By Aggie Mika Microglia—the brain’s own macrophages—can prompt excess eating and subsequent weight gain in mice fed high-fat diets, according to a study published today (July 5) in Cell Metabolism. The researchers demonstrate that an appetite-promoting inflammatory cascade driven by these immune cells occurs within the mediobasal region of the hypothalamus, a structure that, according to a news release, “contains key groups of neurons that regulate food intake and energy expenditure.” Prior studies have demonstrated that when mice are fed a diet high in saturated fat, they consume more while expending fewer calories, leading them to gain weight, the news release states. Additionally, previous work in both obese mice and humans has also shown that microglia within the hypothalamus increase following high-fat feeding, prompting inflammation, the authors write in their report. In the current study, the researchers examined whether microglial activity in the mediobasal hypothalamus had anything to do with the increased food consumption and weight gain observed in mice consuming diets high in fat. First, they used a drug to wipe out microglia in this region brain and found that microglia-lacking, high-fat consuming mice gained less weight than their non-drugged, high-fat counterparts. They then genetically manipulated mice so that their microglia weren’t capable of mounting an inflammatory response, and these mice also ate less and gained less weight than normal mice on the high-fat diets. © 1986-2017 The Scientist

Keyword: Obesity; Glia
Link ID: 23811 - Posted: 07.07.2017

By Mitch Leslie When you have a stuffy nose, a slice of freshly baked apple pie tastes like mush. But not being able to smell your food could have a surprising effect on your metabolism, potentially helping you remain thin even when you eat fatty foods, a new study in mice suggests. “This is a very exciting study, and the outcome is quite compelling,” says neuroendocrinologist Tamas Horvath of Yale School of Medicine, who wasn’t connected to the research. To conduct the study, molecular biologist Andrew Dillin of the University of California, Berkeley, and colleagues turned to a variety of genetically altered mice. The scientists gave them regular doses of the diphtheria toxin—which causes a temporary loss of odor-sensing neurons—to suppress their sense of smell. They then fed the rodents either a normal diet or fatty foods—the mouse equivalent of cheesecake and pizza—that usually induce obesity. After more than 3 months of noshing on regular chow, the odor-deprived rodents weighed slightly less than mice whose sense of smell was intact. In the group on the high-fat diet, however, the mice that couldn’t smell weighed 16% less than animals that could, which became obese. Losing the ability to smell also caused a different group of already-obese mice to lose weight, the researchers reveal today in Cell Metabolism. © 2017 American Association for the Advancement of Science.

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 23810 - Posted: 07.06.2017

Carl Zimmer With fossils and DNA, scientists are piecing together a picture of humanity’s beginnings, an origin story with more twists than anything you would find at the movie theater. The expert consensus now is that Homo sapiens evolved at least 300,000 years ago in Africa. Only much later — roughly 70,000 years ago — did a small group of Africans establish themselves on other continents, giving rise to other populations of people today. To Johannes Krause, the director of the Max Planck Institute for Human History in Germany, that gap seems peculiar. “Why did people not leave Africa before?” he asked in an interview. After all, he observed, the continent is physically linked to the Near East. “You could have just walked out.” In a study published Tuesday in Nature Communications, Dr. Krause and his colleagues report that Africans did indeed walk out — over 270,000 years ago. Based on newly discovered DNA in fossils, the researchers conclude that a wave of early Homo sapiens, or close relatives of our species, made their way from Africa to Europe. There, they interbred with Neanderthals. Then the ancient African migrants disappeared. But some of their DNA endured in later generations of Neanderthals. “This is now a comprehensive picture,” Dr. Krause said. “It brings everything together.” Since the 1800s, paleontologists have struggled to understand how Neanderthals are related to us. Fossils show that they were anatomically distinct, with a heavy brow, a stout body and a number of subtler features that we lack. The oldest bones of Neanderthal-like individuals, found in a Spanish cave called Sima de los Huesos, date back 430,000 years. More recent Neanderthal remains, dating to about 100,000 years ago, can be found across Europe and all the way to southern Siberia. © 2017 The New York Times Company

Keyword: Evolution
Link ID: 23809 - Posted: 07.06.2017

By Linda Geddes BILLIONS of dollars have been spent in search of treatments for psychiatric conditions and brain disorders, when a cheap and effective drug may have been right under our noses: light. Now hospitals are turning to light to treat depression, strokes and Parkinson’s disease, using it to hit the reset button on our internal clocks. From green light soothing the pain of migraine, to blue light reducing organ damage during surgery, recent small studies have uncovered some intriguing effects of this therapy. But apart from easing seasonal affective disorder, we’ve been slow to embrace light as a serious contender for treating neurological conditions. We’ve known for 15 years that a special kind of receptor in our eyes transmits information directly to the body’s master clock, as well as other brain areas that control mood and alertness. These cells are particularly responsive to bluish light, including sunlight. These receptors enable light to act as a powerful reset switch, keeping the clock in our brain synced to the outside world. But this clock can fall out of sync or weaken as part of ageing or a range of disorders – a problem doctors are now starting to treat with light. Most hospitals have small windows and 24-hour lighting, both of which might exacerbate health problems. To tackle this, several hospitals in Europe and the US are installing dynamic “solid state” lighting, which changes like daylight over the course of a day. Such lights can, for example, shine bright whitish-blue in the morning, grow warmer and dimmer throughout the day, and turn orange or switch off at night. © Copyright New Scientist Ltd.

Keyword: Biological Rhythms; Stroke
Link ID: 23808 - Posted: 07.06.2017

By James Gallagher Abnormal deposits that build up in the brain during Alzheimer's have been pictured in unprecedented detail by UK scientists. The team at the MRC Laboratory of Molecular Biology says its findings "open up a whole new era" in neurodegenerative disease. Their work should make it easier to design drugs to stop brain cells dying. The researchers used brain tissue from a 74-year-old woman who died after having Alzheimer's disease. The form of dementia leads to tangles of a protein called tau spreading throughout the brain. The more tau tangles there are, the worse the symptoms tend to be. Doctors have known this has happened for decades but what has been missing is a detailed understanding of what the tangles look like. The team took advantage of the "resolution revolution" in microscopy to take thousands of highly detailed images of the tau inside the woman's brain tissues. And using computer software, they figured out the tangles look like this: Image copyright LMB It is pretty meaningless to an untrained eye, but to scientists this could be one of the most important recent discoveries in tackling dementia. Attempts to develop a drug to slow the pace of dementia have been met by repeated failure. But it is hard to come up with a drug when you do not know the precise chemical structure of what you are targeting. Dr Sjors Scheres, one of the researchers, told the BBC News website: "It's like shooting in the dark - you can still hit something but you are much more likely to hit if you know what the structure is. "We are excited - it opens up a whole new era in this field, it really does." © 2017 BBC.

Keyword: Alzheimers
Link ID: 23807 - Posted: 07.06.2017

By NICHOLAS BAKALAR Poor sleep may be an indication of increased risk for Alzheimer’s disease, a new study of older people suggests. Researchers studied 101 cognitively normal people, average age 63, who completed well-validated sleep questionnaires. They analyzed their spinal fluid for the presence of indicators of the plaques and tangles that are characteristic of Alzheimer’s. The study is in Neurology. After controlling for age, a family history of Alzheimer’s, the ApoE gene that increases Alzheimer’s risk and other factors, they found that poor sleep quality, sleep problems and daytime sleepiness were associated with increased spinal fluid indicators of Alzheimer’s disease. The reason for the association is unclear, but at least one animal study found that during sleep the brain’s capacity to clear toxins like beta amyloid, the toxic protein that forms plaques in the brains of those with Alzheimer’s, improves. It may be that poor sleep interferes with this process in people, too. “Not everyone with sleep problems is destined to develop Alzheimer’s disease,” said the senior author, Barbara B. Bendlin, an associate professor of medicine at the University of Wisconsin School of Medicine and Public Health. “We’re looking at groups of people, and over the whole group we find the association of poor sleep with the markers of Alzheimer’s. But when you look at individuals, not everyone shows that pattern.” © 2017 The New York Times Company

Keyword: Alzheimers; Sleep
Link ID: 23806 - Posted: 07.06.2017

Mike Mariani With its bright colors, anthropomorphic animal motif, and nautical-themed puzzle play mat, Dr. Kimberly Noble’s laboratory at Columbia University looks like your typical day care center—save for the team of cognitive neuroscientists observing kids from behind a large two-way mirror. The Neurocognition, Early Experience, and Development Lab is home to cutting-edge research on how poverty affects young brains, and I’ve come here to learn how Noble and her colleagues could soon definitively prove that growing up poor can keep a child’s brain from developing. Noble, a 40-year-old from outside of Philadelphia who discusses her work with a mix of enthusiasm and clinical restraint, is among the handful of neuroscientists and pediatricians who’ve seen increasing evidence that poverty itself—and not factors like nutrition, language exposure, family stability, or prenatal issues, as previously thought—may diminish the growth of a child’s brain. Now she’s in the middle of planning a five-year, nationwide study that could establish a causal link between poverty and brain development—and, in the process, suggest a path forward for helping our poorest children. It’s the culmination of years of work for Noble, who helped jump-start this fledgling field in the early 2000s when, as a University of Pennsylvania graduate student, she and renowned cognitive neuroscientist Martha Farah began exploring the observation that poor kids tended to perform worse academically than their better-off peers. They wanted to investigate the neurocognitive underpinnings of this relationship—to trace the long-standing correlation between socioeconomic status and academic performance back to specific parts of the brain. “There have been decades of work from social scientists, looking at socioeconomic disparities in broad cognitive outcomes—things like IQ or high school graduation rate,” she says. “But there’s no high school graduation part of the brain.” ©2017 Mother Jones and the Foundation for National Progress.

Keyword: Development of the Brain; Stress
Link ID: 23805 - Posted: 07.04.2017

Blood samples from infants who died of Sudden Infant Death Syndrome (SIDS) had high levels of serotonin, a chemical that carries signals along and between nerves, according to a study funded in part by the National Institutes of Health. The finding raises the possibility that a test could be developed to distinguish SIDS cases from other causes of sleep-related, unexpected infant death. The study, led by Robin L. Haynes, Ph.D., of Boston Children’s Hospital and Harvard Medical School, appears in the Proceedings of the National Academy of Sciences. NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) provided funding for the work. SIDS is the sudden death of an infant under one year of age that remains unexplained after a complete autopsy and death scene investigation. In the current study, researchers reported that 31 percent of SIDS infants (19 of 61) had elevated blood levels of serotonin. In previous studies, the researchers reported multiple serotonin-related brain abnormalities in SIDS cases, including a decrease in serotonin in regions involved in breathing, heart rate patterns, blood pressure, temperature regulation, and arousal during sleep. Taken together, the researchers wrote, the findings suggest that an abnormality in serotonin metabolism could indicate an underlying vulnerability that increases SIDS risk and that testing blood samples for serotonin could distinguish certain SIDS cases from other infant deaths. However, they caution that more research is needed. NICHD’s Safe to Sleep campaign provides information on ways to reduce the risk of SIDS and other sleep-related causes of infant death.

Keyword: Sleep; Development of the Brain
Link ID: 23804 - Posted: 07.04.2017

Elana Gordon By the time Elvis Rosado was 25, he was addicted to opioids and serving time in jail for selling drugs to support his habit. "I was like, 'I have to kick this, I have to break this,' " he says. For Rosado, who lives in Philadelphia, drugs had become a way to disassociate from "the reality that was life." He'd wake up physically needing the drugs to function. His decision to finally stop using propelled him into another challenging chapter of his addiction and one of the most intense physical and mental experiences he could have imagined: detoxing. "The symptoms are horrific," Rosado says. There are recovery and treatment centers that can help people quit using drugs — in fact, it's a multi-billion-dollar industry. But this help can be expensive, and waiting lists for state and city-funded programs are often extremely long. So can detoxing on your own be the solution? In most cases, the answer is no. In fact, a growing movement within the field of addiction medicine is challenging the entire notion of detox and the assumption that when people cleanse themselves of chemicals, they're on the road to recovery. Article continues after sponsorship "That's a really pernicious myth, and it has erroneous implications," says Dr. Frederic Baurer, president of the Pennsylvania Society of Addiction Medicine. But at the time, Rosado says, he needed to end his "longtime love affair" with codeine. Like Oxycontin and morphine, it's an opioid. In jail, these drugs were easily available, Rosado recalls, through friends and cell mates. © 2017 npr

Keyword: Drug Abuse
Link ID: 23803 - Posted: 07.04.2017

By Sandrine Ceurstemont Bird or beast? A cuckoo seems to have learned how to mimic the sounds made by the pig-like peccaries it lives alongside, perhaps to ward off predators. The Neomorphus ground cuckoos live in forests in Central and South America, where they often follow herds of wild peccaries so they can feed on the invertebrates that the peccaries disturb as they plough through the leaf litter. Ecologists have noticed that when the cuckoos clap their beaks together they sound a lot like the tooth clacks the peccaries make to deter large predatory cats. To find out whether this is just coincidence or evidence of mimicry, Cibele Biondo at the Federal University of ABC in Brazil and her team analysed the cuckoo and peccary sounds, and compared them with the beak clapping sounds made by roadrunners – close relatives of the ground cuckoos. Logically, the cuckoos should sound most similar to roadrunners, given that the two are closely related. But the analysis suggested otherwise. “The acoustic characteristics are more similar to the teeth clacking of peccaries,” says Biondo. She suspects that cuckoos have something to gain by imitating the peccaries, particularly in the dark, dense forests where predators rely on hearing as much as vision. “Cuckoos may deceive predators by making it appear that peccaries are present when they are not,” says Biondo. © Copyright New Scientist Ltd.

Keyword: Evolution; Animal Communication
Link ID: 23802 - Posted: 07.04.2017

Fergus Walsh Medical correspondent The world's most detailed scan of the brain's internal wiring has been produced by scientists at Cardiff University. The MRI machine reveals the fibres which carry all the brain's thought processes. It's been done in Cardiff, Nottingham, Cambridge and Stockport, as well as London England and London Ontario. Doctors hope it will help increase understanding of a range of neurological disorders and could be used instead of invasive biopsies. I volunteered for the project - not the first time my brain has been scanned. Computer games In 2006, it was a particular honour to be scanned by the late Sir Peter Mansfield, who shared a Nobel prize for his work on developing Magnetic Resonance Imaging, one of the most important breakthroughs in medicine. He scanned me using Nottingham University's powerful new 7 Tesla scanner. When we looked at the crisp, high resolution images, he told me: "I'm a physicist, so don't ask me to tell you to whether there's anything amiss with your brain - you'd need a neurologist for that." I was the first UK Biobank volunteer to have their brain and other organs imaged as part of the world's biggest scanning project. More recently, I had my brain scanned while playing computer games, as part of research into the effects of sleep deprivation on cognition. So my visit to the Cardiff University's Brain Research Imaging Centre (CUBRIC) held no particular concerns. The scan took around 45 minutes and seemed unremarkable. A neurologist was on hand to reassure me my brain looked normal. My family quipped that they were happy that a brain had been found inside my thick skull. But nothing could have prepared me for the spectacular images produced by the team at Cardiff, along with engineers from Siemens in Germany and the United States. © 2017 BBC.

Keyword: Brain imaging
Link ID: 23801 - Posted: 07.04.2017

By RONI CARYN RABIN It may be the most palatable advice you will ever get from a doctor: Have a glass of wine, a beer or a cocktail every day, and you just might prevent a heart attack and live longer. But the mantra that moderate drinking is good for the heart has never been put to a rigorous scientific test, and new research has linked even modest alcohol consumption to increases in breast cancer and changes in the brain. That has not stopped the alcoholic beverage industry from promoting the alcohol-is-good-for-you message by supporting scientific meetings and nurturing budding researchers in the field. Now the National Institutes of Health is starting a $100 million clinical trial to test for the first time whether a drink a day really does prevent heart attacks. And guess who is picking up most of the tab? Five companies that are among the world’s largest alcoholic beverage manufacturers — Anheuser-Busch InBev, Heineken, Diageo, Pernod Ricard and Carlsberg — have so far pledged $67.7 million to a foundation that raises money for the National Institutes of Health, said Margaret Murray, the director of the Global Alcohol Research Program at the National Institute on Alcohol Abuse and Alcoholism, which will oversee the study. The decision to let the alcohol industry pay the bulk of the cost has raised concern among researchers who track influence-peddling in science. “Research shows that industry-sponsored research almost invariably favors the interests of the industry sponsor, even when investigators believe they are immune from such influence,” said Marion Nestle, a professor of nutrition and food studies at New York University who is the author of several books on the topic, including “Food Politics: How the Food Industry Influences Nutrition and Health.” © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 23800 - Posted: 07.04.2017

By Wallis Snowdon, Ariel Fournier The seizure of a controversial drug in Edmonton is evidence that more research is required on kratom as a possible antidote in Alberta's deadly opioid epidemic, says a leading researcher in the field. "Everything has to be taken with caution, but does that mean you take it off the streets?" said Susruta Majumdar, a chemist who has worked on numerous studies into the drug. "Probably not," said Majumdar, who works in the department of neurology at Sloan Kettering Cancer Center in New York. "It's a little premature to ban it right away and take it out of the public scenario because very little research has been done. It's a weak alkaloid but we need to be cautious about it." In a news release Tuesday, Health Canada said it had seized unauthorized kratom products from two Edmonton head shops. The packets were confiscated from a store called Jupiter on Whyte Avenue and from another called Bogart's Pipes and Papers on 132nd Avenue. Kratom is a coffee-like plant native to southeast Asia. The drug is traditionally consumed by chewing on the leaves, but can also be ingested as a capsule or powder or as a tea. Health Canada said the herbal product has been linked to both "narcotic and stimulant-like effects," and may pose serious health risks including nausea, vomiting, seizures, and liver toxicity. ©2017 CBC/Radio-Canada.

Keyword: Drug Abuse
Link ID: 23799 - Posted: 07.01.2017

ByMaia Szalavitz George Sarlo is throwing cash at research into how drugs like magic mushrooms can help people overcome trauma like his own. Deep in the Mexican jungle, in a village so remote it's only accessible by boat, 74-year-old venture capitalist George Sarlo waited to meet his father. It was the fall of 2012, and Sarlo knew his quest seemed absurd. After all, his father had been dead for decades, and he had no connection to this region of rainforests and beaches and its indigenous peoples. As the financier watched a shaman prepare a ceremonial cup of bitter brown ayahuasca, he couldn't believe that he'd agreed to swallow this nauseating psychedelic brew for a second time. But he had traveled for 12 hours—via plane, boat, and finally on foot—to this primeval place, a newly-built gazebo-like wood platform without walls. He had expressed his intentions in a group therapy session in preparation; he had eaten a special, bland diet and even halted other medications. He also trusted his friend, Dr. Gabor Maté, a fellow Hungarian Holocaust survivor, who led the therapy and had arranged the trip. Maté is perhaps best known for his book, In the Realm of Hungry Ghosts, which explores his work with extremely traumatized injection drug users in Vancouver. He's been offering psychedelic therapy to trauma survivors since learning about the potential of ayahuasca in 2008.

Keyword: Drug Abuse; Stress
Link ID: 23798 - Posted: 07.01.2017

Hannah Devlin Doctors in Bristol are set to begin the world’s first clinical study into the use of MDMA to treat alcohol addiction. Researchers are testing whether a few doses of the drug, in conjunction with psychotherapy, could help patients overcome addiction more effectively than conventional treatments. The small trial was granted ethical approval a few weeks ago and the team expects to give the first dose of MDMA, the active ingredient in ecstasy pills, within the next two months. Ben Sessa, a clinical psychiatrist on the trial and senior research fellow at Imperial College London said: “We know that MDMA works really well in helping people who have suffered trauma and it helps to build empathy. Many of my patients who are alcoholics have suffered some sort of trauma in their past and this plays a role in their addiction.” Twenty patients, recruited through the recreational drug and alcohol services in Bristol, will be given the drug in capsule form during two supervised treatment sessions. The participants will be heavy drinkers – typically consuming the equivalent of five bottles of wine a day – who have relapsed into alcoholism repeatedly after trying other forms of treatment. “After 100 years of modern psychiatry our treatments are really poor,” said Sessa, speaking at the Breaking Convention conference in London. “The chances of relapse for these patients are really high – 90% at three years. No one has ever given MDMA to treat alcoholism before.” © 2017 Guardian News and Media Limited

Keyword: Drug Abuse
Link ID: 23797 - Posted: 07.01.2017

By ABBY GOODNOUGH WASHINGTON — The Senate leadership’s efforts to salvage the Republican health care bill have focused in part on adding $45 billion for states to spend on opioid addiction treatment. That is a big pot of money. But addiction specialists said it was drastically short of what would be needed to make up for the legislation’s deep cuts to Medicaid, which has provided treatment for hundreds of thousands of people caught up in a national epidemic of opioid abuse. The new money would most likely flow to states in the form of grants over 10 years, averaging out to $4.5 billion per year. With hundreds of people dying every week from overdoses of heroin, fentanyl and opioid painkillers, some specialists say a fixed amount of grant money is simply inadequate compared with the open-ended funding stream that Medicaid provides to treat all who qualify for the coverage. “When it comes to other illnesses like breast cancer or heart disease, we’d never rely solely on grants for treatment — because we know that grants are not substitutes for health coverage,” said Linda Rosenberg, president and chief executive of the National Council for Behavioral Health, which represents treatment providers. “Addiction is no different.” The Affordable Care Act vastly expanded access to addiction treatment by designating those services as “essential benefits.” That means they had to be covered through both an expansion of Medicaid to far more low-income adults and the marketplaces set up under the law for people to buy private plans. Both the House and Senate health bills would effectively end the expansion and cap federal Medicaid spending, resulting in the loss of coverage for millions of people, according to the Congressional Budget Office. © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 23796 - Posted: 07.01.2017

Martha Mills So, it turns out I’m getting better at depression. That isn’t to say I’ve stopped suffering it, or that it is any less debilitating when it sneaks up after a two-year hiatus and pile-drives me into a blistering agony of mental carpet burns topped with a patronising tousle of the bed-hair, like a nostalgic school bully. No, what’s “better” about me is spotting it and moving quicker through the self-blame method of diagnosis. We all have down days, and that’s what you hope these are. Only they stopped being a day or two of feeling blue that can be whiled away with the distraction of a conspiratorial sofa and questionable DVD collection, and have merged into weeks since you were last able to feel anything but disappointment on waking up, and the choice between showering or just smelling like a tramp’s undercarriage has gone beyond struggle into pure resignation. Being especially practised at denial, I decided that I, a mere mortal with a solid history of depressive episodes since childhood, could fake my way out of this oncoming tsunami of debilitating black fog using the advice that people who have never experienced depression trot out – an experiment that could surely only succeed [sidelong glance to camera]. I would improve my diet and exercise, force myself to take up hobbies, I would “soldier on until it passed” and thrust myself (reluctantly) into social situations. I even tried “looking on the bright side” but it turned out to just be glare on my TV. © 2017 Guardian News and Media Limited

Keyword: Depression
Link ID: 23795 - Posted: 07.01.2017

By Nicholette Zeliadt Researchers have known that genes contribute to autism since the 1970s, when a team found that identical twins often share the condition. Since then, scientists have been racking up potential genetic culprits in autism, a process that DNA-decoding technologies have accelerated in the past decade. As this work has progressed, scientists have unearthed a variety of types of genetic changes that can underlie autism. The more scientists dig into DNA, the more intricate its contribution to autism seems to be. How do researchers know genes contribute to autism? Since the first autism twin study in 1977, several teams have compared autism rates in twins and shown that autism is highly heritable. When one identical twin has autism, there is about an 80 percent chance that the other twin has it, too. The corresponding rate for fraternal twins is around 40 percent. However, genetics clearly does not account for all autism risk. Environmental factors also contribute to the condition, although researchers disagree on the relative contributions of genes and environment. Some environmental risk factors for autism, such as exposure to a maternal immune response in the womb or complications during birth, may work with genetic factors to produce autism or intensify its features. Is there such a thing as an autism gene? Not really. There are several conditions associated with autism that stem from mutations in a single gene, including fragile X and Rett syndromes. But less than 1 percent of non-syndromic cases of autism stem from mutations in any single gene. © 1996-2017 The Washington Post

Keyword: Autism; Genes & Behavior
Link ID: 23794 - Posted: 07.01.2017

By Mo Costandi You can’t teach an old dog new tricks—or can you? Textbooks tell us that early infancy offers a narrow window of opportunity during which sensory experience shapes the way neuronal circuits wire up to process sound and other inputs. A lack of proper stimulation during this “critical period” has a permanent and detrimental effect on brain development. But new research shows the auditory system in the adult mouse brain can be induced to revert to an immature state similar to that in early infancy, improving the animals’ ability to learn new sounds. The findings, published Thursday in Science, suggest potential new ways of restoring brain function in human patients with neurological diseases—and of improving adults’ ability to learn languages and musical instruments. In mice, a critical period occurs during which neurons in a portion of the brain’s wrinkled outer surface, the cortex, are highly sensitized to processing sound. This state of plasticity allows them to strengthen certain connections within brain circuits, fine-tuning their auditory responses and enhancing their ability to discriminate between different tones. In humans, a comparable critical period may mark the beginning of language acquisition. But heightened plasticity declines rapidly, and this continues throughout life, making it increasingly difficult to learn. In 2011 Jay Blundon, a developmental neurobiologist at Saint Jude Children's Research Hospital, and his colleagues reported that the critical periods for circuits connecting the auditory cortex and the thalamus occur at about the same time. © 2017 Scientific American,

Keyword: Hearing; Development of the Brain
Link ID: 23793 - Posted: 06.30.2017

By Kathryn Casteel It’s no secret that heroin has become an epidemic in the United States. Heroin overdose deaths have risen more than sixfold in less than a decade and a half.1 Yet according to one of the most widely cited sources of data on drug use, the number of Americans using heroin has risen far more slowly, roughly doubling during the same time period.2 Most major researchers believe that source, the National Survey on Drug Use and Health, vastly understates the increase in heroin use. But many rely on the survey anyway for a simple reason: It’s the best data they have. Several other sources that researchers once relied on are no longer being updated or have become more difficult to access. The lack of data means researchers, policymakers and public health workers are facing the worst U.S. drug epidemic in a generation without essential information about the nature of the problem or its scale. “We’re simply flying blind when it comes to data collection, and it’s costing lives,” said John Carnevale, a drug policy expert who served at the federal Office of National Drug Control Policy under both Republican and Democratic administrations. There is anecdotal evidence of how patterns of drug use are changing, Carnevale said, and special studies conducted in various localities are identifying populations of drug users. “But the national data sets we have in place now really don’t give us the answers that we need,” he said.

Keyword: Drug Abuse
Link ID: 23792 - Posted: 06.30.2017