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By Elizabeth Landau Electroconvulsive therapy has a public relations problem. The treatment, which sends electric currents through the brain to induce a brief seizure, has barbaric, inhumane connotations — for example, it was portrayed as a sadistic punishment in the film One Flew Over the Cuckoo’s Nest. But for patients with depression that does not improve with medications, electroconvulsive therapy (ECT) can be highly effective. Studies have found that some 50% to 70% of patients with major depressive disorder see their symptoms improve after a course of ECT. In comparison, medications aimed at altering brain chemistry help only 10% to 40% of depression patients. Still, even after many decades of use, scientists don’t know how ECT alters the brain’s underlying biology. Bradley Voytek, a neuroscientist at the University of California, San Diego, said a psychiatrist once told him that the therapy “reboots the brain” — an explanation he found “really unsatisfying.” Recently, Voytek and his collaborators paired their research into the brain’s electrical patterns with patient data to explore why inducing seizures has antidepressant effects. In two studies published last fall, the researchers observed that ECT and a related seizure therapy increased the unstructured background noise hiding behind well-defined brain waves. Neuroscientists call this background noise “aperiodic activity.” The authors suggested that induced seizures might help restore the brain’s balance of excitation and inhibition, which could have an overall antidepressant effect. “Every time that I talk to someone who’s not in this field about this work they’re like, ‘They still do that? They still use electroshock? I thought that was just in horror movies,’” said Sydney Smith, a graduate student in neuroscience in Voytek’s lab and the first author of the new studies. “Dealing with the stigma around it has become even more of a motivation to figure out how it works.” © 2024 Simons Foundation.

Keyword: Depression; Attention
Link ID: 29199 - Posted: 03.19.2024

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 Gina Jiménez Being pregnant and giving birth changes a person’s brain, but the brain looks different depending on whether it’s examined during pregnancy or after a person gives birth, a recent study found. The research is helping disentangle some of the mysteries in the long-ignored field of maternal neuroscience. The study, published in January in Nature Neuroscience, followed more than 100 new mothers from near the end of their pregnancy until about three weeks on average after they had their baby. Previous research had examined birthing parents’ brain before they gave birth or during the postpartum period, but this study observed them both before and after birth, and it also took into account whether they had a vaginal birth or C-section. The findings reveal temporary changes in some brain regions and more permanent ones in a brain circuit that activates when people are not engaged in an active task and that is also involved in self-reflection and empathizing with others. The study has “ordered” some of the scientific disagreements in the field, says its senior author Susana Carmona, a neuroscience researcher now at Gregorio Marañón General University Hospital in Spain.* “It fills important gaps—that is why it’s novel,” says Joe Lonstein, a neuroscientist who studies animal parenting behaviors at Michigan State University but was not involved with the new paper. “There were things we just didn’t know about the timing of events.” Much of the scientific literature on pregnancy and postpartum neuroscience is only around a decade old. A 2016 study found that gray matter decreased in women after they had a baby for the first time, and the reductions persisted for at least six years after pregnancy. In contrast, other studies have observed that gray matter increases in the first weeks after people give birth. The new paper helps reconcile these results: the researchers found that women indeed lost gray matter during pregnancy and childbirth but got it back in most brain areas after they had their baby. © 2024 SCIENTIFIC AMERICAN,

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 29197 - Posted: 03.19.2024

By Julian E. Barnes New studies by the National Institutes of Health failed to find evidence of brain injury in scans or blood markers of the diplomats and spies who suffered symptoms of Havana syndrome, bolstering the conclusions of U.S. intelligence agencies about the strange health incidents. Spy agencies have concluded that the debilitating symptoms associated with Havana syndrome, including dizziness and migraines, are not the work of a hostile foreign power. They have not identified a weapon or device that caused the injuries, and intelligence analysts now believe the symptoms are most likely explained by environmental factors, existing medical conditions or stress. The lead scientist on one of the two new studies said that while the study was not designed to find a cause, the findings were consistent with those determinations. The authors said the studies are at odds with findings from researchers at the University of Pennsylvania, who found differences in brain scans of people with Havana syndrome symptoms and a control group Dr. David Relman, a prominent scientist who has had access to the classified files involving the cases and representatives of people suffering from Havana syndrome, said the new studies were flawed. Many brain injuries are difficult to detect with scans or blood markers, he said. He added that the findings do not dispute that an external force, like a directed energy device, could have injured the current and former government workers. The studies were published in The Journal of the American Medical Association on Monday alongside an editorial by Dr. Relman that was critical of the findings. © 2024 The New York Times Company

Keyword: Learning & Memory; Depression
Link ID: 29196 - Posted: 03.19.2024

By Heidi Ledford Two preliminary studies suggest that next-generation engineered immune cells show promise against one of the most feared forms of cancer. A pair of papers published on 13 March, one in Nature Medicine1 and the other in The New England Journal of Medicine2, describe the design and deployment of immune cells called chimeric antigen receptor T (CAR T) cells against glioblastoma, an aggressive and difficult-to-treat form of brain cancer. The average length of survival for people with this tumour is eight months. Both teams found early hints of progress using CAR T cells that target two proteins made by glioblastoma cells, thereby marking those cells for destruction. CAR T cells are currently approved for treating only blood cancers, such as leukaemia, and are typically engineered to home in on only one target. But these results add to mounting evidence that CAR T cells could be modified to treat a wider range of cancers. “It lends credence to the potential power of CAR T cells to make a difference in solid tumours, especially the brain,” says Bryan Choi, a neurosurgeon at Massachusetts General Hospital in Boston, and a lead author of the New England Journal of Medicine study. “It adds to the excitement that we might be able to move the needle.” Glioblastomas offer a formidable challenge. Fast-growing glioblastomas can mix with healthy brain cells, forming diffuse tumours that are difficult to remove surgically. Surgery, chemotherapy and radiation therapy are typically the only treatment options for these tumours, and tend to produce short-lived, partial responses. © 2024 Springer Nature Limited

Keyword: Neuroimmunology
Link ID: 29195 - Posted: 03.19.2024

By Elise Cutts In March 2019, on a train headed southwest from Munich, the neuroscientist Maximilian Bothe adjusted his careful grip on the cooler in his lap. It didn’t contain his lunch. Inside was tissue from half a dozen rattlesnake spinal cords packed in ice — a special delivery for his new research adviser Boris Chagnaud, a behavioral neuroscientist based on the other side of the Alps. In his lab at the University of Graz in Austria, Chagnaud maintains a menagerie of aquatic animals that move in unusual ways — from piranhas and catfish that drum air bladders to produce sound to mudskippers that hop around on land on two fins. Chagnaud studies and compares these creatures’ neuronal circuits to understand how new ways of moving might evolve, and Bothe was bringing his rattlesnake spines to join the endeavor. The ways that animals move are just about as myriad as the animal kingdom itself. They walk, run, swim, crawl, fly and slither — and within each of those categories lies a tremendous number of subtly different movement types. A seagull and a hummingbird both have wings, but otherwise their flight techniques and abilities are poles apart. Orcas and piranhas both have tails, but they accomplish very different types of swimming. Even a human walking or running is moving their body in fundamentally different ways. The tempo and type of movements a given animal can perform are set by biological hardware: nerves, muscle and bone whose functions are bound by neurological constraints. For example, vertebrates’ walking tempos are set by circuits in their spines that fire without any conscious input from the brain. The pace of that movement is dictated by the properties of the neuronal circuits that control them. For an animal to evolve a novel way of moving, something in its neurological circuitry has to change. Chagnaud wants to describe exactly how that happens. “In evolution, you don’t just invent the wheel. You take pieces that were already there, and you modify them,” he said. “How do you modify those components that are shared across many different species to make new behaviors?” © 2024 Simons Foundation.

Keyword: Evolution
Link ID: 29194 - Posted: 03.16.2024

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 Meghan Rosen Leakiness in the brain could explain the memory and concentration problems linked to long COVID. In patients with brain fog, MRI scans revealed signs of damaged blood vessels in their brains, researchers reported February 22 in Nature Neuroscience. In these people, dye injected into the bloodstream leaked into their brains and pooled in regions that play roles in language, memory, mood and vision. It’s the first time anyone’s shown that long COVID patients can have leaky blood brain barriers, says study coauthor Matthew Campbell, a geneticist at Trinity College Dublin in Ireland. That barrier, tightly knit cells lining blood vessels, typically keeps riffraff out of the brain, like bouncers guarding a nightclub. If the barrier breaks down, bloodborne viruses, cells and other interlopers can sneak into the brain’s tissues and wreak havoc, says Avindra Nath, a neurologist at the National Institutes of Health in Bethesda, Md. It’s too early to say definitively whether that’s happening in people with long COVID, but the new study provides evidence that “brain fog has a biological basis,” says Nath, who wasn’t involved with the work. That alone is important for patients, he says, because their symptoms may be otherwise discounted by physicians. For some people, brain fog can feel like a slowdown in thinking or difficulty recalling short-term memories, Campbell says. For example, “patients will go for a drive, and forget where they’re driving to.” That might sound trivial, he says, but it actually pushes people into panic mode. © Society for Science & the Public 2000–2024.

Keyword: Attention; Learning & Memory
Link ID: 29192 - Posted: 03.16.2024

By Jan Hoffman The death certificate for Ryan Bagwell, a 19-year-old from Mission, Texas, states that he died from a fentanyl overdose. His mother, Sandra Bagwell, says that is wrong. On an April night in 2022, he swallowed one pill from a bottle of Percocet, a prescription painkiller that he and a friend bought earlier that day at a Mexican pharmacy just over the border. The next morning, his mother found him dead in his bedroom. A federal law enforcement lab found that none of the pills from the bottle tested positive for Percocet. But they all tested positive for lethal quantities of fentanyl. “Ryan was poisoned,” Mrs. Bagwell, an elementary-school reading specialist, said. As millions of fentanyl-tainted pills inundate the United States masquerading as common medications, grief-scarred families have been pressing for a change in the language used to describe drug deaths. They want public health leaders, prosecutors and politicians to use “poisoning” instead of “overdose.” In their view, “overdose” suggests that their loved ones were addicted and responsible for their own deaths, whereas “poisoning” shows they were victims. “If I tell someone that my child overdosed, they assume he was a junkie strung out on drugs,” said Stefanie Turner, a co-founder of Texas Against Fentanyl, a nonprofit organization that successfully lobbied Gov. Greg Abbott to authorize statewide awareness campaigns about so-called fentanyl poisoning. “If I tell you my child was poisoned by fentanyl, you’re like, ‘What happened?’” she continued. “It keeps the door open. But ‘overdose’ is a closed door.” © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29191 - Posted: 03.16.2024

By Alejandra Manjarrez People wear gloves when making a snowman for a reason: Handling cold stuff can hurt. A new mouse study reveals what may be a key player in this response: a protein already known to enable sensory neurons in worms to detect cold. New evidence published this week in Nature Neuroscience confirms that this protein has the same function in mammals. “The paper is exciting,” says Theanne Griffith, a neuroscientist at the University of California, Davis who was not involved in the research. She notes that the protein, called GluK2, is found in the brain and has “traditionally been thought to play a major role in learning and memory.” The new work shows that elsewhere in the body, it has an unsuspected and “completely divergent role.” We perceive touch, pain, and temperature thanks to a system of nerves that extends throughout our bodies. Researchers have identified skin sensors that detect hot and warm stimuli. Cold sensors, though, have proved more challenging to find. Researchers have proposed various candidates but found limited and contradictory evidence for their function. An ion channel named TRPM8 is the exception. Famous for detecting the “cool” sensation of menthol, it also detects cold temperatures and helped earn its discoverers the Nobel Prize in Physiology or Medicine in 2021. “Nobody questions that TRPM8 is a cold sensor,” says sensory neurobiologist Félix Viana of the Institute for Neuroscience in Alicante, Spain. But it could not be the whole story. It works most efficiently at temperatures above roughly 10°C, and mice lacking the gene for TRPM8 can still detect very cold temperatures. A few years ago, University of Michigan neuroscientists Shawn Xu and Bo Duan and their colleagues found another candidate: a protein on certain sensory neurons in the tiny roundworm Caenorhabditis elegans that causes the animals to avoid temperatures between 17°C and 18°C, which are colder than their preferred temperatures. Preliminary data from that study hinted that the equivalent protein in mammals, GluK2, also allowed mice to sense cold.

Keyword: Pain & Touch
Link ID: 29190 - Posted: 03.16.2024

By Ben Seal When Oregon’s first psilocybin service center opened in June 2023, allowing those over 21 to take mind-altering mushrooms in a state-licensed facility, the psychedelic revival that had been unfolding over the past two decades entered an important new phase. Psilocybin is still illegal on the federal level. But now, as researchers explore the therapeutic potential of psilocybin and other psychedelics, including LSD and MDMA (also known as Molly or ecstasy), legal reform efforts are spreading across the country — raising tensions between state and federal laws. As a class, psychedelic drugs were outlawed in the United States by the Controlled Substances Act of 1970. The act designated psychedelics as Schedule I drugs — the most restrictive classification, indicating a high potential for abuse and no accepted medical use. That status limits research to federally approved scientific studies and restricts federal funding to research with “significant medical evidence of a therapeutic advantage.” Despite these limitations, researchers have demonstrated the potential of psychedelics in the treatment of post-traumatic stress disorder, major depressive disorder, anxiety and addiction. A 2020 systematic review of recent research found that psychedelics can lessen symptoms linked to a variety of mental health conditions. While that review found no serious, long-term adverse physical or psychological effects from ingesting psychedelics, more research is needed on the latter. Today, decades after research on the effects of hallucinogens on the brain was sidelined by the act, academic and cultural interest in psychedelics is on the rise. More than 60 percent of Americans now support regulated therapeutic use of psychedelics, while nearly half support decriminalization, and nearly 45 percent support spiritual and religious use. An estimated 5.5 million US adults use psychedelics each year.

Keyword: Depression; Drug Abuse
Link ID: 29189 - Posted: 03.16.2024

By Jake Buehler In the middle of the night in a humid coastal rainforest, a litter of pink, hairless babies snuggle with their mother. They stir and squeak for milk, their mother obliges, and they are sated. But these are no puppies or cubs. They are snake-shaped amphibians, far closer to frogs than foxes. These ringed caecilian moms feed their hatchlings a kind of “milk” brewed in the reproductive tract, researchers report in the March 8 Science. The long, cylindrical creatures are the first egg-laying amphibians known to feed hatchlings this way. The discovery suggests the evolution of parental care across animal life is more diverse than researchers thought. For an animal with so few discernable external features, caecilians are a fount of strange biology. Caecilians are elusive, legless, burrowing amphibians that are nearly blind (SN: 6/19/17). Some species, like the ringed caecilian (Siphonops annulatus) in the new study, have poisonous slime, may be venomous and feed their own skin to their young (SN: 7/3/20). Herpetologist Carlos Jared of the Instituto Butantan in São Paulo and his colleagues have been studying these eccentric animals for years. In previous studies, the team noticed that ringed caecilian hatchlings, which live their first two months out of the egg in their mother’s care, spent much of their time around the end of her body near the shared opening of the reproductive, digestive and urinary systems — an anatomical part called the vent. The female would periodically expel a thick fluid from the vent, which the young would enthusiastically feed on. “Some [young] even stuck their heads inside this opening,” Jared says. In the new work, the team collected 16 females and their newly hatched litters from Bahia state in Brazil, bringing them into the lab for observation. There, the researchers recorded the amphibians’ interactions, accumulating over 240 hours of video footage. The team recorded 36 feedings, which often involved the babies wriggling and nibbling at their mother’s vent while making high-pitched noises. Mom would then raise that end of her body and release the fluid. This happened up to six times per day and appeared to be in response to the babies’ pleas. © Society for Science & the Public 2000–2024.

Keyword: Sexual Behavior
Link ID: 29188 - Posted: 03.09.2024

By Regina G. Barber, Anil Oza, Ailsa Chang, Rachel Carlson Neuroscientist Nathan Sawtell has spent a lot of time studying a funky looking electric fish characterized by its long nose. The Gnathonemus petersii, or elephantnose fish, can send and decipher weak electric signals, which Sawtell hopes will help neuroscientists better understand how the brain pieces together information about the outside world. But as Sawtell studied these electric critters, he noticed a pattern he couldn't explain: the fish tend to organize themselves in a particular orientation. "There would be a group of subordinates in a particular configuration at one end of the tank, and then a dominant fish at the other end. The dominant fish would swim in and break up the group, and they would scatter. A few seconds later, the group would coalesce and it would stay there for hours at a time in this stationary configuration," Sawtell, who runs a lab at Columbia University's Zuckerman Institute says. Initially Sawtell and his team couldn't put together why the fish were always hanging out in this configuration. "What could they really be talking to each other about all of this time?" A new study released this week in Nature by Sawtell and colleagues at Columbia University could have one potential answer: the fish are creating an electrical network that is larger than any field an individual fish can muster alone. In this collective field, the whole school of fish get instantaneous information on changes in the water around them, like approaching predators. Rather than being confused by the flurry of electric signals from other fish, "these fish were clever enough to exploit the pulses of group members to sense their environment," Sawtell says. © 2024 npr

Keyword: Pain & Touch
Link ID: 29187 - Posted: 03.09.2024

By Pam Belluck One of the few treatments the Food and Drug Administration has approved for amyotrophic lateral sclerosis has failed a large clinical trial, and its manufacturer said Friday that it was considering whether to withdraw it from the market. The medication, called Relyvrio, was approved less than two years ago, despite questions about its effectiveness in treating the severe neurological disorder. At the time, the F.D.A.’s reviewers had concluded there was not yet sufficient evidence that the medication could help patients live longer or slow the rate at which they lose functions like muscle control, speaking or breathing without assistance. But the agency decided to greenlight the medication instead of waiting two years for results of a large clinical trial, citing data showing the treatment to be safe and the desperation of patients with a disease that often causes death within two to five years. Since then, about 4,000 patients in the United States have received the treatment, a powder that is mixed with water and either drunk or ingested through a feeding tube and carries a list price of $158,000 a year. Now, results of the 48-week trial of 664 patients are in, and they showed that the treatment did not work better than a placebo. “We are surprised and deeply disappointed,” Justin Klee and Joshua Cohen, the co-chief executive officers of Amylyx Pharmaceuticals, the treatment’s manufacturer, said in a statement. They said they would announce their plans for the medication within eight weeks, “which may include voluntarily withdrawing” it from the market. “We will be led in our decisions by two key principles: doing what is right for people living with A.LS., informed by regulatory authorities and the A.L.S. community, and by what the science tells us,” Mr. Klee and Mr. Cohen said. There are only two other approved A.L.S. medications in the United States: riluzole, approved in 1995, which can extend survival by several months, and edaravone, approved in 2017, which can slow progression by about 33 percent. © 2024 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 29186 - Posted: 03.09.2024

By Daniel Gilbert and David Ovalle The U.S. Food and Drug Administration approved the weight-loss drug Wegovy as a treatment to reduce cardiovascular risk in adults who are overweight, the first approval of its kind that could dramatically expand the already huge market for the drug. Wegovy, which has the same active ingredient as diabetes drug Ozempic, already had FDA approval to treat patients who are obese or overweight. It has become a cultural sensation and a blockbuster, bringing in billions of dollars in revenue for its manufacturer, Novo Nordisk. “Wegovy is now the first weight loss medication to also be approved to help prevent life-threatening cardiovascular events in adults with cardiovascular disease and either obesity or overweight,” John Sharretts, a director in the FDA’s Center for Drug Evaluation and Research, said in a statement Friday. “We recognize how important this moment is for the millions of people who live with excess weight or obesity and known heart disease, and we will continue to advance options that put their needs first,” Doug Langa, head of Novo Nordisk’s North American operations, said in a statement. The FDA’s expansion of Wegovy’s regulatory label comes after a closely watched clinical trial last year found that the drug dramatically reduced the risk of heart problems for overweight people. In a five-year study of more than 17,600 patients, Wegovy cut the risk of strokes, heart attacks and other cardiovascular problems by 20 percent among overweight adults with a history of heart disease. Expanding Wegovy’s regulatory label could also entice more insurers to cover the pricey drug, according to researchers and Wall Street analysts. “The result will pressure insurers and the federal government to cover this medication,” said Harlan Krumholz, a cardiologist at the Yale School of Medicine. “It will be increasingly difficult to deny people access to these medications, as this is not about appearance but concerns health.”

Keyword: Obesity
Link ID: 29185 - Posted: 03.09.2024

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 Lisa Sanders, M.D. Surrounded by the detritus of a Thanksgiving dinner, the woman was loading the dishwasher when a loud thump thundered through the house. She hurried out of the kitchen to find her husband of 37 years sitting on the second-floor landing. Her son and son-in-law, an emergency-room doctor, crouched at his side. Her husband protested that he was fine, then began to scooch himself on his bottom into the bedroom. The two young men helped him to his feet. The man’s body shook with a wild tremor that nearly knocked him down again. “I was getting into bed and fell,” he explained — though the bed was too far away to make this at all likely. “Get some sleep,” the woman said gently once her husband was settled in the bed. “We’ll go to the hospital in the morning.” Her daughter and son-in-law had arrived that morning and already mentioned the change they noticed in the 70-year-old senior. The normally gregarious man was oddly quiet. And the tremor he had for as long as they could remember was much more prominent. His hands shook so much he had trouble using his fork and ended up eating much of his Thanksgiving dinner with his fingers. And now this fall, this confusion — they were worried. His wife was also worried. Just after Halloween, she traveled for business, and when she came back, her husband was much quieter than usual. Even more concerning: When he spoke, he didn’t always make sense. “Have you had a stroke?” she asked her first day home. He was fine, he insisted. But a few days later she came home from work to find his face covered with cuts. He was shaving, he said, but his hand shook so much that he kept cutting himself. “There is something wrong with me,” he acknowledged. It was Thanksgiving week, but she was able to get him an appointment at his doctor’s office the next day. They were seen by the physician assistant (P.A.). She was kind, careful and thorough. After hearing of his confusion, she asked the man what day it was. “Friday?” he offered uncertainly. It was Wednesday. Could he touch his finger to his nose and then to her finger, held an arm’s length away? He could not. His index finger carved jagged teeth in the air as he sought his own nose then stretched to touch her finger. And when she asked him to stand, his entire body wobbled dangerously. “It’s all happened so quickly,” the man’s wife said. The P.A. reviewed his lab tests. They were all normal. She then ordered an M.R.I. of the brain. That, she explained, should give them a better idea of what direction to take. But, she added, if he falls or seems © 2024 The New York Times Company

Keyword: Neurotoxins; Movement Disorders
Link ID: 29182 - 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 Emily Anthes Colombia is a bird watcher’s paradise. Its stunningly diverse ecosystems — which include mountain ranges, mangrove swamps, Caribbean beaches and Amazonian rainforests — are home to more avian species than any other country on Earth. So when Hamish Spencer, an evolutionary biologist at the University of Otago in New Zealand, booked a bird-watching vacation in Colombia, he was hoping to spot some interesting and unusual creatures. He got more than he bargained for. During one outing, in early January 2023, the proprietor of a local farm drew his attention to a green honeycreeper, a small songbird that is common in forests ranging from southern Mexico to Brazil. But this particular green honeycreeper had highly unusual plumage. The left side of its body was covered in shimmering spring-green feathers, the classic coloring for females. Its right side, however, was iridescent blue, the telltale marker of a male. The bird appeared to be a bilateral gynandromorph: female on one side and male on the other. “It was just incredible,” Dr. Spencer said. “We were lucky to see it.” Gynandromorphism has been documented in a variety of birds, as well as insects, crustaceans and other organisms. But it’s a relatively rare and poorly understood phenomenon. The bird Dr. Spencer saw in Colombia is only the second known case of bilateral gynandromorphism in a green honeycreeper — and the first documented in the wild. © 2024 The New York Times Compan

Keyword: Sexual Behavior
Link ID: 29180 - Posted: 03.07.2024