By Rachel E. Gross The first question Sophie Davies had was: Will it affect my memory? In the three weeks since giving birth, Ms. Davies had been in a downward spiral. She checked herself into the mother-and-baby unit of her hospital in East Anglia, England, where doctors ratcheted up the dose of Prozac she took to manage her obsessive-compulsive disorder. But every morning she woke up in tears, and every time she looked at her baby boy, she felt hollow with guilt. “I’m never going to be able to be a mom,” she recalled thinking, “or if I am, I’m not going to be able to be a good one.” A month in, a hospital worker suggested she try a headset that used an electric current to treat depression. The word “electric” gave Ms. Davies, then 34, pause. It sounded like electroconvulsive therapy, or ECT, the scary-sounding treatment that triggers seizures and can result in memory loss. This therapy was different. Transcranial direct-current stimulation, or tDCS, uses a weak electric current to shock the brain and does not produce seizures. “This is as far from ECT as a jet engine is from my bicycle,” Dr. Mark George, of the Medical University of South Carolina, where he is a leading expert in neuromodulation, a term that encompasses all therapies that use electricity to modify brain function. Ms. Davies did an internet search and confirmed that the side effects of tDCS — ringing in the ears, headaches and mild burns or irritation where the electrode pads touched the forehead — were generally transient and didn’t include amnesia. She decided to give it a try. In England, the brain stimulation device has been approved for treating depression since 2019. It can be prescribed by a doctor or purchased over the counter, where it sells for around $530. © 2026 The New York Times Company

Keyword: Depression; Brain imaging
Link ID: 30225 - Posted: 04.29.2026

Chris Simms Olfactory receptors in the mouse nose have been mapped out in unprecedented detail — overturning researchers’ understanding of how noses build a sense of smell. The research, published today in Cell1, shows how around 1,100 olfactory receptors expressed on sensory neurons are organized in tightly regulated spatial locations in the epithelial tissue that lines the nasal cavity. A second study2 provides a complementary atlas of olfactory receptor expression in the olfactory epithelium and their neural connections to the olfactory bulb in the brain. “For 30 years, we’ve taught students that the mouse olfactory epithelium is divided into a handful of broad zones, within which receptor choice is essentially random,” says Johan Lundström, a psychologist and experimental neuroscientist at the Karolinska Institute in Stockholm. In the study, researchers examined about five million neurons from hundreds of individual mice. They first used single-cell sequencing to identify which smell receptors were expressed by neurons in the nose, and then used spatial transcriptomics to map out where key genes were being expressed. This allowed them to pinpoint where the receptors are and show that they are always arranged in horizontal stripes running from the top of the nose to the bottom. “Each receptor adopts a particular position in the nose. Since there are a thousand positions in the nose, each receptor is expressed basically in a stripe that overlaps with other receptor stripes, in a thousand overlapping stripes,” says study co-author Sandeep Robert Datta, a neurobiologist at Harvard Medical School in Boston, Massachusetts. Datta and his colleagues propose that this spatial mapping is organized during development and is controlled by sets of genes. The authors found that a molecule called retinoic acid had a key role in this process. They discovered a gradient in the amount of retinoic acid present at different points in the nose. By tweaking how much this molecule was expressed, they showed that it helps to control gene activity, guiding each neuron to express the correct type of smell receptor for its location. © 2026 Springer Nature Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 30224 - Posted: 04.29.2026

By Siddhant Pusdekar Transcriptional changes are essential for converting new experiences into memories but may not be required to make memories last, a new study suggests. The findings, published in eNeuro in March, conflict with a model proposing that positive feedback loops of transcription can help maintain long-term memories, says study investigator Irina Calin-Jageman, professor of biological sciences at Dominican University. But they open up a set of hypotheses about how transcription maintains long-term memories and indicate that the handful of genes whose regulation persists for up to two weeks could be “really key,” she adds. The results, obtained in the sea slug Aplysia californica, are “one small step on our way to understanding this very important question of: What is the role of transcription in forming long-term memories?” says Wayne Sossin, distinguished James McGill professor of neurology and neurosurgery at McGill University, who is listed as a reviewer for the paper. Disproving models doesn’t “get the attention it deserves, I think, from the scientific community,” he says, but science is built on overturning theory. Irina Calin-Jageman and her colleagues focused on the transcriptional traces of a partially faded memory in the sea slug. When the animal feels threatened, it retracts a breathing apparatus on its back called a siphon. After traumatic experiences—such as induced shocks—the slug retracts its siphon for longer than usual, previous work showed. Also, sensory neurons in the pleural ganglia change their gene expression patterns and remain more excitable for up to 24 hours, and synaptic changes can last for several days to weeks, depending on the training. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30223 - Posted: 04.29.2026

By Emma Yasinski “Relapse is a part of recovery”: That’s a common refrain among professionals who treat substance use disorders. Many people who have completed treatment programs return to substance use and reenter treatment multiple times, after days, weeks or even years of sobriety. Marina Wolf, a behavioral neuroscientist at the Oregon Health & Science University, studies how cells in the brain respond to drug exposure in ways that can lead people to develop powerful cravings even months after they stop using drugs such as cocaine, opioids or alcohol. Specifically, she has focused on an aspect of this problem called cue-induced craving, in which people’s brains come to associate a cue — such as seeing a certain location where they previously used drugs — with the desire to use that drug. These learned associations, as she described in the 2025 Annual Review of Pharmacology and Toxicology, are caused by structural changes to the brain — neuroplasticity — as a result of drug use, including the strengthening of connections, called synapses, between specific nerve cells. These changes don’t disappear as soon as a person, or animal, stops using a drug. Cravings, in fact, can strengthen after abstinence, leaving a person vulnerable to resume using. How did you become interested in neuroplasticity and addiction? I never had any formal training in synaptic plasticity or addiction. As a graduate student and then a postdoctoral fellow, I worked on how neurons are regulated by the neurotransmitter dopamine, but we studied dopamine’s role in antipsychotic drug effects, not addiction. But when I was setting up my own lab in the early 1990s, I had a friend from graduate school who was involved in groundbreaking studies to work out synaptic plasticity mechanisms in the brain’s hippocampus, a region of the brain responsible for encoding memories. This was fascinating work that helped demonstrate a critical role for a neurotransmitter called glutamate in synaptic plasticity, so I followed it closely. © 2026 Annual Reviews

Keyword: Drug Abuse
Link ID: 30222 - Posted: 04.29.2026

By Gina Kolata Before the new obesity drugs came on the market, almost no one used the term food noise. Researchers studying and developing drugs like Ozempic, Wegovy, Mounjaro and Zepbound analyzed doses, side effects, weight loss and improvements in conditions such as diabetes, heart disease and sleep apnea. Incessant thoughts about food and internal dialogues about what to eat, what not to eat, when to eat, how to resist eating — these were not on the research agenda. But if the obesity-drug researchers weren’t talking about food noise, people taking GLP-1s had a lot to say about it. For as long as they could remember, users of the drugs said, they had been plagued by food noise. But they thought it was just a normal part of life. They thought everyone had it. Until they took one of the new drugs. Suddenly, food noise was silenced. And that effect is leading to new questions about the drugs. If researchers can clarify the source of this inner buzz and what makes it go away, that could lead to a clearer understanding of what causes obesity in the first place. ‘You Don’t Want the Salad’ People who struggle with their weight describe relentless thoughts of food. Lena Smith Parker, 53, of Hamden, Conn., spent decades dieting and regaining weight. All the while, she said, she was plagued by internal voices urging her to eat and shaming her for eating. © 2026 The New York Times Company

Keyword: Obesity
Link ID: 30221 - Posted: 04.29.2026

Nicola Davis Science correspondent It has long been known that dogs have less between their ears than wolves, but now research has suggested their brains started to get smaller at least 5,000 years ago. Experts say the results offer fresh insights into the domestication of our canine companions. However, the findings are unlikely to explain why your spaniel will only drink from a muddy puddle: the researchers say a reduction in brain size does not mean dogs are dafter than their wolf-like ancestors. “The way our dogs live nowadays doesn’t give them the opportunity to always express most of their intelligence,” said Dr Thomas Cucchi, first author of the study from the French National Centre for Scientific Research. “But they are extremely clever and domestication didn’t make them stupid, but made them really capable of reading us and communicating with us.” The relationship between humans and canines is ancient, with research revealing the oldest direct genetic evidence for domestic dogs dates back more than 15,000 years. But while a reduction in brain size is typically considered a hallmark of domestication, there has long been debate over exactly when dogs ended up with smaller brains than wolves, with some experts suggesting this may have occurred early in the dog-human relationship. However, others argue smaller brain size is not a hallmark of domestication but instead reflects the emergence of pedigree breeds in the last 200 years. Writing in the journal Royal Society Open Science, Cucchi and colleagues studied CT scans of the skulls of 22 prehistoric wolves and dogs, dating from 35,000 to 5,000 years ago, as well as CT scans from the skulls of 59 modern wolves and 104 modern dogs. The latter included different modern breeds as well as stray or “village” dogs, and dingoes. © 2026 Guardian News & Media Limited

Keyword: Evolution
Link ID: 30220 - Posted: 04.29.2026

By Yasemin Saplakoglu Every experience we have changes our brain, the way a ceramicist reshapes a slab of clay. Every corner we turn, every conversation we have, every shudder we feel causes cascading effects: Chemicals are released, electricity surges, the connections between brain cells tighten, and our mental models update. The brain is “incredibly plastic, and it stays that way throughout the lifespan of a human,” said Christine Grienberger (opens a new tab), a neuroscientist at Brandeis University. This plasticity, the quality of being easily reshaped, makes the brain really good at learning — a quintessential process that allows us to remember the plotline of a novel, navigate a new city, pick up a new language, and avoid touching a hot stove. But neuroscientists are still uncovering fundamental rules that describe how neuroplasticity reshapes brain connections. Recently, neuroscientists described a new form of neuroplasticity that might be helping the brain learn across a timescale of several seconds — long enough to capture the behavioral process of learning from a single experience. In two recent reviews, published in The Journal of Neuroscience (opens a new tab) and Nature Neuroscience (opens a new tab), they describe “behavioral timescale synaptic plasticity,” or BTSP. This type of learning in the hippocampus, the brain’s memory hub, is caused by an electrical change that affects multiple neurons at once and unfolds across several seconds. Researchers suspect that it may help the brain learn in a single attempt. “It’s pretty clear that [BTSP is] a strong, powerful mechanism that can lead to immediate memory formation,” said Daniel Dombeck, a neuroscientist at Northwestern University who was not involved with the theory’s development. “It’s something that has been missing in the field for a long time.” © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30219 - Posted: 04.26.2026

Katherine Bourzac Scientists have discovered that the unsung brain cells called astrocytes form extensive networks in the mouse brain1 — networks similar in some respects to the brain circuits formed by the more celebrated brain cells called neurons. The researchers compiled a whole-brain, 3D map of astrocyte networks, which the authors say is the first of its kind. It , shows that webs of the cells connect far-flung regions of the brain, allowing the cells to exchange molecules with each other over long distances. The ‘silent’ brain cells that shape our behaviour, memory and health “It’s a secret subway system we didn’t know was there,” says Shane Liddelow, a neuroscientist at NYU Grossman School of Medicine in New York City and a co-author of a paper published today in Nature describing the work. “This opens up a whole new avenue of investigation.” Astrocyte networks can bridge the brain’s hemispheres, and they display plasticity, reshaping their connections in response to sensory deprivation, the team found. The work is “a fundamentally important advance in our understanding of nervous system structure”, says David Lyons, a neurobiologist at the University of Edinburgh, UK, who was not involved with the research. He adds that so far, this new evidence of complex astrocyte networks raises more questions than it answers. “Clearly we are some way from understanding what the functional relevance and role of such [networks] is, but there are a myriad of possibilities.” © 2026 Springer Nature Limited

Keyword: Glia; Learning & Memory
Link ID: 30218 - Posted: 04.26.2026

By Calli McMurray Last Saturday, President Donald Trump issued an executive order outlining regulatory tweaks intended to “accelerate” U.S. research on and increase access to psychedelic drugs for mental health treatments. The measures target clinical research, not basic studies on how the drugs work. “This may not be the breakthrough the basic research community has been looking for,” says Shawn Lockery, professor of neuroscience at the University of Oregon. The order directs the U.S. Food and Drug Administration (FDA) to speed up review of psychedelic drugs and allots “at least $50 million” from the Department of Health and Human Services for state governments’ own psychedelics research programs. One section of the order, however, could eventually make it easier for basic researchers to access psychedelics for their work. The U.S. Drug Enforcement Agency (DEA) classifies most psychedelics—including psilocybin, MDMA and LSD—as Schedule I, meaning they have “no currently accepted medical use and a high potential for abuse.” Trump’s order calls for the U.S. attorney general to review “any product containing a Schedule I substance that has successfully completed Phase 3 clinical trials for a serious mental health disorder” and consider it for rescheduling to the less restrictive Schedule III. To study a Schedule I drug, researchers must apply for a license and, if approved, follow strict storage and security requirements. Approval can take up to a year, says Alex Kwan, professor of biomedical engineering at Cornell University, who studies psilocybin’s mechanism of action in the brain. “It’s a decent bar to get it. It’s not easy.” © 2026 Simons Foundation

Keyword: Drug Abuse; Depression
Link ID: 30217 - Posted: 04.26.2026

By Gina Kolata The Food and Drug Administration on Thursday approved a gene therapy that can cure a rare, inherited form of deafness. The treatment is the first to restore normal hearing in children who were born deaf. The maker of the therapy, Regeneron, plans to provide it free to any child who needs it. “We wanted to make a statement,” Dr. George Yancopoulos, Regeneron’s chief scientific officer said on Thursday morning. He explained that the company wants to be sure its treatment “would be able to reach its full potential and help as many people as possible.” Some gene therapies for other diseases, priced in the millions of dollars, have had dismal sales. The therapy called Otarmeni, is intended for children with otoferlin deafness, a rare form of hearing loss caused by a mutation in a single gene. The mutation destroys a protein in the inner ear that is needed to transmit sound to the brain. Although otoferlin deafness accounts for just 2 percent to 8 percent of congenital hearing loss, the new treatment “is groundbreaking,” Dr. Dylan Chan, a pediatric otolaryngologist at the University of California, San Francisco, said. He added, “This is the first time in history that there has been a medical therapy that has enabled deaf children to hear.” Dr. Chan has been a paid adviser to Regeneron and to Eli Lilly, which is also developing a gene therapy for otoferlin deafness. He is also a principal investigator for Lilly’s clinical trial of the treatment. © 2026 The New York Times Company

Keyword: Hearing; Genes & Behavior
Link ID: 30216 - Posted: 04.26.2026

By Jake Currie Chimpanzees and humans share 98 percent of their genomes, so what’s in that 2 percent that makes us uniquely human? According to a new study published in Science Advances, a tiny portion of these genes play an outsized role in our language skills—and Neanderthals had the same sequences. Subscribe to skip ads Featured Video These segments of the human genome, known as Human Ancestor Quickly Evolved Regions (HAQERs) are non-coding sequences that showed accelerated evolution after humans split from the ancestor they shared with apes. Even though they represent only 0.1 percent of our genes, they’re responsible for the neural “hardware” for language. “What we’re seeing is how a very small part of the genome can have an outsized influence, not just on who we were as a species, but on who we are as individuals,” study author Jacob Michaelson of the University of Iowa said in a statement. “These aren’t genes we’re talking about. They’re regulatory regions that act like the volume knob on genes.” The HAQERs also interact with another vital speech gene: FOXP2. Identified in 1998, FOXP2 is a transcription factor active in the development of the neural circuitry of language use, and mutations in the gene can cause speech problems. “So, if the HAQERs are like volume knobs that can be turned, FOXP2 is one of the hands that is turning these volume knobs,” Michaelson said. © Nautilus 2026

Keyword: Language; Evolution
Link ID: 30215 - Posted: 04.26.2026

By Nora Bradford If you were to imagine a waterfall, a misty cascade into an azure pool surrounded by towering trees might come to mind. That mental vision might also be accompanied by the imagined roar of water splashing down. But when it comes to our brains, does imagining a waterfall activate different areas compared with seeing or hearing one in real life? For both sounds and sights, the overlap between imagination and perception appears not in brain areas linked to a single sense, but in high-level areas that accept multiple types of sensory inputs, researchers report March 31 in Neuron. For years, cognitive neuroscientist Rodrigo Braga has been working to determine whether the human brain is processing mental imagery through hearing and other senses or whether something else is at play. “When I was a teenager, I remember the first time realizing that there’s like a voice I can hear in my head and thinking, ‘Oh, that’s really strange’,” says Braga, of Northwestern University Feinberg School of Medicine in Chicago. In this study, he and his colleagues prompted eight participants to imagine scenes, faces, someone else speaking, internal monologues and sounds while in an MRI scanner. The small number of individuals allowed the researchers to collect hours of MRI data to create individualized brain maps rather than averaging across individuals. This technique allowed the team to reliably find individual variation in brain activity during imagination. © Society for Science & the Public 2000–2026.

Keyword: Consciousness; Attention
Link ID: 30214 - Posted: 04.26.2026

Hannah Critchlow About 2 billion years ago, evolution performed an improbable experiment. A larger ancestral cell engulfed a smaller bacterium. It should have been a meal. Instead, it became a merger. The bacterium survived inside its host, and together they forged one of the most consequential partnerships in the history of life. The host offered shelter and access to oxygen. The bacterium supplied something revolutionary: a vastly more efficient way to generate energy. From this intimate alliance emerged the eukaryotic cell – and with it, the possibility of complex life. Every plant, animal and thinking being traces its lineage back to that ancient symbiosis. Our capacity for reflection, imagination and doubt rests upon what was once a free-living microbe. We call these descendants mitochondria. They persist in nearly every cell of our bodies, hundreds to thousands at a time. In total, we carry an estimated 10 million billion of them – collectively accounting for roughly a 10th of our body mass. Red blood cells are the exception: they lack mitochondria, which maximises oxygen transport. Almost every other cell depends on them absolutely. Neurons are especially demanding hosts. Each contains thousands of mitochondria, occupying up to 40 per cent of its volume. These rod-shaped structures are often described as the cell’s powerhouses. Through aerobic metabolism, they generate most of the chemical energy that keeps cells alive and functioning – the molecular fuel that sustains every biological process. Although the brain represents just 2 per cent of body weight, it consumes about 20 per cent of our energy at rest. Every perception, memory, emotion and idea is metabolically expensive. Thought itself is an energy-hungry act. Weight for weight, our brains are more mitochondrial than neural. This is more than a biological curiosity. It suggests that cognition is inseparable from metabolism – that the mind is not only shaped by networks of neurons but by networks of energy. © Aeon Media Group Ltd. 2012-2026.

Keyword: Biomechanics; Evolution
Link ID: 30213 - Posted: 04.22.2026

Ian Sample Science editor A married couple who met over a dissected brain and went on to create the first approved gene therapy for blindness have been awarded one of the most lucrative prizes in science. Molecular biologist Jean Bennett and ophthalmologist Albert Maguire share the $3m (£2.2m) Breakthrough prize for life sciences with physician Katherine High for the 25-year-long project, during which the couple adopted a pair of dogs they had treated for blindness. The therapy, named Luxturna, was approved in the US in 2017 and has transformed the lives of people born with Leber congenital amaurosis (LCA), a genetic disorder that typically causes total blindness by early adulthood. Proof that the therapy worked came in a clinical trial in which one patient described seeing their child’s face for the first time, the fine grain in wooden furniture and branches waving in the wind. Other patients reported similar profound improvements. Nine slices of bread toasted and burned to different degrees, from white to blackened. “I was overwhelmed,” said Bennett, who is now retired from the University of Pennsylvania. “It was one of the most miraculous eureka moments you can imagine.” Bennett said it was a “tremendously exciting time” for scientific and medical research, but warned that the US administration’s attacks on science could “cause damage for generations to come”, leading her to fear a brain drain that the country would struggle to recover from. “Agendas have become politicised, government agencies that support basic and applied research have been undermined, knowledgable advisers and experts have been dismissed or have fled and revised guidelines contradict decades of rigorous research,” she said. © 2026 Guardian News & Media Limited

Keyword: Vision
Link ID: 30212 - Posted: 04.22.2026

By Chand Chandrasekaran Decisions emerge from coordinated activity patterns across many brain areas. The challenge we face as neuroscientists is figuring out how. Technologies such as Neuropixels and optical imaging enable recordings from populations of neurons across many brain areas, leading to enormously impressive datasets with thousands of neurons. But making sense of these data to uncover the computations underlying decision-making has proved elusive. I think it is a great time for the field to design experiments that match the ambition of our tools. By designing decision-making tasks that vary along multiple dimensions and truly challenge our animals, we might finally understand how multiple brain areas coordinate to drive decisions. The starting point of most decision-making experiments is to get animals to perform a task for rewards, such as juice or food. It is often tempting to train the animal to do “something simple” because the training is easy and quick. Later we can get to the “exciting stuff”: Go in with a kitchen sink of experimental tools to collect neurophysiological data and/or perturb the system and use mathematical tools to uncover how activity in the brain leads to the behavior of interest. Though this approach sounds great in principle, analyzing the neural data associated with simple behavioral tasks can be challenging for multiple reasons. First, when the behavior is too simple, the brain does not need to compute much. When many areas could solve a problem, often they do: Relevant signals pop up all over the brain, leaving us with the somewhat puzzling conclusion that the behavior is global. But some tasks may be too trivial to require different computations from different areas, so it’s unsurprising that many areas look similar in such contexts. Second, animals perform simple tasks quickly, generating only a narrow window of neural activity from which to try to make sense of how they reached a decision. You might be left with just 50 milliseconds of potentially very noisy neural data from which to understand decision-related computations. © 2026 Simons Foundation

Keyword: Attention
Link ID: 30211 - Posted: 04.22.2026

Jon Hamilton It's often called the mind's eye. "I can look at an object in the world around me, but I can also close my eyes and imagine the object," says Varun Wadia, a brain scientist at Cedars-Sinai Medical Center and the California Institute of Technology. That sort of visual imagination, Wadia says, is what allows most people to conjure the face of a loved one or navigate to work using a mental map. For 'time cells' in the brain, what matters is what happens in the moment Shots - Health News For 'time cells' in the brain, what matters is what happens in the moment But its neural underpinnings were a mystery until Wadia and a team reported in the journal Science that imagined and perceived objects appear to activate the same neurons and use the same neural code. "This has not been demonstrated before at the neural level," says Kalanit Grill-Spector, a psychology professor at Stanford University's Wu Tsai Neurosciences Institute, who was not involved in the research. With these insights, she says, scientists are one step closer to building computer models that can simulate vision as well as vision disorders like macular degeneration. These models, in turn, could help researchers develop prosthetic devices to restore sight. The research also helps explain how the brain uses imagination to augment visual information, says Thomas Naselaris, a neuroscientist at the University of Minnesota. © 2026 npr

Keyword: Vision; Consciousness
Link ID: 30210 - Posted: 04.22.2026

Ian Sample Science editor Changes to microbes that live in the gut can identify people at greater risk of Parkinson’s disease long before symptoms develop, according to work that also raises hopes for new therapies. Researchers discovered signature changes in the gut microbiome that are more pronounced in people with a genetic risk for Parkinson’s and even more stark in those diagnosed with the disease. The signature could help doctors spot patients at risk of Parkinson’s years before they display clear symptoms and suggests that healthier diets and treatments that reshape the microbiome might prevent or delay the disease. Prof Anthony Schapira, the head of clinical and movement neurosciences at University College London and lead investigator on the study, said it was the first time a microbial signature in Parkinson’s patients had been seen in people with a genetic susceptibility but had yet to develop symptoms. The signature appears to become stronger as the disease progresses. “These same changes can be found in a small proportion of the general population that may put them at increased risk,” Schapira said. Cases of Parkinson’s have doubled in the past 25 years, with more than 8.5 million people globally now living with the condition. The disease causes progressive brain damage, leading to tremors, slow movement and stiff and inflexible muscles. Patients often experience depression, anxiety, sleep and memory problems, and difficulty with balance. © 2026 Guardian News & Media Limited

Keyword: Parkinsons
Link ID: 30209 - Posted: 04.22.2026

By Bethany Brookshire It’s easy to think of the human body as a single, fully integrated unit. After all, stub your toe all the way at one end of your body, and your brain registers it at the other. A suite of muscles works together to hop up-and-down and the lungs fill with air to expel curses from your mouth. In this moment, your body is one organism, one set of cells all pulling together against the world — and whatever it was that hurt your toe. But while our cells all work together to help us walk, eat and argue with each other on the internet, they are not all pulling together toward the same goal all the time. Each one of the body’s 30 trillion to 40 trillion human cells is its own world, with its own set of DNA that accumulates its own changes over time. These mutations can mean nothing, but they can also mean everything. While many mutations are inert, others cause harm. Still others bring hope, and could correct some of the body’s problems, science writer Roxanne Khamsi explains in Beyond Inheritance. The book draws on the latest research across multiple fields of science to show that mutations are with us throughout our lives, shaping our health and our lifespans. Many people might think of mutations as things that arise and take over only in times of trouble such as cancer. Otherwise, mutation is something that matters only if it’s passed down to the next generation — whether it produces a new eye color or a serious genetic disorder. But mutations do far more than determine what we look like when we’re born and the manner in which we die, Khamsi argues. “Our genetic destinies are not necessarily defined by what we inherit from our biological parents,” she writes. © Society for Science & the Public 2000–2026.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 30208 - Posted: 04.22.2026

Miryam Naddaf By analysing more than a million brain cells, researchers have uncovered widespread differences in patterns of gene activity between male and female brains. The work, which defined sex on the basis of a person’s combination of sex chromosomes, could help to explain why the risk of developing some brain conditions — such as schizophrenia and Alzheimer’s disease — differs between males and females. Although the differences were subtle, the team identified more than 100 genes that showed consistent variation in their expression between males and females across several brain regions. The work was published on 16 April in Science1. “Having these gene-expression signatures provides a molecular handle to understanding the biology of how the brains of men and women might be functioning slightly differently in the context of the different hormonal environments that their bodies produce,” says Jessica Tollkuhn, a neuroscientist and molecular biologist at Cold Spring Harbor Laboratory in New York. She adds that “understanding sex differences in disease susceptibility could lead to better treatments to benefit everyone”. Subtle differences Previous studies2,3 have documented sex differences when it comes to a person’s risk of developing various neurological conditions. For example, schizophrenia, attention deficit hyperactivity disorder (ADHD) and Parkinson’s disease are more common in biological males — who typically have XY sex chromosomes. By contrast, Alzheimer’s disease and mood disorders such as depression and anxiety tend to be more common in females, whose sex chromosomes are usually XX. © 2026 Springer Nature Limited

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 30207 - Posted: 04.18.2026

By Pam Belluck Since the approval of new Alzheimer’s drugs in recent years, there has been a lingering question: While data indicated that they could modestly slow cognitive decline for some patients, would that effect be meaningful or too slight to make difference? A new review of research spanning a decade, published on Wednesday, concluded that the clinical benefit of these and similar drugs is negligible. But the way the review was conducted spurred heated criticism from many Alzheimer’s experts, including some who had been skeptical of some of them. The review, published by Cochrane, an international network of health researchers, evaluated studies that were conducted on seven monoclonal antibody drugs developed over the last two decades to target amyloids, proteins that form plaques in the brains of people who have Alzheimer’s disease. Some Alzheimer’s experts said the conclusions were meaningless because the review swept under one umbrella drugs that had shown very dissimilar results and worked differently. The experts noted that data from the two most recent drugs studied — Leqembi and Kisunla — showed they could slow cognitive decline, which led to approval from the Food and Drug Administration and made them the only anti-amyloid drugs available to patients. But a vast majority of the studies analyzed in the review involved four earlier drugs that had failed clinical trials or were never approved and a fifth drug that was pulled from the market. “The problem with the review is the mix of ingredients,” said Dr. Jason Karlawish, a director of the Penn Memory Center at the University of Pennsylvania, who has been skeptical or cautious toward some of the drugs over the years. “They took some of the rotten ingredients and mixed it in with the fresh food, and the result is a stinky stew.” © 2026 The New York Times Company

Keyword: Alzheimers
Link ID: 30206 - Posted: 04.18.2026