By Emily Underwood It’s a classic science fiction trope: Astronauts on an interstellar journey are kept in sleek, refrigerated pods in a state of suspended animation. Although such pods remain purely fictional, scientists have pursued research into inducing a hibernation-like state in humans to lessen the damage caused by medical conditions such as heart attacks and stroke, and to reduce the stress and costs of future long-distance space sojourns. In a study published today in Nature Metabolism, scientists report that they can trigger a similar state in mice by targeting part of their brain with pulses of ultrasound. Some experts are calling it a major technical step toward achieving this feat in humans, whereas others say it’s a stretch to extrapolate the results to our species. "It’s an amazing paper,” says Frank van Breukelen, a biologist who studies hibernation at the University of Nevada, Las Vegas and co-authored an editorial accompanying the study. The work builds on a flurry of recent studies that pinpoint specific populations of neurons in a region called the preoptic area (POA) of the hypothalamus. These cells act like an on-off switch for “torpor”—a sluggish, energy-saving state the animals enter when they’re dangerously cold or malnourished. In previous studies, scientists genetically engineered these neurons to respond to light or certain chemicals, and found they could cause mice to enter a torpid state even when they were warm and well-fed. Such invasive techniques can’t be easily translated to people, however, Breukelen notes. “That’s really not going to happen in people.” The new ultrasound study, led by bioengineer Hong Chen and her team at Washington University in St. Louis required no genetic engineering. Chen knew from previous research that some neurons have specialized pores called TRPM2 ion channels that change shape in response to ultrasonic waves, including the subset of POA cells that controls mouse torpor. To see what effect that had on the animals’ behavior, her team next glued miniature, speakerlike devices on the heads of mice to focus these waves on the POA.

Keyword: Sleep; Brain imaging
Link ID: 28800 - Posted: 05.27.2023

By Amber Dance Maybe it starts with a low-energy feeling, or maybe you’re getting a little cranky. You might have a headache or difficulty concentrating. Your brain is sending you a message: You’re hungry. Find food. Studies in mice have pinpointed a cluster of cells called AgRP neurons near the underside of the brain that may create this unpleasant hungry, even “hangry,” feeling. They sit near the brain’s blood supply, giving them access to hormones arriving from the stomach and fat tissue that indicate energy levels. When energy is low, they act on a variety of other brain areas to promote feeding. By eavesdropping on AgRP neurons in mice, scientists have begun to untangle how these cells switch on and encourage animals to seek food when they’re low on nutrients, and how they sense food landing in the gut to turn back off. Researchers have also found that the activity of AgRP neurons goes awry in mice with symptoms akin to those of anorexia, and that activating these neurons can help to restore normal eating patterns in those animals. Understanding and manipulating AgRP neurons might lead to new treatments for both anorexia and overeating. “If we could control this hangry feeling, we might be better able to control our diets,” says Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center in Philadelphia. AgRP neurons appear to be key players in appetite: Deactivating them in adult mice causes the animals to stop eating — they may even die of starvation. Conversely, if researchers activate the neurons, mice hop into their food dishes and gorge themselves. © 2023 Annual Reviews

Keyword: Obesity
Link ID: 28799 - Posted: 05.27.2023

By Carolyn Wilke Costello the octopus was napping while stuck to the glass of his tank at the Rockefeller University in New York. He snoozed quietly for half an hour, and then entered a more active sleep stage, his skin cycling through colors and textures used for camouflage — typical behavior for a cephalopod. But soon things became strange. A minute later, Costello scuttled along the glass toward his tank’s sandy bottom, curling his arms over his body. Then he spun like a writhing cyclone. Finally, Costello swooped down and clouded half of his tank with ink. As the tank’s filtration system cleared the ink, Eric Angel Ramos, a marine scientist, noticed that Costello was grasping a pipe with unusual intensity, “looking like he was trying to kill it,” he said. “This was not a normal octopus behavior,” said Dr. Ramos, who is now at the University of Vermont. It’s not clear when or if Costello woke up during the episode, Dr. Ramos said. But afterward, Costello returned to normal, eating and later playing with his toys. “We were completely dumbfounded,” said Marcelo O. Magnasco, a biophysicist at Rockefeller. Perhaps Costello was having a nightmare, he and a team of researchers speculated. They shared this idea and other possible explanations in a study uploaded this month to the bioRxiv website. It has yet to be formally reviewed by other scientists. After the incident, Dr. Ramos reviewed the footage of Costello’s activity, which was recorded as part of a behavior and cognition study (the lab was also observing another octopus, Abbott; both were named after the heptapod aliens in the movie “Arrival”). In total, the team found three more shorter instances that appeared similar. To Dr. Magnasco, the behaviors exhibited in Costello’s longest spell evoked the acting out of a dream. The curling of arms over his body looked like a defensive posture, he said. In the footage, the animal is seen perhaps trying to make himself look larger, and then he tries an evasive maneuver — inking. When he fails to escape, it seems like Costello seeks to subdue a threat by strangling the pipe, Dr. Magnasco said, adding, “This is the sequence of a fight.” © 2023 The New York Times Company

Keyword: Sleep; Evolution
Link ID: 28798 - Posted: 05.27.2023

By Robert Martone Neurological conditions can release a torrent of new creativity in a few people as if opening some mysterious floodgate. Auras of migraine and epilepsy may have influenced a long list of artists, including Pablo Picasso, Vincent van Gogh, Edvard Munch, Giorgio de Chirico, Claude Monet and Georges Seurat. Traumatic brain injury (TBI) can result in original thinking and newfound artistic drive. Emergent creativity is also a rare feature of Parkinson’s disease. But this burst of creative ability is especially true of frontotemporal dementia (FTD). Although a few rare cases of FTD are linked to improvements in verbal creativity, such as greater poetic gifts and increased wordplay and punning, enhanced creativity in the visual arts is an especially notable feature of the condition. Fascinatingly, this burst of creativity indicates that the potential to create may rest dormant in some of us, only to be unleashed by a disease that also causes a loss of verbal abilities. The emergence of a vibrant creative spark in the face of devastating neurological disease speaks to the human brain’s remarkable potential and resilience. A new study published in JAMA Neurology examines the roots of this phenomenon and provides insight into a possible cause. As specific brain areas diminish in FTD, the researchers find, they release their inhibition, or control, of other regions that support artistic expression. Frontotemporal dementia is relatively rare—affecting about 60,000 people in the U. S.—and distinct from the far more common Alzheimer’s disease, a form of dementia in which memory deficits predominate. FTD is named for the two brain regions that can degenerate in this disease, specifically the frontal and temporal lobes.

Keyword: Alzheimers; Attention
Link ID: 28797 - Posted: 05.27.2023

By Jennie Erin Smith José Echeverría spends restless days in a metal chair reinforced with boards and padded with a piece of foam that his mother, Nohora Vásquez, adjusts constantly for his comfort. The chair is coming loose and will soon fall apart. Huntington’s disease, which causes José to move his head and limbs uncontrollably, has already left one bed frame destroyed. At 42, he is still strong. José’s sister Nohora Esther Echeverría, 37, lives with her mother and brother. Just two years into her illness, her symptoms are milder than his, but she is afraid to walk around her town’s steep streets, knowing she could fall. A sign on the front door advertises rum for sale that does not exist. The family’s scarce resources now go to food — José and Nohora Esther must eat frequently or they will rapidly lose weight — and medical supplies, like a costly cream for Jose’s skin. Huntington’s is a hereditary neurodegenerative disease caused by excess repetitions of three building blocks of DNA — cytosine, adenine, and guanine — on a gene called huntingtin. The mutation results in a toxic version of a key brain protein, and a person’s age at the onset of symptoms relates, roughly, to the number of repetitions the person carries. Early symptoms can include mood disturbances — Ms. Vásquez remembers how her late husband had chased the children out of their beds, forcing her to sleep with them in the woods — and subtle involuntary movements, like the rotations of Nohora Esther’s delicate wrists. The disease is relatively rare, but in the late 1980s a Colombian neurologist, Jorge Daza, began observing a striking number of cases in the region where Ms. Vásquez lives, a cluster of seaside and mountain towns near Barranquilla. Around the same time, American scientists led by Nancy Wexler were working with an even larger family with Huntington’s in neighboring Venezuela, gathering and studying thousands of tissue samples from them to identify the genetic mutation responsible. © 2023 The New York Times Company

Keyword: Huntingtons; Genes & Behavior
Link ID: 28796 - Posted: 05.23.2023

By Laura Sanders Scientists can see chronic pain in the brain with new clarity. Over months, electrodes implanted in the brains of four people picked up specific signs of their persistent pain. This detailed view of chronic pain, described May 22 in Nature Neuroscience, suggests new ways to curtail the devastating condition. The approach “provides a way into the brain to track pain,” says Katherine Martucci, a neuroscientist who studies chronic pain at Duke University School of Medicine. Chronic pain is incredibly common. In the United States from 2019 to 2020, more adults were diagnosed with chronic pain than with diabetes, depression or high blood pressure, researchers reported May 16 in JAMA Network Open. Chronic pain is also incredibly complex, an amalgam influenced by the body, brain, context, emotions and expectations, Martucci says. That complexity makes chronic pain seemingly invisible to an outsider, and very difficult to treat. One treatment approach is to stimulate the brain with electricity. As part of a clinical trial, researchers at the University of California, San Francisco implanted four electrode wires into the brains of four volunteers with chronic pain. These electrodes can both monitor and stimulate nerve cells in two brain areas: the orbitofrontal cortex, or OFC, and the anterior cingulate cortex, or ACC. The OFC isn’t known to be a key pain influencer in the brain, but this region has lots of neural connections to pain-related areas, including the ACC, which is thought to be involved in how people experience pain. But before researchers stimulated the brain, they needed to know how chronic pain was affecting it. For about 3 to 6 months, the implanted electrodes monitored brain signals of these people as they went about their lives. During that time, the participants rated their pain on standard scales two to eight times a day. © Society for Science & the Public 2000–2023.

Keyword: Pain & Touch; Brain imaging
Link ID: 28795 - Posted: 05.23.2023

By Priyanka Runwal Researchers have for the first time recorded the brain’s firing patterns while a person is feeling chronic pain, paving the way for implanted devices to one day predict pain signals or even short-circuit them. Using a pacemaker-like device surgically placed inside the brain, scientists recorded from four patients who had felt unremitting nerve pain for more than a year. The devices recorded several times a day for up to six months, offering clues for where chronic pain resides in the brain. The study, published on Monday in the journal Nature Neuroscience, reported that the pain was associated with electrical fluctuations in the orbitofrontal cortex, an area involved in emotion regulation, self-evaluation and decision making. The research suggests that such patterns of brain activity could serve as biomarkers to guide diagnosis and treatment for millions of people with shooting or burning chronic pain linked to a damaged nervous system. “The study really advances a whole generation of research that has shown that the functioning of the brain is really important to processing and perceiving pain,” said Dr. Ajay Wasan, a pain medicine specialist at the University of Pittsburgh School of Medicine, who wasn’t involved in the study. About one in five American adults experience chronic pain, which is persistent or recurrent pain that lasts longer than three months. To measure pain, doctors typically rely on patients to rate their pain, using either a numerical scale or a visual one based on emojis. But self-reported pain measures are subjective and can vary throughout the day. And some patients, like children or people with disabilities, may struggle to accurately communicate or score their pain. “There’s a big movement in the pain field to develop more objective markers of pain that can be used alongside self-reports,” said Kenneth Weber, a neuroscientist at Stanford University, who was not involved in the study. In addition to advancing our understanding of what neural mechanisms underlie the pain, Dr. Weber added, such markers can help validate the pain experienced by some patients that is not fully appreciated — or is even outright ignored — by their doctors. © 2023 The New York Times Company

Keyword: Pain & Touch; Brain imaging
Link ID: 28794 - Posted: 05.23.2023

By Carl Zimmer One of the greatest transformations in the history of life occurred more than 600 million years ago, when a single-celled organism gave rise to the first animals. With their multicellular bodies, animals evolved into a staggering range of forms, like whales that weigh 200 tons, birds that soar six miles into the sky and sidewinders that slither across desert dunes. Scientists have long wondered what the first animals were like, including questions about their anatomy and how they found food. In a study published on Wednesday, scientists found tantalizing answers in a little-known group of gelatinous creatures called comb jellies. While the first animals remain a mystery, scientists found that comb jellies belong to the deepest branch on the animal family tree. The debate over the origin of animals has endured for decades. At first, researchers relied largely on the fossil record for clues. The oldest definitive animal fossils date back about 580 million years, although some researchers have claimed to find even older ones. In 2021, for example, Elizabeth Turner, a Canadian paleontologist, reported finding 890-million-year-old fossils of possible sponges. Sponges would make sense as the oldest animal. They are simple creatures, with no muscles or nervous system. They anchor themselves to the ocean floor, where they filter water through a maze of pores, trapping bits of food. Sponges are so simple, in fact, that it can come as a surprise that they are animals at all, but their molecular makeup reveals their kinship. They make certain proteins, such as collagen, that are produced only by animals. What’s more, their DNA shows they are more closely related to animals than to other forms of life. Starting in the 1990s, as scientists gathered DNA from more animal species, they tried to draw the animal family tree. In some studies, the sponges ended up on the deepest branch of the tree. In this scenario, animals evolved a nervous system only after the sponges branched off. © 2023 The New York Times Company

Keyword: Evolution
Link ID: 28793 - Posted: 05.23.2023

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