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Laura Sanders Alzheimer’s disease destroys command centers in the brain that keep people awake. That finding could explain why the disease often brings daytime drowsiness. Sleep problems can precede dementias, including Alzheimer’s, sometimes by decades. But the new result, described online August 12 in Alzheimer’s & Dementia, suggests that disordered sleeping isn’t just an early harbinger of Alzheimer’s. Instead, sleep trouble is “part of the disease,” says Lea Grinberg, a neuropathologist at the University of California, San Francisco. Grinberg and colleagues focused on the brain stem and a structure perched above it called the hypothalamus. Together, these parts of the nervous system oversee crucial jobs such as keeping people awake and paying attention. Though important, the brain stem and its neighbors have been largely overlooked in studies of dementia, Grinberg says. In particular, the researchers searched for evidence of tau, a protein that can form tangles inside nerve cells, in postmortem brains of people who died with Alzheimer’s disease. Three small regions of the hypothalamus and brain stem, all of which usually contain nerve cells that keep people awake during the day, were packed with tau, the team found. And two of the three areas had lost over 70 percent of their nerve cells, or neurons. These areas “are hit hard, and they are hit by tau,” Grinberg says. That destruction could be part of the reason people with Alzheimer’s disease often feel tired during the day, even if they slept the night before. |© Society for Science & the Public 2000 - 2019.
Keyword: Alzheimers
Link ID: 26509 - Posted: 08.17.2019
By John Williams The first, startling epigraph in Nicci Gerrard’s new book, “The Last Ocean,” comes from Emily Dickinson: “Abyss has no Biographer.” Gerrard sets out to tell the story of dementia, a disease that can appear to consume those it afflicts. After her father, John, died in 2014, the author — who writes best-selling thrillers with her husband under the name Nicci French — embarked on learning more about the disease as both a journalist and an activist. The result is a tender, inquisitive tour of a subject that can be raw and painful. Below, Gerrard talks about loss, art that punches you in the solar plexus and the experience of writing a book that doesn’t answer questions. When did you first get the idea to write this book? I first had the idea when my father, who’d been living with dementia for over 10 years, went into hospital in February 2014. After four weeks without anyone to see him — we were allowed in for very limited times and then not at all, because of a norovirus outbreak — I barely recognized him. I will, for the rest of my life, feel terribly that I didn’t get him out earlier. Then he lived at home for nine months. He had become skeletal, immobile, inarticulate, and in a way he felt utterly lost, like a ghost in our lives and in his own life. He would lay downstairs in a hospital bed, looking outside at the garden he used to love. There was this clear sense that he’d already lost everything he had, everything he was, all his capacity, there was nothing left — and yet somehow that he didn’t lose himself. In the book I say that if I were religious, I would call that self he retained his soul. Something very indelible remained. © 2019 The New York Times Company
Keyword: Alzheimers
Link ID: 26508 - Posted: 08.17.2019
Nicola Davis A new organ involved in the sensation of pain has been discovered by scientists, raising hopes that it could lead to the development of new painkilling drugs. Researchers say they have discovered that the special cells that surround the pain-sensing nerve cells that extend into the outer layer of skin appear to be involved in sensing pain – a discovery that points to a new organ behind the feeling of “ouch!”. The scientists say the finding offers new insight into pain and could help answer longstanding conundrums. “The major question for us now is whether these cells are actually the cause for certain kinds of chronic pain disorders,” Prof Patrik Ernfors, a co-author of the research from the Karolinska Institute in Sweden, told the Guardian. Writing in the journal Science, the researchers reveal how they examined the nature of cells in the skin that, they say, have largely been overlooked. These are a type of Schwann cell, which wrap around and engulf nerve cells and help to keep them alive. The study has revealed these Schwann cells have an octopus-like shape. After examining tissues, the team found the body of the cells sits below the outer layer of the skin, but that the cells have long extensions that wrap around the ends of pain-sensing nerve cells that extend up into the epidermis, the outer layer of the skin. The scientists were surprised at the findings because it has long been believed that the endings of nerve cells in the epidermis were bare or unwrapped. “In the pain field, we talk about free nerve endings that are responsible for pain sensation. But actually they are not free,” Ernfors said. © 2019 Guardian News & Media Limited
Keyword: Pain & Touch; Glia
Link ID: 26507 - Posted: 08.16.2019
Statistics Canada says Canadian men are almost twice as likely to use cannabis as women. New data from the National Cannabis Survey today shows 16 per cent of Canadians over 15 years old report using pot in April, May or June. That's down slightly from 17.5 per cent in the first three months of the year. Almost five million Canadians consumed cannabis in some form during the three month period. One quarter of men, and 16 per cent of women, reported they plan to consume it in the next three months. The survey suggests men are more likely to use cannabis daily or weekly than women, and are also more likely to use it for non-medicinal purposes. About four in 10 marijuana users say they bought cannabis illegally. Smoking the drug remains the most common way of consuming it, with 68 per cent of men and 62 per cent of women consumers choosing this method. At 14 per cent, women were almost three times more likely than men (five per cent) to have consumed cannabis through "other methods," including edible and topical variants. Recreational marijuana became legal in Canada last October and Statistics Canada is tracking consumption habits every three months. ©2019 CBC/Radio-Canada.
Keyword: Drug Abuse; Sexual Behavior
Link ID: 26506 - Posted: 08.16.2019
By Dylan Loeb McClain Kary B. Mullis, a biochemist who won the 1993 Nobel Prize in Chemistry for discovering a way to analyze DNA easily and cheaply and thus pave the way for major advances in medical diagnostics, molecular biology and forensic science, died on Aug. 7 at his home in Newport Beach, Calif. He was 74. The cause was heart and respiratory failure brought on by pneumonia, his wife, Nancy Cosgrove Mullis, said. The process for analyzing DNA that Dr. Mullis invented is called polymerase chain reaction, or PCR. It replicates a single strand of DNA millions of times, enabling scientists to pinpoint a segment of the strand and amplify it for identification. Polymerase, an enzyme that synthesizes polymers and nucleic acids, is essential in creating DNA and RNA, the molecules that are responsible for coding DNA. Before PCR, amplifying DNA took weeks, because it had to be generated in bacteria. Once Dr. Mullis’s process was perfected, it took only hours, opening up a world of possibilities. We’ll bring you stories that capture the wonders of the human body, nature and the cosmos. Today, his method is used to detect genetic mutations that can lead to diagnoses of diseases, like sickle cell anemia; analyze ancient sources of DNA, like bones; assist in obtaining crime scene evidence; and determine paternity. It was used as well to decode and map the entire human DNA as part of the Human Genome Project, the landmark international research effort that ran from 1990 to 2003. As he told the story in his Nobel lecture, Dr. Mullis found his inspiration one night in 1983 while driving to his cabin in Mendocino, Calif. © 2019 The New York Times Company
Keyword: Genes & Behavior
Link ID: 26505 - Posted: 08.16.2019
By Bret Stetka Among the human body’s many maladies, few have stumped medical researchers like those that decimate the brain. After decades of effort, effectively treating—let alone curing—neurodegenerative disorders such as Huntington’s and Alzheimer's disease has been a source of frustration for many, as old theories are questioned and clinical trials fail. Basic scientists have achieved some progress. Over the past few decades, they have made serious headway in identifying single inherited genes responsible for genetic forms of various neurodegenerative diseases such as Alzheimer’s—and also the molecular and neural mechanisms behind nongenetic, or sporadic, forms of brain maladies. Yet translating these findings into working therapies has proved challenging. With genetic engineering technologies, such as CRISPR, that literally rewrite our DNA still a ways away from routine use, a number of clinical researchers have turned to a more immediate genome-based approach to treat disorders of the brain: manipulating RNA to modify levels of proteins associated with disease. DNA provides our genetic code, with its sister molecule RNA translating that code into the proteins that run our brains and myriad bodily functions. Scientists can now use molecules called antisense oligonucleotides (ASOs) to modify this process by binding to RNA and altering translation. ASOs are DNA-like molecules that greatly resemble the DNA that produced the RNA they correspond to in the first place. Depending on where they are designed to bind, these antisense molecules can prevent an RNA from being translated into a protein, which reduces levels of that protein in the body or brain. Alternatively, these same DNA-like molecules can be crafted to interfere with RNA machinery that normally inhibits or slows translation. In this case, more protein is made. © 2019 Scientific American
Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 26504 - Posted: 08.15.2019
By Kate Murphy Maybe it was because when the waiter asked, “Still or sparkling?” you chose sparkling. It could have also been that you were ravenous and ate a little too much. Or, possibly, it was your ex, who happened to be dining at the same restaurant and stood a little too long over your table making awkward small talk. All of these things, hic, might cause spasms, hic, in your diaphragm, hic. Referred to in the medical literature as singultus (from the Latin singult, which means gasp or sob), hiccups are familiar to anyone who has ever taken a breath. In fact, you begin to hiccup while still in the womb. Most people hiccup the most during childhood, with the bouts becoming less frequent over time, but even in adulthood, hiccups are still a common, and annoying, occurrence. Just as we all have our own particular way of sneezing, we all have a unique way of hiccuping that can range from four to 60 hiccups per minute. Most hiccups are benign and last only a few minutes or hours. But sometimes hiccups are indicative of a more serious health issue, particularly when they recur or don’t go away for days, weeks or years. Beyond being embarrassing, the muscle contractions can be physically exhausting. They can interrupt sleep and make it hard to eat. Approximately 4,000 people in the United States are admitted to the hospital every year for hiccups. The patient with the longest recorded case, according to Guinness World Records, was Charles Osborne of Anthon, Iowa, who hiccuped for 68 years straight. He claimed it started while attempting to weigh a hog before slaughtering it. Doctors say there are as many causes for hiccups as there are crazy remedies, including tugging on your tongue, standing on your head and swallowing granulated sugar. Some actually work. Others are more likely just entertainment for friends and family who watch while you try to cure yourself. © 2019 The New York Times Company
Keyword: Miscellaneous
Link ID: 26503 - Posted: 08.15.2019
Etelka Lehoczky Like any good story about a scientific discovery, Walter A. Brown's account of the history of lithium features plenty of improvisation, conjecture and straight-up kismet. Unlike many such stories, though, it also features a fair share of personal bias, senseless puttering and random speculation — on part of these scientific researchers. Brown, a practicing psychiatrist and university professor of more than 40 years, seems to have been drawn to write Lithium: A Doctor, A Drug and a Breakthrough as much because of lithium's fluky history and overlooked importance (for many years, he argues, it was "the Cinderella of psychiatric drugs") as by the profound impact it's had on countless sufferers of bipolar disorder and depression. Lithium is a homage, not just to a drug, but to the renegade side of science. Its heroes are researchers scattered around the globe, short on funding and frequently unaware of each other's work, without whom a commonly available substance would never have been recognized as a treatment for one of the most baffling psychiatric illnesses. By celebrating these men, Brown hopes to do a lot more than simply raise awareness about an underappreciated substance. He aims to demolish what remains of the myth that scientific progress is driven by rigorous dispassion. The story of lithium's use in medicine is certainly colorful, as is the history of the illness it's become known for. Brown doesn't stint on either tale. He goes all the way back to the first century to find a would-be description of manic depression by the Greek doctor Aretaeus of Cappadocia. These patients, Aretaeus wrote, "'laugh, play, dance night and day, and sometimes go openly to the market crowned, as if victors in some contest of skill,'" only to become "'torpid, dull and sorrowful.'" © 2019 npr
Keyword: Schizophrenia
Link ID: 26502 - Posted: 08.15.2019
By Sheila Kaplan Nearly three dozen young people have been hospitalized around the country in recent weeks for severe respiratory problems after vaping either nicotine or marijuana, stumping doctors treating them. The Illinois, Minnesota and Wisconsin public health departments are investigating these cases and at least 20 additional emergency admissions that doctors suspect are related to vaping some substance, possibly even illegal street drugs or adulterated liquids laced with T.H.C., the ingredient that produces marijuana’s high. There are also cases in California, which appear to be associated with vaping cannabis or cannabidiol oil. Most of the patients were having difficulty breathing when they arrived at the hospital. Some patients also reported chest pain, vomiting and other ailments. The cases have ranged in severity, with some patients suffering severe lung damage that required weeks of treatment in the intensive care units. Each of the patients reported using e-cigarettes or other vaping devices in the weeks leading up to the emergency. But officials are not yet clear whether vaping caused the injuries, and if so, what ingredient in the e-cigarette or vaping systems was responsible. “We know the children have been injured. We don’t yet know the causative agent,” said Dr. David D. Gummin, medical director of the Wisconsin Poison Center, and professor and chief of medical toxicology at the Medical College of Wisconsin. “We have no leads pointing to a specific substance other than those that are associated with smoking or vaping.” Initially, Dr. Gummin said, doctors suspected that the patients were suffering from an infectious disease. But the patients’ failure to respond to antibiotics led the doctors to believe they had been harmed by a toxic substance. A common practice among their patients was vaping. © 2019 The New York Times Company
Keyword: Drug Abuse
Link ID: 26501 - Posted: 08.15.2019
Patti Neighmond Most children enrolled in Medicaid who get a diagnosis of attention deficit hyperactivity disorder don't get timely or appropriate treatment afterward. That's the conclusion of a report published Thursday by a federal watchdog agency, the Department of Health and Human Services' Office of Inspector General. "Nationwide, there were 500,000 Medicaid-enrolled children newly prescribed an ADHD medication who did not receive any timely follow-up care," says Brian Whitley, a regional inspector general with OIG. The report analyzed Medicaid claims data from 2014 and 2015. Those kids didn't see a health care provider regarding their ADHD within a month of being prescribed the medication, though pediatric guidelines recommend that, he says. And one in five of those children didn't get the two additional check-ins with a doctor they should get within a year. "That's a long time to be on powerful medications without a practitioner checking for side effects or to see how well the medication is working," Whitley says. Additionally, according to the OIG report, "Nearly half of Medicaid-enrolled children who were newly prescribed an ADHD medication did not receive behavioral therapy," though that, too, is recommended by pediatricians. Elizabeth Cavey, who lives with her family in Arlington, Va., knows just how important it is to get a child with ADHD accurately diagnosed and treated. Kindergarten, Cavey says, was a disaster for her daughter. "She was constantly being reprimanded and forced to sit still," Cavey recalls. "And she's a bright child, but she kept falling further and further behind in learning letters and language, because she could not concentrate." © 2019 npr
Keyword: ADHD; Development of the Brain
Link ID: 26500 - Posted: 08.15.2019
By Joseph D. Stern, M.D. My patient had arrived from another hospital in the middle of the night. He was a wiry older man, restless but alert. He had a blood clot compressing the dominant hemisphere of his brain. He did not speak or move the right side of his body but fidgeted with his left hand and leg: pulling at his IV; removing his oxygen tubing and the ECG contacts pasted to his chest. He did not seem to understand what was happening and could neither assent to nor refuse the surgery I was recommending. Yet just hours earlier, he had been his normal self. His wife, whom I later learned was developing dementia, accompanied him in the ambulance. She was frail, thin and appeared disheveled and confused. She knew little about his medications and medical problems and didn’t know if he was on blood thinners. Still, given his rapid decline over a few hours, I took him to surgery. The craniotomy went well and he seemed to recover smoothly. But my patient made little improvement over the next two days. A repeat CT scan showed that the blood I had removed had re-accumulated. This is a known complication of a craniotomy for subdural hematoma. Still, it felt like a personal failure. The easiest thing to do would have been to take my patient back to surgery. But was it the right thing to do? Two weeks earlier I had attended a conference on palliative care held by the Archdiocese of Boston. Dr. Mary Buss, a hematologist/oncologist and chief of palliative care at Beth Israel Deaconess Medical Center, related some recent research on moral distress in neurosurgery she had conducted with Dr. Stephen Miranda. Dr. Miranda, who was then a medical student and is now a neurosurgical resident at the University of Pennsylvania, interviewed neurosurgery residents about the decision to operate on an elderly patient with early dementia and on blood thinners with a subdural hematoma and a poor neurological exam. © 2019 The New York Times Company
Keyword: Brain Injury/Concussion; Stroke
Link ID: 26499 - Posted: 08.15.2019
Anna Moore On a lazy Sunday morning in May last year, Isobel Lloyd was at her boyfriend’s house, having coffee with his mum. The conversation had worked around to Lloyd’s grandma – her mother’s mother – who’d died in her 50s, when Lloyd was very young. Lloyd’s only memories of her had been hospice visits where her grandma lay bedbound, unable to talk or swallow, with no control over how her body moved. Lloyd had forgotten the name of her grandma’s disease, hadn’t thought about it in years. Like most 20-year-olds, she was future-focused – a student from Yorkshire, keen on her studies, in love with her boyfriend of four years. Sitting in his family kitchen, they began reeling off degenerative diseases. Motor neurone. Multiple sclerosis. Parkinson’s. Alzheimer’s. Then finally Huntington’s disease (HD). In a flash of recognition, Lloyd knew that was the one her grandma had. “It just clicked,” she says. “I Googled it on my phone – and that’s when I read that it was genetic. My mum had a 50% risk of getting it – and if she did, I had a 50% risk, too.” She didn’t tell her boyfriend’s mother what she’d just learned, “But I felt the colour rush out of my face,” says Lloyd, an only child. “I thought, ‘No way, that can’t be true.’ I was 20 years old and no one had told me?” In fact, that’s not so unusual. Secrecy, evasion and lies are frequent features for families grappling with genetic disease. Whether it’s HD, a breast cancer gene, inheritable bowel cancer, early-onset Alzheimer’s, it’s not uncommon for younger generations to stumble upon their inheritance by noticing patterns, asking questions. By then, they’re faced not just with their frightening at-risk status, but also anger at all those years in the dark. © 2019 Guardian News & Media Limited
Keyword: Huntingtons; Genes & Behavior
Link ID: 26498 - Posted: 08.15.2019
By Tiffany Hsu Scientists at Virginia Commonwealth University in Richmond, Va., were concerned when a young man contacted their department last year complaining of a heart-pounding, hallucinogenic high he had neither expected nor wanted to have. The team, led by the forensic toxicologist Michelle R. Peace, had published a study about mysterious ingredients in vaping liquids. That’s how the man, a graduate student Dr. Peace declined to name, knew to tell it about his experience. He said he had vaped a liquid, from a company called Diamond CBD, that contained CBD, or cannabidiol. A compound reputed to have soothing properties, CBD has been marketed by the fast-growing cannabis industry as an ingredient in sleeping masks, kombucha, Carl’s Jr. burgers and Martha Stewart-backed dog treats. It is not supposed to cause a psychoactive experience. Dr. Peace decided to run some tests of Diamond CBD vaping liquids, some from the graduate student and some bought from the manufacturer. In four of nine samples, all marketed on the company’s website as 100 percent natural, her lab discovered a synthetic compound, 5F-ADB. That ingredient has been linked by the Drug Enforcement Administration to anxiety, convulsions, psychosis, hospitalization and death. Diamond CBD has often promoted its products as health aids meant to “help your body to heal and recover” and “to make you feel the best version of yourself.” The company’s parent, PotNetwork Holdings, said in a statement that independent tests did not show “any unnatural or improper derivative.” The company said it planned to run more tests on its products and materials and would issue a recall if it found any problems. The efforts of cannabis companies to go mainstream could be hampered by CBD advertising that depends on misleading or unproven claims, entrepreneurs and researchers said. Dr. Peace compared the marketing efforts of some companies to snake-oil scams in the 1800s, “when guys in wagons were selling sham tinctures in glass bottles.” © 2019 The New York Times Company
Keyword: Drug Abuse; Stress
Link ID: 26497 - Posted: 08.14.2019
In a nationwide study, researchers used magnetic resonance imaging (MRI) to scan the brains of hundreds of participants in the National Institutes of Health’s Systolic Blood Pressure Intervention Trial (SPRINT) and found that intensively controlling a person’s blood pressure was more effective at slowing the accumulation of white matter lesions than standard treatment of high blood pressure. The results complement a previous study published by the same research group which showed that intensive treatment significantly lowered the chances that participants developed mild cognitive impairment. “These initial results support a growing body of evidence suggesting that controlling blood pressure may not only reduce the risk of stroke and heart disease but also of age-related cognitive loss,” said Walter J. Koroshetz, M.D., director of the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “I strongly urge people to know your blood pressure and discuss with your doctors how to optimize control. It may be a key to your future brain health.” Brain white matter is made up of billions of thin nerve fibers, called axons, that connect the neurons with each other. The fibers are covered by myelin, a white fatty coating that protects axons from injury and speeds the flow of electrical signals. White matter lesions, which appear bright white on MRI scans, represent an increase in water content and reflect a variety of changes deep inside the brain, including the thinning of myelin, increased glial cell reactions to injury, leaky brain blood vessels, or multiple strokes. These changes are associated with high blood pressure, or “hypertension”.
Keyword: Alzheimers
Link ID: 26496 - Posted: 08.14.2019
Todd Golde and Steven DeKosky Dr. Todd Golde is a co-founder of Lacerta Therapeutics, Inc. and serves on their scientific advisory board (SAB). He is on the SAB for Promis Neuroscience, Inc. In the past he has served, ad hoc, on SABs related to neurodegenerative disease programs for Eli Lilly, Novartis, Bristol Myers Squib, Abbvie, Lundbeck, Biogen and Pfizer. He is co-editor in chief of Alzheimer’s Research and Therapy for which he receives an honorarium. He has served on the medical and scientific advisory board for the Alzheimer’s Association. He serves as a scientific advisor and participates in grant reviews for BrightFocus Foundation and the American Federation for Aging Research. He is a co-inventor on multiple patents and patent applications relating to AD therapeutics. He currently receives funding from the NIH. Steven DeKosky receives grant funding from the National Institute of Aging, serves as a consultant for Amgen, Biogen, and Cognition Therapeutics, and serves as editor for dementia for Up-To-Date, a point-of-care electronic textbook. He has chaired study sections for the NIH, served on two NIH councils, for the National Center for Complementary and Alternative Medicine (now the National Center for Complementary and Integrative Health; NCCIH) and the Director's Council (Council of Councils). He has served on the board of the Alzheimer's Association and chaired their Medical and Scientific Advisory Council, as well as chairing the Medical and Scientific Advisory Panel of Alzheimer's Disease International. © 2010–2019, The Conversation US, Inc.
Keyword: Alzheimers
Link ID: 26495 - Posted: 08.14.2019
Meredith Fore A long-standing controversy in neuroscience centers on a simple question: How do neurons in the brain share information? Sure, it’s well-known that neurons are wired together by synapses and that when one of them fires, it sends an electrical signal to other neurons connected to it. But that simple model leaves a lot of unanswered questions—for example, where exactly in neurons’ firing is information stored? Resolving these questions could help us understand the physical nature of a thought. Two theories attempt to explain how neurons encode information: the rate code model and the temporal code model. In the rate code model, the rate at which neurons fire is the key feature. Count the number of spikes in a certain time interval, and that number gives you the information. In the temporal code model, the relative timing between firings matters more—information is stored in the specific pattern of intervals between spikes, vaguely like Morse code. But the temporal code model faces a difficult question: If a gap is "longer" or "shorter," it has to be longer or shorter relative to something. For the temporal code model to work, the brain needs to have a kind of metronome, a steady beat to allow the gaps between firings to hold meaning. Every computer has an internal clock to synchronize its activities across different chips. If the temporal code model is right, the brain should have something similar. Some neuroscientists posit that the clock is in the gamma rhythm, a semiregular oscillation of brain waves. But it doesn’t stay consistent. It can speed up or slow down depending on what a person experiences, such as a bright light. Such a fickle clock didn't seem like the full story for how neurons synchronize their signals, leading to ardent disagreements in the field about whether the gamma rhythm meant anything at all. © 2018 Condé Nast.
Keyword: Consciousness; Biological Rhythms
Link ID: 26494 - Posted: 08.13.2019
A new study analyzing samples from patients with and without acute flaccid myelitis (AFM) provides additional evidence for an association between the rare but often serious condition that causes muscle weakness and paralysis, and infection with non-polio enteroviruses. The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, funded the research, which was conducted by investigators at Columbia University’s Center for Infection and Immunity and investigators from the Centers for Disease Control and Prevention. The findings are reported in the online journal mBio. There have been 570 confirmed cases since CDC began tracking AFM in August 2014. AFM outbreaks were reported to the CDC in 2014, 2016 and 2018. AFM affects the spinal cord and is characterized by the sudden onset of muscle weakness in one or more limbs. Spikes in AFM cases, primarily in children, have coincided in time and location with outbreaks of EV-D68 and a related enterovirus, EV-A71. Both of these viruses typically cause mild respiratory illness from which most people recover fully. Despite the epidemiological link between enterovirus circulation and AFM cases, evidence of direct causality has not been found. The researchers first looked for direct evidence of enterovirus infection in the cerebrospinal fluid (CSF) of 13 children and one adult diagnosed with AFM in 2018. They also examined five CSF samples taken from people with other central nervous system diseases. The team used a new tool they developed called VirCapSeq-VERT, which can detect any viral genetic material that is at least 60% like that of any known vertebrate virus. They found enteroviral genetic material (EV-A71) in only the one adult AFM case and genetic material from another enterovirus (echovirus 25) in one of the non-AFM cases.
Keyword: Movement Disorders; Neuroimmunology
Link ID: 26493 - Posted: 08.13.2019
By Ryan P. Dalton Subject cDa29—well-known yet anonymous—resides somewhere in the north of England. You can almost see it: the peat stacks and old textile mills; the limestone and turf ruins where, on divine calling, Hadrian marked the northernmost reach of the Roman Empire. But even were you there, you wouldn’t see it the way cDa29 does. That’s because cDa29 is tetrachromatic: while most people see their world as a mix of three colors—red, green and blue—cDa29 sees hers in four. Difficult to imagine as that world may be for trichromats, your sense of smell provides access to an even richer world, one painted not in four colors but 400. You can almost smell it: the peat, the mills, the turf. How do your senses build these worlds? They begin with sensory “receptors,” which sit on the surfaces of cells and are activated by specific stimuli. In the case of vision, there are three color photoreceptors in your retina—activated by red, green or blue light. By keeping these receptors separated—such that no two photoreceptors occur together in one cell—your retina can keep track of what colors came from where. As a counterexample, you have a few dozen “bitter receptors” on your tongue, but each bitter taste cell contains several of them. This arrangement allows you to detect many different bitter compounds, but it does not help you distinguish between them. As these examples illustrate, you must both be able to detect a wide range of stimuli and to discriminate between those stimuli—and generally, your senses strike a balance between these two objectives. Ever the romantic, your sense of smell casts aside the suggestion of balance and optimizes for both detection and discrimination. Olfactory neurons in your nose have evolved some 400 odor receptors, and each neuron contains only one. Receptors are tuned to detect a few basic odors apiece: some detect geranium petals or pine needles, while others detect the by-products of putrefaction. To organize all this information, your olfactory neurons wire into an “olfactory map” on your brain’s olfactory bulb. Olfactory neurons are one of the few types of neurons that are born throughout your life, and each of the roughly 10,000 such neurons born each day in your nose subsequently wires into the olfactory map in your brain. © 2019 Scientific American
Keyword: Chemical Senses (Smell & Taste)
Link ID: 26492 - Posted: 08.13.2019
Laura Sanders A season of head hits left its mark on college football players’ brains, even when those hits didn’t cause concussions. Routine head bumps over the course of a season were linked to abnormal brain tissue in part of players’ brain stems, researchers report August 7 in Science Advances. It’s unclear if these brain stem changes affect mental performance, or whether the changes are permanent. But the study suggests that in addition to the big hits that cause concussions, these smaller knocks could cause trouble. During the 2011, 2012 and 2013 football seasons, a team led by researchers at the University of Rochester in New York recruited players from the university to participate in a study looking at head impacts and brain health. Each player wore an accelerometer in his helmet to capture the forces at play during all practices and games during a single season. The players also underwent pre- and post-season brain scans. A measure called fractional anisotropy let researchers estimate how well stretches of white matter brain tissue can carry neural signals, a key job of healthy brain tissue. The 38 players included in the study collectively took 19,128 hits. And by the end of their season, the players on average had lower measures of fractional anisotropy in their right midbrains — a part of the brain stem. These declines were more tightly linked to the number of hits that twisted heads, as opposed to direct head-on hits. Those rotational forces might be particularly damaging to brain tissue, a finding that fits with results from earlier studies, the researchers write. |© Society for Science & the Public 2000 - 2019.
Keyword: Brain Injury/Concussion
Link ID: 26491 - Posted: 08.13.2019
Laura Sanders The golf ball–sized chunk of brain is not cooperating. It’s thicker than usual, and bloodier. One side has a swath of tissue that looks, to my untrained eye, like gristle. Nick Dee, the neuroscientist charged with quickly cutting the chunk into neat pieces, confers with his colleagues. “We can trim off that ugliness on the side,” he says. The “ugliness” is the brain’s connective tissue called white matter. To produce useful slices for experiments, the brain tissue must be trimmed, superglued to a lipstick-sized base and then fed into a lab version of a deli slicer. But this difficult chunk isn’t cutting nicely. Dee and colleagues pull it off the base, trim it again and reglue. Half an hour earlier, this piece of neural tissue was tucked inside a 41-year-old woman’s head, on her left side, just above the ear. Surgeons removed the tissue to reach a deeper part of her brain thought to be causing severe seizures. Privacy rules prevent me from knowing much about her; I don’t know her name, much less her first memory, favorite meal or sense of humor. But within this piece of tissue, which the patient generously donated, are clues to how her brain — all of our brains, really — create the mind. Dee’s team is working fast because this piece of brain is alive. Some of the cells can still behave as if they are a part of a person’s brain, which means they hold enormous potential for scientists who want to understand how we remember, plan, behave and feel. After Dee and his team do their part, pieces of the woman’s brain will be whisked into the hands of eager scientists, where the cells will be photographed, zapped with electricity, relieved of their genetic material and even infected with viruses that make them glow green and red. © Society for Science & the Public 2000 - 2019
Keyword: Brain imaging; Evolution
Link ID: 26490 - Posted: 08.12.2019


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