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By Casey Schwartz Kay Redfield Jamison arrives punctually at a towering marble statue of Jesus Christ in the entrance of the old hospital building on Johns Hopkins Medical Campus. Next to it, two guest books are left open to receive the wishes and prayers of those who pass through these halls. “Dear God please help our daughter feel better. …” “Dear Lord, please heal my grandpa and let him live happily. …” This building, decorated with rows of oil paintings of Hopkins doctors and nurses through the ages, is redolent of the history of healing. The desperate, uncertain, even heroic attempt to heal is at the center of Jamison’s new book, “Fires in the Dark: Healing the Unquiet Mind,” out on May 23 from Knopf. “If I could have subtitled it ‘A Love Song to Psychotherapy,’ I would have,” she said. Jamison, 76, her blond hair cut into a bob, wears a colorful floral dress as she makes her way through hallways filled with people in scrubs to a quiet corridor reserved for psychiatry. She is the co-director of the Center for Mood Disorders and a professor of psychiatry. Her bookcase displays her many publications: her psychobiography of the poet Robert Lowell, which was nominated for the Pulitzer Prize, and her books on suicide, on exuberance and on the connection between mania and artistic genius. And, of course, her best-known work, “An Unquiet Mind,” a memoir she published in 1995 in which she went public with her own manic depression, at considerable personal cost. Jamison had been a thriving, sporty high school senior in the Pacific Palisades neighborhood of Los Angeles until suddenly, falling into a deep depression after a mild mania, “I couldn’t count on my mind being on my side,” she said. She was bewildered by what she was going through. Her high school English teacher handed her a book of poems by Robert Lowell, who had struggled all his life with manic-depression, and with whom she felt an instant connection. That same teacher also gave her “Sherston’s Progress,” by the English poet Siegfried Sassoon. More than fifty years later, Sassoon’s book would become one of the central inspirations of “Fires in the Dark.” © 2023 The New York Times Company

Keyword: Schizophrenia; Depression
Link ID: 28792 - Posted: 05.23.2023

By Marla Broadfoot In Alexandre Dumas’s classic novel The Count of Monte-Cristo, a character named Monsieur Noirtier de Villefort suffers a terrible stroke that leaves him paralyzed. Though he remains awake and aware, he is no longer able to move or speak, relying on his granddaughter Valentine to recite the alphabet and flip through a dictionary to find the letters and words he requires. With this rudimentary form of communication, the determined old man manages to save Valentine from being poisoned by her stepmother and thwart his son’s attempts to marry her off against her will. Dumas’s portrayal of this catastrophic condition — where, as he puts it, “the soul is trapped in a body that no longer obeys its commands” — is one of the earliest descriptions of locked-in syndrome. This form of profound paralysis occurs when the brain stem is damaged, usually because of a stroke but also as the result of tumors, traumatic brain injury, snakebite, substance abuse, infection or neurodegenerative diseases like amyotrophic lateral sclerosis (ALS). The condition is thought to be rare, though just how rare is hard to say. Many locked-in patients can communicate through purposeful eye movements and blinking, but others can become completely immobile, losing their ability even to move their eyeballs or eyelids, rendering the command “blink twice if you understand me” moot. As a result, patients can spend an average of 79 days imprisoned in a motionless body, conscious but unable to communicate, before they are properly diagnosed. The advent of brain-machine interfaces has fostered hopes of restoring communication to people in this locked-in state, enabling them to reconnect with the outside world. These technologies typically use an implanted device to record the brain waves associated with speech and then use computer algorithms to translate the intended messages. The most exciting advances require no blinking, eye tracking or attempted vocalizations, but instead capture and convey the letters or words a person says silently in their head. © 2023 Annual Reviews

Keyword: Brain imaging; Language
Link ID: 28791 - Posted: 05.21.2023

Katharine Sanderson Researchers have developed an electronic skin that can mimic the same process that causes a finger, toe or limb to move when poked or scalded. The technology could lead to the development of a covering for prosthetic limbs that would give their wearers a sense of touch, or help to restore sensation in people whose skin has been damaged. The ‘e-skin’ was developed in the laboratory of chemical engineer Zhenan Bao at Stanford University in California. Her team has long been trying to make a prosthetic skin that is soft and flexible, but that can also transmit electrical signals to the brain to allow the wearer to ‘feel’ pressure, strain or changes in temperature. The latest work, published on 18 May in Science1, describes a thin, flexible sensor that can transmit a signal to part of the motor cortex in a rat’s brain that causes the animal’s leg to twitch when the e-skin is pressed or squeezed. “This current e-skin really has all the attributes that we have been dreaming about,” says Bao. “We have been talking about it for a long time.” In healthy living skin, mechanical receptors sense information and convert it into electrical pulses that are transmitted through the nervous system to the brain. To replicate this, an electronic skin needs sensors and integrated circuits, which are usually made from rigid semiconductors. Flexible electronic systems are already available, but they typically work only at high voltages that would be unsafe for wearable devices. To make a fully soft e-skin, Bao’s team developed a flexible polymer for use as a dielectric — a thin layer in a semiconductor device that determines the strength of the signal and the voltage needed to run the device. The researchers then used the dielectric to make stretchy, flexible arrays of transistors, combined into a sensor that was thin and soft like skin. © 2023 Springer Nature Limited

Keyword: Pain & Touch; Robotics
Link ID: 28790 - Posted: 05.21.2023

By Claudia Lopez Lloreda Ketamine is a powerful anesthetic and sometimes recreational drug that causes people to feel dissociated from their own bodies. Recent studies suggest the drug may help treat people with depression who have tried more conventional treatments without success. But there are major questions about what makes it work. Is it the weird dissociative experience? Some molecular effect on the brain? Or just the experience of being in a clinical trial? In a new study that is yet to be peer reviewed, researchers attempted to find the answer in a unique way: They gave volunteers ketamine while they were under general anesthesia, theoretically preventing the participants from going on a trip. The approach alleviated the subjects’ depression, but not any better than a placebo did. The authors interpret this as evidence that ketamine’s effects on depression are strongly tied to a patient’s experience of being seen by medical professionals. But other experts say the study’s implications may be more complicated. Ketamine causes “dissociative” effects such as out-of-body experiences. Patients sometimes also report visual and auditory hallucinations—the voices of friends and family members who aren’t there, for example. The dissociative effects of ketamine have been linked to a stronger antidepressant response, possibly by helping patients reframe their experience from an outside perspective. But it’s a problem for researchers running double-blinded clinical trials, as participants can usually tell whether they have received ketamine or a placebo. To disentangle the subjective experience of ketamine from the biochemical effects of the drug, researchers at Stanford University recruited 40 participants who were preparing to undergo general surgery and who also had mild to moderate depression. The scientists gave the volunteers ketamine or saline as placebo right after they were put under anesthesia, but before their surgery, essentially blinding them to any psychedelic or dissociative effects. Then, for the next 3 days, the researchers surveyed the participants on their depression symptoms, scoring them on such factors as sadness, loss of appetite, and lack of sleep.

Keyword: Depression; Drug Abuse
Link ID: 28789 - Posted: 05.21.2023

By David Ovalle It had been four days since Kevin Hargrove last took the medication that stilled his dangerous cravings. He awoke with a queasy stomach and achy muscles, then vomited on the sidewalk as he set off from his encampment under a D.C. bridge this month. Hargrove recently changed his Medicare-funded insurance company and was unable to fill his prescription for buprenorphine, the medication he has taken for years to treat his opioid addiction. The withdrawals proved too much. The 66-year-old found a dealer on the street, paid $6 for two pills he believed were codeine painkillers and washed them down with a can of Olde English 800 malt liquor. Less than an hour later, Hargrove passed out inside his sister’s Columbia Heights apartment, overdosing on what was suspected to be fentanyl. “Don’t tell me!” his sister cried. “You’ve been doing so well!” Hargrove’s story illustrates the challenges often faced by those struggling with opioid addiction — especially people of color — in receiving buprenorphine, a medication that public health experts believe should play a critical role in curbing an addiction-and-overdose crisis fueled by fentanyl. His overdose happened this month as a newly published national study from the Harvard T.H. Chan School of Public Health showed that White patients are up to 80 percent more likely to receive buprenorphine than Black patients, and that Black patients receive a more limited supply. “There are lots of totally counterproductive insurance restrictions on this drug, particularly for populations in which the need is the greatest,” said the study’s lead author, Michael L. Barnett, an associate professor of health policy and management at Harvard’s School of Public Health.

Keyword: Drug Abuse
Link ID: 28788 - Posted: 05.21.2023

By Yasemin Saplakoglu Memories are shadows of the past but also flashlights for the future. Our recollections guide us through the world, tune our attention and shape what we learn later in life. Human and animal studies have shown that memories can alter our perceptions of future events and the attention we give them. “We know that past experience changes stuff,” said Loren Frank, a neuroscientist at the University of California, San Francisco. “How exactly that happens isn’t always clear.” A new study published in the journal Science Advances now offers part of the answer. Working with snails, researchers examined how established memories made the animals more likely to form new long-term memories of related future events that they might otherwise have ignored. The simple mechanism that they discovered did this by altering a snail’s perception of those events. The researchers took the phenomenon of how past learning influences future learning “down to a single cell,” said David Glanzman, a cell biologist at the University of California, Los Angeles who was not involved in the study. He called it an attractive example “of using a simple organism to try to get understanding of behavioral phenomena that are fairly complex.” Although snails are fairly simple creatures, the new insight brings scientists a step closer to understanding the neural basis of long-term memory in higher-order animals like humans. Though we often aren’t aware of the challenge, long-term memory formation is “an incredibly energetic process,” said Michael Crossley, a senior research fellow at the University of Sussex and the lead author of the new study. Such memories depend on our forging more durable synaptic connections between neurons, and brain cells need to recruit a lot of molecules to do that. To conserve resources, a brain must therefore be able to distinguish when it’s worth the cost to form a memory and when it’s not. That’s true whether it’s the brain of a human or the brain of a “little snail on a tight energetic budget,” he said. All Rights Reserved © 2023

Keyword: Learning & Memory; Attention
Link ID: 28787 - Posted: 05.18.2023

Sara Reardon Researchers have identified a man with a rare genetic mutation that protected him from developing dementia at an early age. The finding, published on 15 May in Nature Medicine1, could help researchers to better understand the causes of Alzheimer’s disease and potentially lead to new treatments. For nearly 40 years, neurologist Francisco Lopera at the University of Antioquia in Medellín, Colombia, has been following an extended family whose members develop Alzheimer’s in their forties or earlier. Many of the approximately 6,000 family members carry a genetic variant called the paisa mutation that inevitably leads to early-onset dementia. But now, Lopera and his collaborators have identified a family member with a second genetic mutation — one that protected him from dementia until age 67. “Reading that paper made the hair on my arms stand up,” says neuroscientist Catherine Kaczorowski at the University of Michigan in Ann Arbor. “It’s just such an important new avenue to pursue new therapies for Alzheimer’s disease.” Lopera and his colleagues analysed the genomes and medical histories of 1,200 Colombians with the paisa mutation, which causes dementia around ages 45—50. They identified the man with the second mutation when he was 67 and had only mild cognitive impairment. When the researchers scanned his brain, they found high levels of the sticky protein complexes known as amyloid plaques, which are thought to kill neurons and cause dementia, as well as a protein called tau that accumulates as the disease progresses. The brain looked like that of a person with severe dementia, says study co-author Joseph Arboleda, an ophthalmologist at Harvard Medical School in Boston, Massachusetts. But a small brain area called the entorhinal cortex, which coordinates skills such as memory and navigation, had low levels of tau. © 2023 Springer Nature Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 28786 - Posted: 05.18.2023

By Meredith Wadman A groundbreaking epidemiological study has produced the most compelling evidence yet that exposure to the chemical solvent trichloroethylene (TCE)—common in soil and groundwater—increases the risk of developing Parkinson’s disease. The movement disorder afflicts about 1 million Americans, and is likely the fastest growing neurodegenerative disease in the world; its global prevalence has doubled in the past 25 years. The report, published today in JAMA Neurology, involved examining the medical records of tens of thousands of Marine Corps and Navy veterans who trained at Marine Corps Base Camp Lejeune in North Carolina from 1975 to 1985. Those exposed there to water heavily contaminated with TCE had a 70% higher risk of developing Parkinson’s disease decades later compared with similar veterans who trained elsewhere. The Camp Lejeune contingent also had higher rates of symptoms such as erectile dysfunction and loss of smell that are early harbingers of Parkinson’s, which causes tremors; problems with moving, speaking, and balance; and in many cases dementia. Swallowing difficulties often lead to death from pneumonia. About 90% of Parkinson’s cases can’t be explained by genetics, but there have been hints that exposure to TCE may trigger it. The new study, led by researchers at the University of California, San Francisco (UCSF), represents by far the strongest environmental link between TCE and the disease. Until now, the entire epidemiological literature included fewer than 20 people who developed Parkinson’s after TCE exposure. The Camp Lejeune analysis “is exceptionally important,” says Briana De Miranda, a neurotoxicologist at the University of Alabama at Birmingham who studies TCE’s pathological impacts in the brains of rats. “It gives us an extremely large population to assess a risk factor in a very carefully designed epidemiological study.”

Keyword: Parkinsons; Neurotoxins
Link ID: 28785 - Posted: 05.18.2023

By Leo Sands Just under half of obese adolescents administered the latest in a new generation of recently approved weight-loss drugs were no longer considered to be clinically obese by the end of a 16-month trial, a study found. The findings support a small but growing body of evidence that the drug semaglutide, which goes by the brand names of Ozempic and Wegovy, can be an effective treatment option for chronic weight management for a range of ages. Obesity rates for children and adolescents are now alarmingly high in many countries, with such significant implications for young lives that the World Health Organization considers childhood obesity “one of the most serious public health challenges of the 21st century.” The authors of the new peer-reviewed study, published Wednesday in the journal Obesity, found that semaglutide was “highly effective” in reducing body mass index among teens. The weights of 134 clinically obese adolescents were monitored for 68 weeks, with participants given a 2.4 milligram injection of semaglutide weekly. By the end of the study, 45 percent of the group recorded a drop in BMI to below the clinical threshold for obesity. Just 12 percent of participants in a separate group who received a placebo were no longer considered to be obese at the end of the trial. Both groups also got lifestyle counseling and had a daily goal of 60 minutes of moderate- to high-intensity physical activity.

Keyword: Obesity
Link ID: 28784 - Posted: 05.18.2023

By Cordula Hölig, Brigitte Röder, Ramesh Kekunnaya Growing up in poverty or experiencing any adversity, such as abuse or neglect, during early childhood can put a person at risk for poor health, including mental disorders, later in life. Although the underlying mechanisms are poorly understood, some studies have shown that adverse early childhood experience leaves persisting (and possibly irreversible) traces in brain structure. As neuroscientists who are investigating sensitive periods of human brain development, we agree: safe and nurturing environments are a prerequisite for healthy brain development and lifelong well-being. Thus, preventing early childhood adversity undoubtedly leads to healthier lives. Poverty and adversity can cause changes in brain development. Harms can come from exposure to violence or toxins or a lack of nutrition, caregiving, perceptual and cognitive stimulation or language interaction. Neuroscientists have demonstrated that these factors crucially influence human brain development. Advertisement We don’t know whether these changes are reversed by more favorable circumstances later in life, however. Investigating this question in humans is extremely difficult. For one, multiple biological and psychological factors through which poverty and adversity affect brain development are hard to disentangle. That’s because they often occur together: a neglected child often experiences a lack of caregiving simultaneously with malnutrition and exposure to physical violence. Secondly, a clear beginning and end of an adverse experience is hard to define. Finally, it is almost impossible to fully reverse harsh environments in natural settings because most of the time it is impossible to move children out of their families or communities.. © 2023 Scientific American

Keyword: Development of the Brain; Learning & Memory
Link ID: 28783 - Posted: 05.13.2023

By Ula Chrobak A couple of weeks after I adopted my dog, Halle, I realized she had a problem. When left alone, she would pace, bark incessantly, and ignore any treats I left her in favor of chewing my belongings. When I returned, I’d find my border collie mix panting heavily with wide, fearful eyes. As frustrated as I was, though, I restrained the urge to scold her, realizing her destruction was born out of panic. Halle’s behavior was a textbook illustration of separation anxiety. Distressed over being left alone, an otherwise perfectly mannered pup might chomp the couch, scratch doors, or relieve themselves on the floor. Problem behaviors like these tend to be interpreted as acts of willful defiance, but they often stem from intense emotions. Dogs, like humans, can act out of character when they are distressed. And, as with people, some dogs may be neurologically more prone to anxiety. So concluded a recent brain imaging study, published in PLOS One, in which researchers performed resting-state functional magnetic resonance imaging on 25 canines that were deemed behaviorally “normal,” and 13 that had been diagnosed with anxiety, based on a behavioral evaluation. The scans revealed that anxious dogs had stronger connections between several of five brain regions that the researchers called the anxiety circuit: the amygdala, frontal lobe, hippocampus, mesencephalon, and thalamus. The team also saw weaker connections between the hippocampus and midbrain in anxious dogs, which can signal difficulties in learning and might explain why the owners reported decreased trainability in these dogs. That the neurological architecture of anxious dogs seems to parallel the signatures of human anxiety comes as little surprise to many animal behavior experts.

Keyword: Emotions; Evolution
Link ID: 28782 - Posted: 05.13.2023

Jean Bennett Gene therapy is a set of techniques that harness DNA or RNA to treat or prevent disease. Gene therapy treats disease in three primary ways: by substituting a disease-causing gene with a healthy new or modified copy of that gene; turning genes on or off; and injecting a new or modified gene into the body. Get facts about the coronavirus pandemic and the latest research How has gene therapy changed how doctors treat genetic eye diseases and blindness? In the past, many doctors did not think it necessary to identify the genetic basis of eye disease because treatment was not yet available. However, a few specialists, including me and my collaborators, identified these defects in our research, convinced that someday treatment would be made possible. Over time, we were able to create a treatment designed for individuals with particular gene defects that lead to congenital blindness. This development of gene therapy for inherited disease has inspired other groups around the world to initiate clinical trials targeting other genetic forms of blindness, such as choroideremia, achromatopsia, retinitis pigmentosa and even age-related macular degeneration, all of which lead to vision loss. There are at least 40 clinical trials enrolling patients with other genetic forms of blinding disease. Gene therapy is even being used to restore vision to people whose photoreceptors – the cells in the retina that respond to light – have completely degenerated. This approach uses optogenetic therapy, which aims to revive those degenerated photoreceptors by adding light-sensing molecules to cells, thereby drastically improving a person’s vision. © 2010–2023, The Conversation US, Inc.

Keyword: Vision; Genes & Behavior
Link ID: 28781 - Posted: 05.13.2023

Scott Hensley In a split vote, advisers to the Food and Drug Administration recommended that the agency approve the first gene therapy for Duchenne muscular dystrophy, the most common form of the genetic illness. The vote, 8 to 6, came after a day of testimony from speakers for Sarepta Therapeutics, the maker of the gene therapy called SRP-9001, FDA scientists and families whose children have Duchenne muscular dystrophy. The question before the panel was whether the benefits for the treatment outweigh the risks. While the FDA is not bound by the recommendations of its outside advisers, it usually follows them. The agency is expected to decide by the end of May. Gene therapy for muscular dystrophy stirs hopes and controversy Duchenne muscular dystrophy is the most common inherited neuromuscular disorder among children. It affects an estimated 10,000 to 12,000 children in the U.S. The genetic condition mainly afflicts boys and leads to progressive muscle damage, loss of ability to movement and eventually death. Sarepta's treatment involves a single infusion of viruses that has been genetically modified to carry a gene to patients' muscles to produce a miniature version of a protein called dystrophin. Patients with Duchenne muscular dystrophy are missing the muscle-protecting protein or don't make enough of it. While not a cure, Sarepta argues that its "micro-dystrophin" treatment can help slow the progression of the disease. The company's request for approval rested mainly on how much micro-dystrophin the treatment produces in patients' muscles instead of waiting for clear, real-world evidence that it's actually helping patients. © 2023 npr

Keyword: Muscles; Movement Disorders
Link ID: 28780 - Posted: 05.13.2023

By Jan Hoffman Despite the continuing rise in opioid overdose deaths, one of the most effective treatments for opioid addiction is still drastically underprescribed in the United States, especially for Black patients, according to a large new study. From 2016 through 2019, scarcely more than 20 percent of patients diagnosed with opioid use disorder filled prescriptions for buprenorphine, the medication considered the gold standard in opioid addiction treatment, despite repeated visits to health care providers, according to the study, which was published Wednesday in the New England Journal of Medicine. Within six months following a high-risk event like an overdose, white patients filled buprenorphine prescriptions up to 80 percent more often than Black patients, and up to 25 percent more often than Latino patients, the study found. Rates of use for methadone, another effective treatment, were generally even lower. “It was disheartening to see that buprenorphine or methadone treatments were so low, even among patients who just left the hospital with an overdose or other addiction-related issue,” said Dr. Michael L. Barnett, the lead author, who teaches health policy and management at Harvard. “And not only that, but people of color received lifesaving treatment at a fraction of the rate that white patients did.” Access to medical care, a reason often used to explain racial disparities in treatment, was not necessarily at work here, said Dr. Barnett, an associate professor at the Harvard T.H. Chan School of Public Health. Noting that all the patients regardless of race encountered doctors roughly once a month, he said, “There are two mechanisms left that could explain disparities this large. One is where people of color get their health care, which we know is highly segregated, and another is racial differences in patient trust and demand for buprenorphine.“ Buprenorphine, often marketed under the brand name Suboxone, is a synthetic opioid that satisfies a patient’s cravings for other opioids and prevents withdrawal, without providing a high. It was approved for addiction treatment by the Food and Drug Administration more than two decades ago, but still faces some resistance and stigma because it, too, is an opioid. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 28779 - Posted: 05.13.2023

Heidi Ledford When Naomi Rance first started studying menopause and the brain, she pretty much had the field to herself. And what she was discovering surprised her. In studies of post-mortem brains, she had found neurons in a region called the hypothalamus that roughly doubled in size in women after menopause1. “This was changing so much in postmenopausal women,” says Rance, a neuropathologist at the University of Arizona in Tucson. “It had to be important.” This was the 1990s, and few other researchers were interested. Rance forged ahead on her own, painstakingly unravelling what the neurons were doing and finessing a way to study menopause symptoms in rats by tracking tiny temperature changes in their tails as a measure of hot flushes, a common symptom of menopause that is thought to be triggered in the hypothalamus. Thirty years later, a drug called fezolinetant, based on Rance’s discoveries, is being evaluated by the US Food and Drug Administration, with an approval decision expected in the first half of this year. If approved, fezolinetant could be a landmark: the first non-hormonal therapy to treat the source of hot flushes, a symptom that has become nearly synonymous with menopause and one that is experienced by about 80% of women going through the transition. (This article uses ‘women’ to describe people who experience menopause, while recognizing that not all people who identify as women go through menopause, and not all people who go through menopause identify as women.) Rance and others in the field, fezolinetant’s progress to this point is a sign that research into the causes and effects of menopausal symptoms is finally being taken seriously. In the next few years, the global number of postmenopausal women is expected to surpass one billion. But many women still struggle to access care related to menopause, and research into how best to manage such symptoms has lagged behind. That is slowly changing. Armed with improved animal models and a growing literature on the effects of existing treatments, more researchers are coming into the field to fill that gap. © 2023 Springer Nature Limited

Keyword: Hormones & Behavior; Learning & Memory
Link ID: 28778 - Posted: 05.10.2023

John Katsaras Charles Patrick Collier Dima Bolmatov Your brain is responsible for controlling most of your body’s activities. Its information processing capabilities are what allow you to learn, and it is the central repository of your memories. But how is memory formed, and where is it located in the brain? Although neuroscientists have identified different regions of the brain where memories are stored, such as the hippocampus in the middle of the brain, the neocortex in the top layer of the brain and the cerebellum at the base of the skull, they have yet to identify the specific molecular structures within those areas involved in memory and learning. Research from our team of biophysicists, physical chemists and materials scientists suggests that memory might be located in the membranes of neurons. Neurons are the fundamental working units of the brain. They are designed to transmit information to other cells, enabling the body to function. The junction between two neurons, called a synapse, and the chemistry that takes place between synapses, in the space called the synaptic cleft, are responsible for learning and memory. At a more fundamental level, the synapse is made of two membranes: one associated with the presynaptic neuron that transmits information, and one associated with the postsynaptic neuron that receives information. Each membrane is made up of a lipid bilayer containing proteins and other biomolecules. The changes taking place between these two membranes, commonly known as synaptic plasticity, are the primary mechanism for learning and memory. These include changes to the amounts of different proteins in the membranes, as well as the structure of the membranes themselves.

Keyword: Learning & Memory
Link ID: 28777 - Posted: 05.10.2023

By Erin Blakemore Newly published research suggests that the sons of women with polycystic ovary syndrome (PCOS) are up to twice as likely to develop obesity as their peers. The study in Cell Reports Medicine used data from cohort research following 467,275 male infants born in Sweden between July 2006 and December 2015. Of those, 9,828 were born to a mother with PCOS — and 147 of those boys were eventually diagnosed with obesity. About 2 in 100 Swedish boys who were born to mothers with PCOS became obese during childhood, compared with about 1 in 100 for boys whose mothers did not have PCOS. The risk was higher among the sons of women who had PCOS and a body mass index (BMI) greater than 25 and highest among the sons of women who both had PCOS and did not take metformin during pregnancy. Researchers followed up the analysis with an RNA sequencing study that found higher cholesterol in sons of Chilean women with PCOS than controls. In another analysis, researchers fed a group of mice a fatty, sugary diet and exposed them to high levels of dihydrotestosterone, a hormone that mimics that of pregnant women with PCOS. Their sons were born with metabolic problems that persisted into adulthood, even when they ate a healthy diet throughout their lives. “We could see that these male mice had more fat tissue, larger fat cells, and a disordered basal metabolism, despite eating a healthy diet,” says Elisabet Stener-Victorin, a reproductive endocrinology and metabolism investigator at the Karolinska Institute in Sweden and the study’s lead author, in a news release.

Keyword: Obesity; Hormones & Behavior
Link ID: 28776 - Posted: 05.10.2023

Scientists at the National Institutes of Health have identified new genetic risk factors for two types of non-Alzheimer’s dementia. These findings were published in Cell Genomics and detail how researchers identified large-scale DNA changes, known as structural variants, by analyzing thousands of DNA samples. The team discovered several structural variants that could be risk factors Lewy body dementia (LBD) and frontotemporal dementia (FTD). The project was a collaborative effort between scientists at the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA) at NIH. Structural variants have been implicated in a variety of neurological disorders. Unlike more commonly studied mutations, which often affect one or a few DNA building blocks called nucleotides, structural variants represent at least 50 but often hundreds, or even thousands, of nucleotides at once, making them more challenging to study. “If you imagine that our entire genetic code is a book, a structural variant would be a paragraph, page, or even an entire chapter that has been removed, duplicated, or inserted in the wrong place,” said Sonja W. Scholz, M.D., Ph.D., investigator in the neurogenetics branch of NINDS and senior author of this study. By combining cutting-edge computer algorithms capable of mapping structural variations across the whole genome with machine learning, the research team analyzed whole-genome data from thousands of patient samples and several thousand unaffected controls. A previously unknown variant in the gene TCPN1 was found in samples from patients with LBD, a disease, that like Parkinson’s disease, is associated with abnormal deposits of the protein alpha-synuclein in the brain. This variant, in which more than 300 nucleotides are deleted from the gene, is associated with a higher risk for developing LBD. While this finding is new for LBD, TCPN1 is a known risk factor for Alzheimer’s disease, which could mean that this structural variant plays a role in the broader dementia population.

Keyword: Alzheimers; Genes & Behavior
Link ID: 28775 - Posted: 05.10.2023

By Freda Kreier Pregnancy can do weird things to the body. For some bats, it can hamper their ability to “see” the world around them. Kuhl’s pipistrelle bats (Pipistrellus kuhlii) echolocate less frequently while pregnant, researchers report March 28 in BMC Biology. The change may make it harder for the tiny bats to detect prey and potential obstacles in the environment. The study is among the first to show that pregnancy can shape how nonhuman mammals sense their surroundings, says Yossi Yovel, a neuroecologist at Tel Aviv University in Israel. Nocturnal bats like Kuhl’s pipistrelles famously use sound to navigate and hunt prey in the dark (SN: 9/20/17). Their calls bounce off whatever is nearby and bats use the echoes to reconstruct what’s around them, a process aptly named echolocation. The faster a bat makes calls, the better it can make out its surroundings. But rapid-fire calling requires breathing deeply, which is something that pregnancy can get in the way of. “Although I’ve never been pregnant, I know that when I eat a lot, it’s more difficult to breathe,” Yovel says. So pregnancy — which can add a full gram to a 7-gram Kuhl’s pipistrelle and may push up on the lungs — might hamper echolocation. Yovel and colleagues tested their hypothesis by capturing 10 Kuhl’s pipistrelles, five of whom were pregnant, and training the bats to find and land on a platform. Recordings of the animals’ calls revealed that bats that weren’t pregnant made around 130 calls on average while searching for the platform. But bats that were pregnant made only around 110 calls, or 15 percent fewer. © Society for Science & the Public 2000–2023.

Keyword: Hearing; Hormones & Behavior
Link ID: 28774 - Posted: 05.10.2023

Sara Reardon For the second time, an experimental drug has been shown to reduce the cognitive decline associated with Alzheimer’s disease. On 3 May, pharmaceutical company Eli Lilly announced in a press release that its monoclonal antibody donanemab slowed mental decline by 35% for some participants in a 1,736-person trial — a rate comparable to that for competitor drug lecanemab. But researchers warn that until the full results are published, questions remain as to the drug’s clinical usefulness, as well as whether the modest benefit outweighs the risk of harmful side effects. Like lecanemab, donanemab targets amyloid protein, which is thought to cause dementia by accumulating in the brain and damaging neurons. The trial results provide strong evidence that amyloid is a key driver of Alzheimer’s, says Jeffrey Cummings, a neuroscientist at the University of Nevada, Las Vegas. “These are transformative in an enormously important way from a scientific point of view,” he adds. “They’re terrific.” But Marsel Mesulam, a neurologist at Northwestern University in Chicago, is more cautious. “The results that are described are extremely significant and impressive, but clinically their significance is doubtful,” he says, adding that the modest effect suggests that factors other than amyloid contribute to Alzheimer’s disease progression. “We’re heading to a new era — there’s room to cheer, but it’s an era that should make us all very sober, realizing that there will be no single magic bullet.” In the press release, Eli Lilly said that people with mild Alzheimer’s who received donanemab showed 35% less clinical decline over 18 months than did those who received a placebo, and 40% less decline in their ability to perform daily tasks. The company, based in Indianapolis, Indiana, says that it will present the full results at a conference in July and publish them in a peer-reviewed journal. It plans to apply for approval by the US Food and Drug Administration (FDA) in the next two months. Promising treatments © 2023 Springer Nature Limited

Keyword: Alzheimers
Link ID: 28773 - Posted: 05.06.2023