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By William Schwalbe More than three years ago, I came down with a mysterious illness I thought might be a flu, but turned out to be something entirely different. My blizzard of symptoms began innocuously in November 2016 with terribly cold feet. So cold that even when I got under the covers with a hot water bottle between them, and they were warm to the touch, they still felt like painful ice-blocks. At other times, I had the equally unpleasant sensation that my feet and shins were burning or already burnt. A few weeks later, I started to experience intense throbbing pain in all my toes, as if someone had seconds before stomped on them with heavy boots, which made walking or standing difficult. Often my legs were so heavy that I could barely move them. Occasionally, my feet turned bright red. And every few hours came shooting pains, electric shocks that traveled up my legs. In my 55 years on earth, I’d never felt pain like that — except when a dentist drilled without Novocain. All the symptoms increased at night, so sleep became elusive. I wound up sticking my feet outside the covers because even a sheet brushing against them proved too painful to bear. Before long, the same panoply of pains had moved to my hands and then arms — and occasionally my face and stomach. Heat made the symptoms worse; cold and damp made them much worse. But often these pains flared for no discernible reason. Totally unrelated, or so I thought, were other things that began to go wrong with me over the next few months: I often found myself pouring with sweat from my forehead, but became unable to sweat on my legs and arms; I lost all the hair on my lower legs; I was increasingly faint and dizzy, with my heart racing whenever I changed position or had a shower; and I was experiencing a fatigue and bone-pain so profound that every few hours I needed to stop whatever I was doing and lie down on the floor. © 1996-2020 The Washington Post

Keyword: Pain & Touch
Link ID: 27334 - Posted: 06.29.2020

By Richard Sandomir Dr. William Dement, whose introduction to the mysteries of slumber as a postgraduate student in the 1950s led him to become an eminent researcher of sleep disorders and to preach the benefits of a good night’s sleep, died on June 17 in Stanford, Calif. He was 91. His son, Nick, a physician, said the cause was complications of a heart procedure. Dr. Dement spent his working life as a popular professor in the department of psychiatry at Stanford University, where he started what is believed to be the world’s first successful sleep disorders clinic. He taught a class on sleep and dreams that drew as many as 1,200 students. When he awakened dozing students with spritzes from a water gun, Dr. Dement gave them extra credit if they recovered and shouted, “Drowsiness is red alert!” — his rallying cry to make sleep deprivation a public health priority. Drowsiness was the last step before falling asleep, he often said. Sleep deprivation put people at a higher risk of an accident on the road, diminished their productivity, increased the likelihood of their making mistakes, made them irritable and actually hurt their ability to fall asleep. “Bill Dement was an evangelist about sleep,” Dr. Rafael Pelayo, a Stanford psychiatry professor who succeeded Dr. Dement in leading the sleep class, said in a phone interview. “He felt that not enough people knew about sleep disorders, and he thought of his students as multipliers who would tell the world about them.” Dr. Dement’s expertise led to his appointment as chairman of a federal commission on sleep disorders. The commission reported in 1992 that 40 million Americans had undiagnosed, untreated, mistreated or chronic sleep problems — findings that led Congress to establish the National Center on Sleep Disorders Research, within the National Institutes of Health, in 1993. When Dr. Dement testified on Capitol Hill five years later about the sleep center’s progress, he said he was pleased with its research but disappointed that the government had not sounded loud enough alarms about the serious, sometimes fatal, consequences of unhealthful sleep. © 2020 The New York Times Company

Keyword: Sleep
Link ID: 27333 - Posted: 06.29.2020

By Bruce Bower An aptitude for mentally stringing together related items, often cited as a hallmark of human language, may have deep roots in primate evolution, a new study suggests. In lab experiments, monkeys demonstrated an ability akin to embedding phrases within other phrases, scientists report June 26 in Science Advances. Many linguists regard this skill, known as recursion, as fundamental to grammar (SN: 12/4/05) and thus peculiar to people. But “this work shows that the capacity to represent recursive sequences is present in an animal that will never learn language,” says Stephen Ferrigno, a Harvard University psychologist. Recursion allows one to elaborate a sentence such as “This pandemic is awful” into “This pandemic, which has put so many people out of work, is awful, not to mention a health risk.” Ferrigno and colleagues tested recursion in both monkeys and humans. Ten U.S. adults recognized recursive symbol sequences on a nonverbal task and quickly applied that knowledge to novel sequences of items. To a lesser but still substantial extent, so did 50 U.S. preschoolers and 37 adult Tsimane’ villagers from Bolivia, who had no schooling in math or reading. Those results imply that an ability to grasp recursion must emerge early in life and doesn’t require formal education. Three rhesus monkeys lacked humans’ ease on the task. But after receiving extra training, two of those monkeys displayed recursive learning, Ferrigno’s group says. One of the two animals ended up, on average, more likely to form novel recursive sequences than about three-quarters of the preschoolers and roughly half of the Bolivian villagers. © Society for Science & the Public 2000–2020.

Keyword: Language; Evolution
Link ID: 27332 - Posted: 06.27.2020

Jon Hamilton A research effort based at the Allen Institute in Seattle, Wash., will tap leading scientists from several institutions to dive even deeper into brain genetics and physiology. The aim: Find clues to the earliest beginnings of Alzheimer's. Allen Institute Three research institutions in Seattle have joined forces to study how Alzheimer's disease takes root in the brain. The consortium will create a new research center at the Allen Institute for Brain Science to study tissue from brains donated by people who died with Alzheimer's. UW Medicine and the Kaiser Permanente Washington Health Research Group are also part of the effort, which will be funded by a five-year $40.5 million grant from the National Institute on Aging, a part of the National Institutes of Health. The project, with its emphasis on basic research, represents part of a global do-over for the Alzheimer's field, which has weathered a series of failed attempts to develop a drug that could slow or stop the disease. "The premise of this project here is that we need to take a step back," says Ed Lein, a senior scientist at the Allen Institute and the center's lead investigator. That's a marked change from a decade ago, when there was great excitement about experimental drugs that could scrub away the sticky brain plaques thought to cause Alzheimer's. Studies have shown that the drugs do their job, removing a toxic protein called amyloid-beta from the brain. But they don't help patients avoid memory loss or cognitive problems. © 2020 npr

Keyword: Alzheimers
Link ID: 27331 - Posted: 06.27.2020

By Laura Sanders COVID-19 cases described by U.K. doctors offer a sharper view of the illness’s possible effects on the brain. Strokes, confusion and psychosis were found among a group of 125 people hospitalized with infections of SARS-CoV-2, the coronavirus behind the pandemic. The results, described June 25 in Lancet Psychiatry, come from a group of severely sick people, so they can’t answer how common these types of neurological symptoms may be in a more general population. Still, these details bring scientists closer to better understanding COVID-19. Brain-related symptoms of COVID-19 patients can slip through the cracks. “These relatively rare but incredibly severe complications get missed, like needles in a haystack,” says Benedict Michael, a neurologist at the University of Liverpool in England. So he and his colleagues designed a survey to uncover these symptoms. Sign up for e-mail updates on the latest coronavirus news and research In April, neurologists, stroke physicians, psychiatrists and other doctors across the United Kingdom entered COVID-19 patient details to a centralized database as part of the survey. Targeting these scientific specialties meant that the patients included were likely to have brain-related symptoms. Of the 125 patients described fully, 77 experienced an interruption of blood flow in the brain, most often caused by a blood clot in the brain. Blood clots are a well-known and pernicious COVID-19 complication (SN: 6/23/20), and strokes have been seen in younger people with COVID-19. About a third of the 125 patients had a shift in mental state, including confusion, personality change or depression. Eighteen of 37 patients with altered mental states were younger than 60. So far, it’s unclear exactly how SARS-CoV-2 causes these symptoms. © Society for Science & the Public 2000–2020.

Keyword: Stroke
Link ID: 27330 - Posted: 06.27.2020

By Abigail Zuger, M.D. Do I dare to eat a Cheeto? I do not; I can’t even let one into the house. The same goes for its delectably plump twin, the Cheez Doodle; its tasty rotund cousin, the Cheez Ball; and its heavenly brother by another mother, that sandwich of two Cheezy crackers glued together with peanut butter. I dare not even walk down the supermarket aisle where this neon orange family lives, for while others may succumb to chocolate or pastry, my Waterloo is this cheesy goodness — let’s call it Cheez. One Cheez Doodle would lead to a bag, then to more bags, and then to the certain catastrophe of a larger, sicker me. I know these delicacies are terrible for a person’s health. How exactly do I know that? It’s not because I’m a medical professional, that’s for sure; there were zero discussions of Cheez in our pre- or post-graduate training. I know because I just know, is all. Overprocessed chemical-laden stuff is bad for you; it’s pure malevolent junk. Everyone knows that. George Zaidan, an MIT-trained chemist of contrarian bent, knows it too. That is, he knows it to be piously reiterated received wisdom, and thus legitimate fodder for dissection, examination, refutation, and cheerfully self-indulgent obscenity-laden riffs. Further, he has chosen this junk food truth as an excellent starting point for “Ingredients: The Strange Chemistry of What We Put in Us and On Us,” an entertaining and enlightening jaunt around the perimeters of exactly what we can ever hope science can teach us about stuff that is good and bad for us. And it all begins with a single Cheeto, the putative first brick on the winding golden road to nutritional hell.

Keyword: Obesity
Link ID: 27329 - Posted: 06.27.2020

By Jack J. Lee For some bottlenose dolphins, finding a meal may be about who you know. Dolphins often learn how to hunt from their mothers. But when it comes to at least one foraging trick, Indo-Pacific bottlenose dolphins in Western Australia’s Shark Bay pick up the behavior from their peers, researchers argue in a report published online June 25 in Current Biology. While previous studies have suggested that dolphins learn from peers, this study is the first to quantify the importance of social networks over other factors, says Sonja Wild, a behavioral ecologist at the University of Konstanz in Germany. Cetaceans — dolphins, whales and porpoises — are known for using clever strategies to round up meals. Humpback whales (Megaptera novaeangliae) off Alaska sometimes use their fins and circular bubble nets to catch fish (SN: 10/15/19). At Shark Bay, Indo-Pacific bottlenose dolphins (Tursiops aduncus) use sea sponges to protect their beaks while rooting for food on the seafloor, a strategy the animals learn from their mothers (SN: 6/8/05). These Shark Bay dolphins also use a more unusual tool-based foraging method called shelling. A dolphin will trap underwater prey in a large sea snail shell, poke its beak into the shell’s opening, lift the shell above the water’s surface and shake the contents into its mouth. © Society for Science & the Public 2000–2020.

Keyword: Learning & Memory; Evolution
Link ID: 27328 - Posted: 06.26.2020

Hemant Khanna In recent months, even as our attention has been focused on the coronavirus outbreak, there have been a slew of scientific breakthroughs in treating diseases that cause blindness. Researchers at U.S.-based Editas Medicine and Ireland-based Allergan have administered CRISPR for the first time to a person with a genetic disease. This landmark treatment uses the CRISPR approach to a specific mutation in a gene linked to childhood blindness. The mutation affects the functioning of the light-sensing compartment of the eye, called the retina, and leads to loss of the light-sensing cells. According to the World Health Organization, at least 2.2 billion people in the world have some form of visual impairment. In the United States, approximately 200,000 people suffer from inherited forms of retinal disease for which there is no cure. But things have started to change for good. We can now see light at the end of the tunnel. I am an ophthalmology and visual sciences researcher, and am particularly interested in these advances because my laboratory is focusing on designing new and improved gene therapy approaches to treat inherited forms of blindness. The eye as a testing ground for CRISPR Gene therapy involves inserting the correct copy of a gene into cells that have a mistake in the genetic sequence of that gene, recovering the normal function of the protein in the cell. The eye is an ideal organ for testing new therapeutic approaches, including CRISPR. That is because the eye is the most exposed part of our brain and thus is easily accessible. © 2010–2020, The Conversation US, Inc.

Keyword: Vision
Link ID: 27327 - Posted: 06.26.2020

Nicola Davis People living with inflammatory bowel disease (IBD) have more than twice the risk of developing dementia, researchers have revealed in the latest study to link gut health to neurological diseases. A growing body of research suggests changes in the gastrointestinal tract may affect the brain through two-way communication known as the gut-brain axis. Scientists have previously found signs that the abnormally folded proteins involved in Parkinson’s disease may arise in the gut and travel to the brain via the vagus nerve, while changes to the microbial community in the gut – the gut microbiome – have been linked with conditions ranging from mental health problems to motor neurone disease and Parkinson’s disease. In addition, previous work has shown people with IBD have a higher risk of Parkinson’s disease. Researchers now say they have found that people with IBD – inflammatory conditions including ulcerative colitis and Crohn’s disease, which have symptoms including stomach pain and bloody stools – have a greater chance of developing dementia than those without, and tend to be diagnosed with dementia several years earlier. “The findings suggest that there may be a connection between IBD and neurocognitive decline,” said Dr Bing Zhang, first author of the research from the University of California San Francisco. While the study does not prove IBD causes dementia, Zhang and his colleagues outlined a number of ways the two may be linked, noting chronic inflammation has been suggested to trigger processes involved in Alzheimer’s disease, and blood clots and stroke – features involved in vascular dementia. © 2020 Guardian News & Media Limited or its affiliated companies.

Keyword: Alzheimers; Neuroimmunology
Link ID: 27326 - Posted: 06.26.2020

by Peter Hess / Inherited mutations in a gene called ACTL6B lead to autism, epilepsy and intellectual disability, according to a new study1. The mutations are recessive, which means that they lead to autism only if a person inherits them in both copies of the gene — one from each parent, who are silent carriers. Most other mutations implicated in autism are spontaneous, or ‘de novo,’ mutations, which are not inherited. The study suggests that recessive mutations in ACTL6B could be a relatively common cause of autism, says co-lead researcher Joseph Gleeson, professor of neurosciences and pediatrics at the University of California, San Diego. ACTL6B helps to control the expression of other genes in brain cells by encoding part of a protein complex called BAF. This complex tightens and loosens chromatin, the bundle of DNA and protein crammed inside a cell’s nucleus, during transcription. Scientists have linked autism to mutations in many other chromatin regulation genes — including several that encode other parts of the BAF complex. ACTL6B mutations have previously been associated with neurodevelopmental conditions, but the new study makes a strong case that they are tied to autism, says Gaia Novarino, professor of neuroscience at the Institute of Science and Technology in Klosterneuburg, Austria, who was not involved in the study. The work also provides a comprehensive look at how mutations in ACTL6B affect the brains of people, mice and flies, and suggests that the gene plays a common role across species. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27325 - Posted: 06.26.2020

Ruth Williams Turning off just one factor in the brain’s astrocyte cells is sufficient to convert them into neurons in live mice, according to a paper published in Nature today (June 24) and one this spring by another research team in Cell. By flipping this cellular identity switch, researchers have, to some extent, been able to reverse the neuron loss and motor deficits caused by a Parkinson’s-like illness. Not everyone is entirely convinced by the claims. “I think this is very exciting work,” says Pennsylvania State University’s Gong Chen of the Nature paper. It reaffirms that “using the brain’s internal glial cells to regenerate new neurons is a really new avenue for the treatment of brain disorders,” he continues. Chen, who is also based at Jinan University and is the chief scientific officer for NeuExcell—a company developing astrocyte-to-neuron conversion therapies—has performed such conversions in the living mouse brain by a different method but was not involved in the new study. In Parkinson’s disease, dopaminergic neurons within the brain’s substantia nigra—a region in the midbrain involved in movement and reward—gradually die. This results in a deterioration of motor control, characterized by tremors and other types of dyskinesia, with other faculties such as cognition and mood sometimes affected too, especially at later stages of the disease. While treatments to boost diminishing dopamine levels, such as the drug levodopa, can ameliorate symptoms, none can stop the underlying disease process that relentlessly eats away at the patient’s neurological functions and quality of life. © 1986–2020 The Scientist.

Keyword: Parkinsons; Glia
Link ID: 27324 - Posted: 06.26.2020

By David Grimm Last year marked the 60th anniversary of one of the most influential concepts in lab animal welfare—the three Rs. To promote the humane treatment of laboratory animals, these principles urge scientists to replace animals with new technologies, reduce the number of animals used in experiments, and refine lab protocols to minimize animal suffering. First outlined in the 1959 book, The Principles of Humane Experimental Technique, the three Rs have become a cornerstone of lab animal legislation and oversight throughout the world. But as millions of animals continue to be used in biomedical research each year, and new legislation calls on federal agencies to reduce and justify their animal use, some have begun to argue that it’s time to replace the three Rs themselves. “It was an important advance in animal research ethics, but it’s no longer enough,” Tom Beauchamp told attendees last week at a lab animal conference. Beauchamp, an emeritus professor of ethics at Georgetown University, has studied the ethics of animal research for decades. He also co-authored the influential Belmont Report of 1978, which has guided ethical principles for conducting research on human subjects. Beauchamp recently teamed up with David DeGrazia, a bioethicist at George Washington University and a senior research fellow in the Department of Bioethics at the U.S. National Institutes of Health (NIH), to lay out six principles for the ethical use of lab animals, which would replace the three Rs. The pair published both a scientific article and book on the topic late last year. © 2020 American Association for the Advancement of Science.

Keyword: Animal Rights
Link ID: 27323 - Posted: 06.26.2020

Kerry Grens William Dement, whose research and leadership were integral to the expansion of sleep science and medicine in the 20th century, died June 17 at age 91. He made fundamental contributions to understanding the phases of sleep and the array of sleep disorders people experience. In 1970, he launched one of the first sleep disorders clinic in the world. “William Dement was a force of nature. A pioneering researcher and clinician, and a legendary teacher, his passion to uncover sleep’s secrets and to share these discoveries was unquenchable,” Lloyd Minor, the dean of Stanford University School of Medicine, where Dement was a faculty member for half a century, says in a university obituary. “Not only did he make great contributions to Stanford, but his efforts directly led to the birth and development of the field of sleep medicine.” Dement was born in Wenatchee, Washington, in 1928. He served in the US Army in Japan and earned his bachelor’s degree from the University of Washington. At the University of Chicago, where he received a PhD and an MD, Dement worked with Nathaniel Kleitman to describe the physiology of rapid eye movement (REM) sleep and its relationship to dreaming. “The groundbreaking research and use of polysomnography by Kleitman, [Eugene] Aserinsky, and Dement in the U.S., and by Michel Jouvet in France, laid the foundation for the fields of sleep and circadian science and clinical sleep medicine,” according to a memoriam by the American Academy of Sleep Medicine (AASM), the first professional organization for sleep disorders that Dement helped launch in 1975. © 1986–2020 The Scientist.

Keyword: Sleep
Link ID: 27322 - Posted: 06.26.2020

By Brian Resnick@B_resnickbrian@vox.com Fix your gaze on the black dot on the left side of this image. But wait! Finish reading this paragraph first. As you gaze at the left dot, try to answer this question: In what direction is the object on the right moving? Is it drifting diagonally, or is it moving up and down? Remember, focus on the dot on the left. It appears as though the object on the right is moving diagonally, up to the right and then back down to the left. Right? Right?! Actually, it’s not. It’s moving up and down in a straight, vertical line. See for yourself. Trace it with your finger. This is a visual illusion. That alternating black-white patch inside the object suggests diagonal motion and confuses our senses. Like all misperceptions, it teaches us that our experience of reality is not perfect. But this particular illusion has recently reinforced scientists’ understanding of deeper, almost philosophical truths about the nature of our consciousness. “It’s really important to understand we’re not seeing reality,” says neuroscientist Patrick Cavanagh, a research professor at Dartmouth College and a senior fellow at Glendon College in Canada. “We’re seeing a story that’s being created for us.” Most of the time, the story our brains generate matches the real, physical world — but not always. Our brains also unconsciously bend our perception of reality to meet our desires or expectations. And they fill in gaps using our past experiences. All of this can bias us. Visual illusions present clear and interesting challenges for how we live: How do we know what’s real? And once we know the extent of our brain’s limits, how do we live with more humility — and think with greater care about our perceptions?

Keyword: Vision
Link ID: 27321 - Posted: 06.24.2020

As we open computers to connect with each other remotely, motor neurons in our spinal cord are opening synaptic pathways to connect with our muscles physically. We rarely think about these electrical signals passing back and forth between computers or our neurons and muscles, until those signals are lost. Kennedy’s disease, a neuromuscular degenerative disease, affects 1 in 40,000 men every year. Little progress has been made in understanding its biological basis since it was identified in the 1960s, but one promising lead may be a family of proteins known as neurotrophic factors. MSU scientists Cynthia Jordan, professor in the College of Natural Science Neuroscience Program, and Katherine Halievski, former Ph.D. student in Jordan’s Lab and lead author, published a benchmark study in the Journal of Physiology describing the key role of one of these proteins in Kennedy’s disease: Brain-Derived Neurotrophic Factor (BDNF). “There were stories that neurotrophic factors could slow down neurodegenerative diseases, but where they fell short was really understanding how they slow down the disease,” Jordan explained. “Where this paper and Katherine’s work stand alone is in using classic neuroscience techniques to understand how BDNF improved neuromuscular function at the cellular level.” Motor neurons are cells that carry signals from the brain to every muscle in the body — fast twitch muscles that perform quick, high impact movements such as jumping, and slow-twitch muscles that sustain long contractions such as standing. At each step in the pathway — from the neuron, along the synaptic pathway and to the muscle — BDNF supports the process, giving both neurons and muscles what they need to connect, survive and thrive. © Michigan State University

Keyword: Movement Disorders; Hormones & Behavior
Link ID: 27320 - Posted: 06.24.2020

By Andrew McCormick The psychiatrist was bald, with kind eyes, a silver goatee and the air of exhaustion that follows a person who works hard in a difficult field. It was March 2019, and having let an old prescription expire months earlier, I had gone to the Veterans Affairs hospital in Manhattan — my first time at a V.A. — hoping to get antidepressants. In a small, sparsely decorated office, the doctor and I faced each other across a wide desk. He told me about various V.A. programs — counseling, group therapy, a veterans’ yoga class, each accompanied by a flier — and described at length the V.A.’s crisis hotline. I appreciated his care, but I wasn’t there to break any new emotional ground; I really just wanted a prescription and to be on my way. I answered briskly as he worked through the questions any mental health worker asks you on a first visit. Did I have a history of anxiety or depression? Yes. Had I had thoughts of hurting myself or of suicide? Not really. Did anyone in my family have a history of mental health issues? Suddenly, my brain went foggy and my thoughts failed to connect. My speech slowed, and I began struggling to form sentences. Weird, I thought. I hadn’t felt sick. I worried the doctor might think he’d hit a nerve, when in fact I had answered questions like these many times before, including in post-deployment health evaluations in the Navy. My vision blurred. Eyes aflutter, I motioned to the doctor to give me a minute. I think I laughed. With the calm dispassion of a man who’s seen it all, the doctor picked up a phone beside him: “I’m going to need some help,” he said. “He’s about to pass out. . . . Yeah, he looks like he might throw up.” I swallowed hard. I tried not to. “Yeah, he just threw up.” © 2020 The New York Times Company

Keyword: Depression; Stress
Link ID: 27319 - Posted: 06.24.2020

By Elizabeth Pennisi Though not much bigger than a wooden match stick, snapping shrimp (Alpheus heterochaelis, pictured) are already famous for their loud, quick closing claws, the sound of which stuns their prey and rivals. Now, researchers have discovered these marine crustaceans have the eyesight to match this speed. In the new study, scientists stuck a thin conducting wire into the eye of a chilled, live shrimp and recorded electrical impulses from the eye in response to flickering light. The crustaceans refresh their view 160 times a second, the team reports today in Biology Letters. That’s one of the highest refresh rates of any animal on Earth. Pigeons come close, being able to sample their field of view 143 times per second, whereas humans top out at a relatively measly 60 times a second. Only some day-flying insects beat the snapping shrimp, the researchers report. As a result, what people—perhaps even Superman—and all other vertebrates see as a blur, the shrimp detects as discrete images moving across its field of vision. Until a few years ago, most researchers assumed snapping shrimp didn’t see very well because they have a hard hood called a carapace that extends over their eyes. Although the hood seems transparent, with some coloration, it wasn’t clear how well it transmitted light. But it appears to be no impediment to the shrimp detecting fast moving prey or even predators whipping by. This might be important because the shrimp tend to live in cloudy water, so they don’t have much notice when another critter is approaching them. Posted in: © 2020 American Association for the Advancement of Science.

Keyword: Vision; Evolution
Link ID: 27318 - Posted: 06.24.2020

By Nicholas Bakalar Five behaviors are associated with a lower risk for Alzheimer’s disease, a new study in Neurology suggests, and the more of them you follow, the lower your risk. Researchers used detailed diet and lifestyle information from two databases, one of 1,845 people whose average age was 73, the other of 920 people whose average age was 81. All were free of Alzheimer’s disease at the start of the study. They followed them for an average of about six years, during which 608 developed Alzheimer’s disease. The researchers scored the participants on their adherence to five behaviors: not smoking, consistent moderate or intense physical activity, light to moderate alcohol consumption, a high-quality Mediterranean-style diet, and engagement in late-life cognitively challenging activity. Compared to those with none or one of the healthy lifestyle factors, those with two or three had a 37 percent reduced risk for Alzheimer dementia, and those with four or five had a 60 percent reduced risk. The lead author, Dr. Klodian Dhana, an assistant professor of medicine at Rush Medical College, said that the paper focuses on modifiable risk factors. All five of these factors are related to each other, he added, and work best in combination. “My top recommendations are to engage in cognitively stimulating activities such as reading books and newspapers and playing brain-stimulating games, like chess and checkers,” he said. “Also, exercising regularly and following a diet for a healthy brain that includes green leafy vegetables every day, berries, nuts, poultry, fish, and limited fried food.” © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27317 - Posted: 06.24.2020

By Elizabeth Preston A clown fish uses his fins to fan water across a glistening mass of eggs, keeping them aerated. A silver arowana scoops up his fertilized eggs with his mouth and holds them gently for two months, until a host of miniature adults swims free from his jaws. A seahorse drifts through coral, his belly pouch swollen with unborn young. Most fish are uninvolved parents. They dump their eggs and sperm, then swim off and let nature take its course. But some species of fish take their parental duties more seriously — and among them, the majority of caring parents are dads. Care from mothers, or from both parents at once, is much less common. In a study published last fall in Evolution, researchers found evidence that paternal care, the system in which dads are the sole caretakers, has evolved dozens of times in fish. These fish aren’t exactly helicopter dads. Their most common parenting style is simply guarding eggs after they’re fertilized. “Some people are surprised this is considered care,” said Frieda Benun Sutton, an evolutionary biologist at the City University of New York. But it does count. To learn more about why this type of care in fish usually comes from dads, Dr. Benun Sutton and her co-author, Anthony Wilson, of Brooklyn College, took a deep dive into the family history of fish parents. They started with an evolutionary tree, built by other researchers in 2017 using genetic data, that shows how almost 2,000 fish species are related. Then they mapped onto the tree all the information they could find about parental care in those species: Were young cared for by fathers, mothers, both or nobody? They also added other factors including the size and number of each fish’s eggs and how they’re fertilized. The completed tree showed that care by fathers is no evolutionary accident: It has arisen at least 30 separate times. Hundreds of the species in this sample have absent mothers and caring fathers. But why? © 2020 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 27316 - Posted: 06.22.2020

By Bret Stetka How do humans and other animals distinguish between the smell of rotting seafood or the enticing allure of a ripe banana? New research at New York University Langone Health and their colleagues uses artificially created odors to help reveal the intricate chain of events that allow one odor to be distinguished from another. The results were published today in Science. In the deep recesses of the nose are millions of sensory neurons that, along with our eyes and ears, help conjure the world around us. When stimulated by a chemical with a smell, or an odorant, they send nerve impulses to thousands of clusters of neurons in the glomeruli, which make up the olfactory bulb, the brain’s smell center. Different patterns of glomerular activation are known to generate the sensation of specific odors. Firing one set of glomeruli elicits the perception of pineapples; firing another evokes pickles. Unlike other sensations, such as sight and hearing, scientists do not know which qualities of a particular smell are used by the brain to perceive it. When you see a person’s face, you may remember the eyes, which helps you recognize that individual in the future. But the ears and nose might be less important in how the brain represents that person. The authors of the new study sought to identify distinguishing features involved in forming the representation of odors in the brain. To do so, they used a technique called optogenetics to activate glomeruli in mice. Optogenetics uses light to stimulate specific neurons in the brain. And it can help determine the function of particular brain regions. © 2020 Scientific American

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27315 - Posted: 06.22.2020