopkins Bloomberg School of Public Health, said in a news release. The study suggested that residential blocks with predominantly Black and Hispanic populations were less likely to be tested for lead, but also disproportionately exposed to contaminated water. Gina Ramirez, Midwest regional lead of environmental health for the Natural Resources Defense Council, said she grew up in Chicago drinking bottled water, but now uses filtered water for her own family, because of a generational awareness of “not trusting my tap” to be safe. The study “confirmed my worst fears that children living in vulnerable populations in the city are the most impacted,” she said. “All children deserve to grow up in a healthy city, and to learn that something inside their home is impacting so many kids health and development is a huge wake-up call.”

Keyword: Neurotoxins; Development of the Brain
Link ID: 29207 - Posted: 03.23.2024

By Tomasz Nowakowski, Karthik Shekhar Diverse neurons and their equally diverse circuits are the foundation of the brain’s remarkable ability to process information, store memories, regulate behavior and enable conscious thought. High-throughput, single-cell profiling technologies have made it possible to classify these cells more comprehensively than ever before, offering a 360-degree view of the sheer magnitude of neural diversity in the mammalian brain. A recent effort to define the complete set of transcriptomic cell types in the adult whole mouse brain, for example, defined roughly 5,000 distinct cell types distributed across dozens of brain areas. This landmark accomplishment is a critical step toward integrating information about function and connectivity, and extending similar efforts to the adult human brain. But this impressive gestalt conveys little, if any, information about how such diversity arises and develops in the first place. Single-cell atlases developed to date have been limited to a few points in time, focusing largely on the endpoint of neural development. How is this exquisite panoply of neurons generated and organized into precise and orderly circuits that last a lifetime? Providing the answer is the central task of developmental neuroscience. We want to understand the many transitions that unfold — where cells come from, the paths they take, and when terminal cell states emerge. The comprehensive nature of single-cell technologies offers tremendous promise for defining cell types and reconstructing the trajectories of gene expression that underlie their differentiation. Initial efforts to apply these technologies to development, including in the prenatal human brain, hint at the insights these approaches can bring. Single-cell transcriptomics has helped map the diversity of neural progenitor cells, for example, most notably identifying progenitors that are expanded in humans, and their associated molecular adaptations. Further insights into development will require methods that reveal the specific history of every neuron type, including those that can more densely sample brain cells’ trajectories over time and novel approaches for tracking fate transitions in individual cells. These discoveries will in turn help us to understand neurodevelopmental conditions, many of which are associated with genomic variation, and neurological disorders, such as brain tumors. © 2024 Simons Foundation

Keyword: Development of the Brain
Link ID: 29198 - Posted: 03.19.2024

By Esther Landhuis In January 2023, the US Food and Drug Administration (FDA) approved lecanemab — an antibody medication that decreases β-amyloid protein build-up in the brain — as a treatment for Alzheimer’s disease. Pivotal evidence came from a large, randomized trial of people with early-stage Alzheimer’s, which afflicts around 32 million people worldwide. By the end of that 18-month study1, patients in the placebo group scored on average 1.66 points worse than their performance at baseline on a standard dementia test, which assesses cognitive and functional changes over time through interviews with a patient and their caregiver. The mean score of treated participants, by comparison, worsened by 1.21 points — a 27% slowing of cognitive decline. But is this improvement meaningful for patients and their families? There are two major categories of drugs used to treat Alzheimer’s disease and other progressive conditions: symptomatic drugs, which treat the symptoms, and disease-modifying drugs, which target the root cause. Donepezil and rivastigmine, for example, are symptomatic drugs that boost the activity of chemicals in the brain to compensate for declines in cognitive and memory function caused by Alzheimer’s disease, but they cannot stop its progression. Lecanemab, developed jointly by Japanese pharmaceutical company Eisai and American biotechnology firm Biogen, targets the underlying issue of amyloid build-up in the brain, and in doing so, could fundamentally change the course of the disease. An important feature of disease-modifying drugs is that their benefits are cumulative. Studies of patients with multiple sclerosis, for example, have shown the benefits of starting disease-modifying drugs earlier in the course of the disease compared with later, including improved mortality rates and reduced disability in the long term. Being able to quantify how long a disease-modifying drug can delay or halt the progression of Alzheimer’s disease could change how researchers understand — and communicate — its benefits. © 2024 Springer Nature Limited

Keyword: Alzheimers
Link ID: 29193 - Posted: 03.16.2024

By Ellen Barry Twins are a bonanza for research psychologists. In a field perpetually seeking to tease out the effects of genetics, environment and life experience, they provide a natural controlled experiment as their paths diverge, subtly or dramatically, through adulthood. Take Dennis and Douglas. In high school, they were so alike that friends told them apart by the cars they drove, they told researchers in a study of twins in Virginia. Most of their childhood experiences were shared — except that Dennis endured an attempted molestation when he was 13. At 18, Douglas married his high school girlfriend. He raised three children and became deeply religious. Dennis cycled through short-term relationships and was twice divorced, plunging into bouts of despair after each split. By their 50s, Dennis had a history of major depression, and his brother did not. Why do twins, who share so many genetic and environmental inputs, diverge as adults in their experience of mental illness? On Wednesday, a team of researchers from the University of Iceland and Karolinska Institutet in Sweden reported new findings on the role played by childhood trauma. Their study of 25,252 adult twins in Sweden, published in JAMA Psychiatry, found that those who reported one or more trauma in childhood — physical or emotional neglect or abuse, rape, sexual abuse, hate crimes or witnessing domestic violence — were 2.4 times as likely to be diagnosed with a psychiatric illness as those who did not. If a person reported one or more of these experiences, the odds of being diagnosed with a mental illness climbed sharply, by 52 percent for each additional adverse experience. Among participants who reported three or more adverse experiences, nearly a quarter had a psychiatric diagnosis of depressive disorder, anxiety disorder, substance abuse disorder or stress disorder. © 2024 The New York Times Company

Keyword: Depression; Genes & Behavior
Link ID: 29184 - Posted: 03.07.2024

By Laura Dattaro Steven McCarroll just wanted to compare how different cell types express genes in people with and without schizophrenia. But when he sequenced the transcriptomes of more than 1 million cortical cells from 191 postmortem brains, what leapt out from the data went far beyond his simple case-control comparison: Astrocytes and neurons from all of the brains coordinate their expression of certain genes needed for healthy synapses, a relationship the team dubbed the Synaptic Neuron-and-Astrocyte Program (SNAP) and described in a paper published in Nature today. “The data led us to something much more exciting and surprising than what we set out to do,” says McCarroll, professor of biomedical science and genetics at Harvard Medical School. SNAP is an intricate dance, McCarroll and his colleagues found: The more a person’s neurons express synaptic genes, so too do their astrocytes, but this coordination wanes in older people and those with schizophrenia. Because astrocytes — a type of glial cell — and neurons are in constant communication and the findings are correlational, it’s unclear which cell type choreographs this dance. But other evidence suggests that astrocytes take the lead, says Stephen Quake, professor of bioengineering at Stanford University, who was not involved in McCarroll’s work. In mice trained to fear a foot shock, for example, neurons involved in memory formation express neurotensin, whereas astrocytes express a receptor for it, Quake and his colleagues reported last month in Nature. But when they inhibited the animals’ astrocytes during fear training, the mice performed worse on memory tests, suggesting those cells play an active role in long-term memory formation, Quake says — and govern the relationship McCarroll found. © 2024 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 29183 - Posted: 03.07.2024

By Veronique Greenwood It can be hard to tell, at first, when a cell is on the verge of self-destruction. It appears to be going about its usual business, transcribing genes and making proteins. The powerhouse organelles called mitochondria are dutifully churning out energy. But then a mitochondrion receives a signal, and its typically placid proteins join forces to form a death machine. They slice through the cell with breathtaking thoroughness. In a matter of hours, all that the cell had built lies in ruins. A few bubbles of membrane are all that remains. “It’s really amazing how fast, how organized it is,” said Aurora Nedelcu, an evolutionary biologist at the University of New Brunswick who has studied the process in algae. Apoptosis, as this process is known, seems as unlikely as it is violent. And yet some cells undergo this devastating but predictable series of steps to kill themselves on purpose. When biologists first observed it, they were shocked to find self-induced death among living, striving organisms. And although it turned out that apoptosis is a vital creative force for many multicellular creatures, to a given cell it is utterly ruinous. How could a behavior that results in a cell’s sudden death evolve, let alone persist? The tools for apoptosis, molecular biologists have found, are curiously widespread. And as they have sought to understand its molecular process and origins, they’ve found something even more surprising: Apoptosis can be traced back to ancient forms of programmed cell death undertaken by single-celled organisms — even bacteria — that seem to have evolved it as a social behavior. © 2024 the Simons Foundation.

Keyword: Apoptosis; Development of the Brain
Link ID: 29181 - Posted: 03.07.2024

By Katherine Ellison Jonel Dershem first noticed problems with her memory in 2016 after her breast cancer surgery. She was only 50 and at first blamed the lapses on chemotherapy, and then on her busy, stressful life. So did her husband and friends — and doctor. “I kept blowing it off,” said Dershem, an obstetrician from Voorhees, N.J., whose challenges began with little things like leaving a faucet running and progressed to trouble finishing routine tasks. “I was our family’s primary breadwinner. I didn’t want there to be any serious problems.” In December 2022, nearly seven years after her memory loss began, Dershem was diagnosed with mild cognitive impairment (MCI). Her delayed diagnosis wasn’t unusual, but experts say that needs to change. More than occasional forgetfulness, MCI causes problems that disrupt daily life but don’t make it impossible to function, said Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center and the Mayo Clinic Study of Aging. It is often but not always a precursor to dementia, he added. “It’s a subtle condition,” said Petersen, who in 1999 led the first study differentiating patients with MCI from healthy subjects and those with dementia. If you miss a golf date once, no worries, he said, but if “that happened a couple of times last week and people in your family are starting to worry about you — well, that may be MCI.” “With MCI, people can still drive, pay their bills and do their taxes — they just do so less efficiently,” Petersen said. A 2022 study in the journal Alzheimer’s & Dementia projected that 14.4 million people in the United States would have MCI in 2025, and 19.3 million in 2050. An American Academy of Neurology subcommittee estimated that about 1 in 10 people ages 70 to 74 had MCI, and 1 in 4 ages 80 to 84 in 2018.

Keyword: Alzheimers; Learning & Memory
Link ID: 29178 - Posted: 03.05.2024

By Paula Span Determining whether someone has Alzheimer’s disease usually requires an extended diagnostic process. A doctor takes a patient’s medical history, discusses symptoms, administers verbal and visual cognitive tests. The patient may undergo a PET scan, an M.R.I. or a spinal tap — tests that detect the presence of two proteins in the brain, amyloid plaques and tau tangles, both associated with Alzheimer’s. All of that could change dramatically if new criteria proposed by an Alzheimer’s Association working group are widely adopted. Its final recommendations, expected later this year, will accelerate a shift that is already underway: from defining the disease by symptoms and behavior to defining it purely biologically — with biomarkers, substances in the body that indicate disease. The draft guidelines, Revised Criteria for Diagnosis and Staging of Alzheimer’s Disease, call for a simpler approach. That could mean a blood test to indicate the presence of amyloid. Such tests are already available in some clinics and doctors’ offices. “Someone who has biomarker evidence of amyloid in the brain has the disease, whether they’re symptomatic or not,” said Dr. Clifford R. Jack Jr., the chair of the working group and an Alzheimer’s researcher at the Mayo Clinic. “The pathology exists for years before symptom onset,” he added. “That’s the science. It’s irrefutable.” He and his colleagues on the panel do not recommend testing people who have no symptoms of cognitive decline. But skeptics predict that’s likely to happen nonetheless. If so, a sizable proportion would test positive for amyloid and would therefore be diagnosed with Alzheimer’s. A 2015 Dutch study estimated that more than 10 percent of cognitively normal 50-year-olds would test positive, as would almost 16 percent of 60-year-olds and 23 percent of 70-year-olds. Most of those individuals would never develop dementia. © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29177 - Posted: 03.05.2024

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