Hannah Devlin Science correspondent They are diseases that threaten more than physical health: memories, personality, and the ability to move and speak are incrementally stolen. And until this year neurodegenerative diseases, from Alzheimer’s to ALS, had been entirely unstoppable. However, a breakthrough in Huntington’s disease this week suggests this bleak picture could be about to change. The landmark trial was the first to show that the genetic defect that causes Huntington’s could be corrected, raising hopes that the drug will become the first to slow the progress of the disease – or even stop it. The Huntington’s results alone would have been remarkable enough, but they come just a month after the same experimental class of drugs were revealed to help patients with a different degenerative disease, called Spinal Muscular Atrophy (SMA). Babies with the most severe form of SMA normally never develop the strength to sit up or roll over, but after four years on the drug, some of these children are starting to stand and take their first steps with a walker. The two trials have triggered a wave of optimism that drugs built on similar principles could be used to target a wide range of deadly brain disorders, possibly even Alzheimer’s and Parkinson’s. “I don’t want to overstate this too much, but this could be a turning point,” said Prof John Hardy, a neuroscientist at University College London who was awarded the Breakthrough prize for his work on Alzheimer’s. © 2017 Guardian News and Media Limited

Keyword: Huntingtons; Movement Disorders
Link ID: 24429 - Posted: 12.16.2017

By Roni Dengler Our brains don’t rest when we sleep. Electrical waves ripple through our noggins as our neurons talk to each other. Now, researchers have shown that when these waves don’t interact properly, we can lose our long-term memory. The work may help explain why older adults are so forgetful, and it could lead to new therapies to treat memory loss. To find out how sleep contributes to memory loss in old age, Randolph Helfrich, a neuroscientist at the University of California (UC), Berkeley, and his team gave healthy 70- and 20-year-olds a memory test. Participants were trained to match 120 common, short words—for example, “bird”—with nonsense words made of combinations of random syllables, like “jubu.” Once they learned the word-nonsense word combos, the volunteers played a version of the game “memory.” They had to match the word pairs twice: once about 10 minutes after they’d mastered the task, and again a few hours after waking from a full night’s rest. While they slept, researchers recorded the electrical activity in their brains. As expected, the older adults’ ability to remember the word pairs in the morning was worse than their young counterparts’. The electrical recordings revealed one reason. Two kinds of brain waves—slow oscillations, large undulations that promote restorative sleep, and sleep spindles, transient bursts of short waves—are tell-tale marks of deep, typically dreamless, non–rapid eye movement sleep. But these waves are out of sync in older people, the researchers report today in Neuron. This out-of-step activity, they say, interrupts communication between the parts of our brains that store short- and long-term memories. In effect, Helfrich says, the prefrontal cortex where long-term memories are stored needs to tell the hippocampus—the part of the brain where all memories go first—that it’s ready to receive information; if brain waves aren’t in sync, this communication gets lost. So do the memories. © 2017 American Association for the Advancement of Science

Keyword: Learning & Memory; Alzheimers
Link ID: 24428 - Posted: 12.15.2017

By PAM BELLUCK As the first babies born with brain damage from the Zika epidemic become 2-year-olds, the most severely affected are falling further behind in their development and will require a lifetime of care, according to a study published Thursday by the Centers for Disease Control and Prevention. The study, the first to comprehensively assess some of the oldest Zika babies in Brazil, focused on 15 of the most disabled children born with abnormally small heads, a condition called microcephaly. At about 22 months old, these children had the cognitive and physical development of babies younger than 6 months. They could not sit up or chew, and they had virtually no language. “A child might be making those raspberry sounds, but they are not making even the sort of consonant sounds like ‘mama, baba, dada,’” said Dr. Georgina Peacock, an author of the study and the director of the division of human development and disability at the C.D.C.’s National Center on Birth Defects and Developmental Disabilities. It is unclear how many of the nearly 3,000 Brazilian Zika babies born with microcephaly will have outcomes as severe as the children in the study, but the experiences of doctors working in Brazil suggest it could be hundreds. “It’s heartbreaking,” the C.D.C. director, Dr. Brenda Fitzgerald, said in an interview. “We would expect that these children are going to require enormous amounts of work and require enormous amounts of care.” The new study, conducted with the Brazilian Ministry of Health and other organizations, evaluated children in Paraíba state, part of Brazil’s northeastern region, which became the epicenter of the Zika crisis. The researchers initially studied 278 babies born in Paraíba between October 2015 and the end of January 2016. Of those, 122 families agreed to participate in follow-up evaluations this year. The study released Thursday involves what were considered the most severe of those cases, Dr. Peacock said. © 2017 The New York Times Company

Keyword: Development of the Brain
Link ID: 24427 - Posted: 12.15.2017

Scientists have identified differences in a group of genes they say might help explain why some people need a lot more sleep — and others less — than most. The study, conducted using fruit fly populations bred to model natural variations in human sleep patterns, provides new clues to how genes for sleep duration are linked to a wide variety of biological processes. Researchers say a better understanding of these processes could lead to new ways to treat sleep disorders such as insomnia and narcolepsy. Led by scientists with the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health, the study will be published on Dec. 14 in PLOS Genetics. “This study is an important step toward solving one of the biggest mysteries in biology: the need to sleep,” says study leader Susan Harbison, Ph.D., an investigator in the Laboratory of Systems Genetics at NHLBI. “The involvement of highly diverse biological processes in sleep duration may help explain why the purpose of sleep has been so elusive.” Scientists have known for some time that, in addition to our biological clocks, genes play a key role in sleep and that sleep patterns can vary widely. But the exact genes controlling the duration of sleep and the biological processes that are linked to these genes have remained unclear. To learn more, scientists artificially bred 13 generations of wild fruit flies to produce flies that were either long sleepers (sleeping 18 hours each day) or short sleepers (sleeping three hours each day). The scientists then compared genetic data between the long and short sleepers and identified 126 differences among 80 genes that appear to be associated with sleep duration. They found that these genetic differences were tied to several important developmental and cell signaling pathways. Some of the genes identified have known functions in brain development, as well as roles in learning and memory, the researchers said.

Keyword: Sleep; Genes & Behavior
Link ID: 24426 - Posted: 12.15.2017

By NICHOLAS BAKALAR A new study suggests that vigorous physical activity may increase the risk for vision loss, a finding that has surprised and puzzled researchers. Using questionnaires, Korean researchers evaluated physical activity among 211,960 men and women ages 45 to 79 in 2002 and 2003. Then they tracked diagnoses of age-related macular degeneration, from 2009 to 2013. Macular degeneration, the progressive deterioration of the central area of the retina, is the leading cause of vision loss in the elderly. They found that exercising vigorously five or more days a week was associated with a 54 percent increased risk of macular degeneration in men. They did not find the association in women. The study, in JAMA Ophthalmology, controlled for more than 40 variables, including age, medical history, body mass index, prescription drug use and others. The authors write that excessive exercise might affect the eye’s choroid, a sensitive vascular membrane that surrounds the retina, but “epidemiologic studies cannot provide any evidence for the mechanism or pathology.” The authors acknowledge that the study depends partly on self-reports, which are not always reliable, and that it is an observational study that does not prove cause and effect. © 2017 The New York Times Company

Keyword: Vision
Link ID: 24425 - Posted: 12.15.2017

Amy Maxmen A study of some of the world’s most obscure marine life suggests that the central nervous system evolved independently several times — not just once, as previously thought1. The invertebrates in question belong to families scattered throughout the animal evolutionary tree, and they display a diversity of central nerve cord architectures. The creatures also activate genes involved with nervous system development in other, well-studied animals — but they often do it in non-neural ways, report the authors of the paper, published on 13 December in Nature. “This puts a stake in the heart of the idea of an ancestor with a central nerve cord,” says Greg Wray, an evolutionary developmental biologist at Duke University in Durham, North Carolina. “That opens up a lot of questions we don’t have answers to — like, if central nerve cords evolved independently in different lineages, why do they have so many similarities?” In 1875, German zoologist Anton Dohrn noted anatomical similarities between the central nerve cord that runs length-wise through the bodies of annelids — a group of invertebrates that includes earthworms — and the nerve cord in the spine of vertebrates. He proposed that the groups’ ancient common ancestor had a nerve cord that ran along its belly-side, as seen in annelids. He also suggested that this cord flipped to the back of the body in a more recent animal that gave rise to all vertebrates. © 2017 Macmillan Publishers Limited,

Keyword: Evolution; Development of the Brain
Link ID: 24424 - Posted: 12.14.2017

By GRETCHEN REYNOLDS Intense treadmill exercise can be safe for people who have recently been given diagnoses of Parkinson’s disease and may substantially slow the progression of their condition, according to an important new study of adults in the early stages of the disease. But the same study’s results also indicate that gentler exercise, while safe for people with Parkinson’s, does not seem to delay the disease’s advance. As most of us know, Parkinson’s disease is a progressive neurological disorder that involves problems with motor control. Symptoms like weakness, stiffness, loss of balance and falls can make exercise difficult and potentially hazardous. Though Parkinson’s is currently incurable, its symptoms can be eased for a time with various drugs. But most of those drugs lose their effectiveness in people over time. So some researchers have begun searching for other treatment options, particularly for use in the beginning stages of the disease. If people with early Parkinson’s could brake the disease’s advance and delay their need to start medications, the researchers have reasoned, they might change the arc of their disease, delaying its most severe effects. That possibility recently led a consortium of researchers from Northwestern University, the University of Colorado’s Anschutz Medical Campus in Aurora and other institutions to look at exercise as a treatment. There were precedents. Animal studies already had shown that exercise reduced symptoms and slowed physical decline in a rodent version of Parkinson’s. But rodents are not people. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 24423 - Posted: 12.14.2017

By Jessica Hamzelou An Italian family that is barely able to sense pain has had the genetic root of their shared disorder uncovered. Understanding this gene may lead to new painkiller drugs. The affected family members include a 78-year-old woman, her two middle-aged daughters, and their three children. All of them fail to sense pain in the way most of us do, and don’t notice when they are being injured. When they were assessed, the family members were found to have bone fractures in their arms and legs that they hadn’t realised were there. “Sometimes they feel pain in the initial break but it goes away very quickly,” says James Cox, of University College London. “For example, Letizia broke her shoulder while skiing, but then kept skiing for the rest of the day and drove home. She didn’t get it checked out until the next day.” To find the cause of their lack of pain sensitivity, Cox and his colleagues performed a series of tests on the family members. The team found that all six individuals had normal numbers of nerves in their skin, but that they all had a mutation in a gene called ZFHX2. When the team deleted this gene entirely in mice, they found that the animals were not as good at sensing when painful pressure was applied to their tails, but they were hypersensitive to heat sensations. This suggests the gene may play a role in controlling whether stimuli are painful or not. © Copyright New Scientist Ltd.

Keyword: Pain & Touch; Genes & Behavior
Link ID: 24422 - Posted: 12.14.2017

Tina Hesman Saey PHILADELPHIA — Flat brains growing on microscope slides may have revealed a new wrinkle in the story of how the brain folds. Cells inside the brains contract, while cells on the outside grow and push outward, researchers at the Weizmann Institute of Science in Rehovot, Israel, discovered from working with the lab-grown brains, or organoids. This push and pull results in folds in the organoids similar to those found in full-size brains. Orly Reiner reported the results December 5 at the joint meeting of the American Society for Cell Biology and the European Molecular Biology Organization. Reiner and her colleagues sandwiched human brain stem cells between a glass microscope slide and a porous membrane. The apparatus allowed the cells access to nutrients and oxygen while giving the researchers a peek at how the organoids grew. The cells formed layered sheets that closed up at the edges, making the organoids resemble pita bread, Reiner said. Wrinkles began to form in the outer layers of the organoids about six days after the mini brains started growing. These brain organoids may help explain why people with lissencephaly — a rare brain malformation in which the ridges and folds are missing — have smooth brains. The researchers used the CRISPR/Cas9 gene-editing system to make a mutation in the LIS1 gene. People with lissencephaly often have mutations in that gene. Cells carrying the mutation didn’t contract or move normally, the team found. |© Society for Science & the Public 2000 - 2017.

Keyword: Development of the Brain
Link ID: 24421 - Posted: 12.14.2017

Eating is prompted, in part, by brain regions that help to maintain the body’s energy levels. But hunger pangs are not the only motivation for a trip to the snack bar. In an effort to understand how the brain’s emotional and cognitive machinery influences appetite, Yunlei Yang and his colleagues at the State University of New York Upstate Medical University in Syracuse examined the medial septal complex, a group of brain cells that has a role in emotion. Some of the complex’s cells produce a signalling chemical called glutamate. When the scientists turned on these glutamate-producing cells in mice, the animals ate less than half as much as control mice. That makes the region a good starting point for studies of emotionally triggered eating, the team says. Proc. Natl Acad. Sci. USA (2017)

Keyword: Obesity; Emotions
Link ID: 24420 - Posted: 12.14.2017

Hannah Devlin Science correspondent A landmark trial for Huntington’s disease has announced positive results, suggesting that an experimental drug could become the first to slow the progression of the devastating genetic illness. The results have been hailed as “enormously significant” because it is the first time any drug has been shown to suppress the effects of the Huntington’s mutation that causes irreversible damage to the brain. Current treatments only help with symptoms, rather than slowing the disease’s progression. Prof Sarah Tabrizi, director of University College London’s Huntington’s Disease Centre who led the phase 1 trial, said the results were “beyond what I’d ever hoped ... The results of this trial are of ground-breaking importance for Huntington’s disease patients and families,” she said. The results have also caused ripples of excitement across the scientific world because the drug, which is a synthetic strand of DNA, could potentially be adapted to target other incurable brain disorders such as Alzheimer’s and Parkinson’s. The Swiss pharmaceutical giant Roche has paid a $45m licence fee to take the drug forward to clinical use. Huntington’s is an incurable degenerative disease caused by a single gene defect that is passed down through families. The first symptoms, which typically appear in middle age, include mood swings, anger and depression. Later patients develop uncontrolled jerky movements, dementia and ultimately paralysis. Some people die within a decade of diagnosis. © 2017 Guardian News and Media Limited

Keyword: Huntingtons; Genes & Behavior
Link ID: 24419 - Posted: 12.11.2017

Hannah Devlin Huntington’s has blighted Peter Allen’s family for generations. He watched his mother, Stephanie, slowly die from the disease and before that his grandmother, Olive, fell victim to the same illness. At 51 years old, Peter is the first of his generation to show signs of the illness, but his sister, Sandy, and brother, Frank, know they are also carrying the gene. The onset of Huntington’s is insidious. Psychological changes typically come first – tiredness, mood swings, apathy and anger. Four years ago, Peter was formally diagnosed as symptomatic when he began suffering anxiety and panic attacks so severe he would become convinced that he couldn’t swallow. In retrospect, the depression he suffered in his thirties may have been an earlier manifestation of changes happening his brain. In person, Peter is articulate, funny and exudes affection for his wife and siblings, but there are small signs of the changes that are underway. Every now and then he pauses to search for the right word. A loss of dexterity means he can no longer write or sign his name, his balance is unsteady and, when tired, his speech becomes slurred. “You know that you’re gradually lessening,” he says. A lack of awareness about the disease and its symptoms means people sometimes assume he is drunk. “I’ve been asked to leave pubs before I’ve even had a drink,” he says. “I don’t go to those pubs any more.” Peter took redundancy from his marketing job at Network Rail in 2015 and has not returned to full-time work, although he is retraining to become a garden designer. Anti-depressant drugs have helped bring the psychological symptoms under control. In future, he will be offered other drugs to stiffen his muscles, which helps reduce involuntary movements. But no current treatments can slow the relentless progression of the disease, the loss of memory, motor control and eventually the ability to think. © 2017 Guardian News and Media Limited

Keyword: Huntingtons; Genes & Behavior
Link ID: 24418 - Posted: 12.11.2017

/ By Rae Ellen Bichell In mid-October, Dr. David Bennett, a neurologist who directs the Alzheimer’s Disease Center at Rush University Medical Center in Chicago, stood in a St. Louis auditorium packed with nuns. His goal: To convince them — particularly the ones without brain disease — to donate their brains to science. “We are beginning to understand how little we actually know about the human brain.” Politicians, Bennett is fond of saying, can walk into a room and separate people from their money. “I can walk into a room and separate people from their brains.” To Bennett, making such acquisitions is, in some ways, more crucial than ever. Demand for brains for scientific research is rising across the board — driven in varying degrees by increased funding for research on brain disorders, rising incidence of age-related brain disease, big technological leaps in scientific tools used to analyze the brain, and a growing sense that sometimes, studying animals just isn’t good enough to understand and fix human disease. But more than this, scientists like Bennett are realizing that the brains they have traditionally studied (Bennett maintains 4,000 square feet of cabinets and freezers full of brain slices in Chicago), are too often riddled with the signs of end stage Alzheimer’s and other maladies that contribute to dementia. Far more rare are comparatively healthy brains that can allow scientists to more accurately identify what causes dementia — and what protects us from it. That deficiency now has Bennett and other scientists working hard to stock their shelves with a particularly precious resource: the brains of people like Sister Carleen Reck, who heard Bennett speak and thought his request for brain donations was a good idea, so she signed an anatomical gift act. Copyright 2017 Undark

Keyword: Alzheimers; Brain imaging
Link ID: 24417 - Posted: 12.11.2017

By PERRI KLASS, M.D. What does the child who can’t say goodbye to a parent without breaking down have in common with the child who is cripplingly terrified of dogs and the one who gets a bad stomach ache reliably on Monday morning? Anxieties and worries of all kinds are common in children, necessarily part of healthy development, but also, when they interfere with the child’s functioning, the most common pediatric mental health problems. From separation anxiety to social anxiety to school avoidance to phobias to generalized anxiety disorder, many children’s lives are at some point touched by anxiety that gets out of hand. “I often tell parents, anxiety and fears are totally a normal and healthy part of growing up,” said Dr. Sabrina Fernandez, an assistant professor of pediatrics at the University of California, San Francisco, who has written about strategies for primary care doctors to use in dealing with anxiety disorders. “I worry that it’s becoming something more when it interferes with the child’s ability to do their two jobs: to learn in school and to make friends.” Children whose lives are being seriously derailed by their anxieties often get psychotherapy or medication, or both. And a meta-analysis published in November in JAMA looked at the two best-studied treatments for anxiety disorders, cognitive behavioral therapy and psychotropic medication. The technique of a meta-analysis allows scientists to pull in a whole range of different studies, weight the results according to the size and rigor of the research, and then consider the wider array of data gleaned from multiple investigations. “We included panic disorder, social anxiety disorder, specific phobias, generalized anxiety disorder and separation anxiety,” said the lead author, Zhen Wang, an associate professor of health services research at the Mayo Clinic College of Medicine and Science (they did not include children with post-traumatic stress disorder or obsessive-compulsive disorder). The study looked at the effectiveness of treatments in reducing the symptoms of anxiety, and at ending the anxiety disorder state. And they also looked at any reports of adverse events associated with the treatments, from sleep disturbances to suicide. © 2017 The New York Times Company

Keyword: Development of the Brain; Stress
Link ID: 24416 - Posted: 12.11.2017

By Ferris Jabr Chickens are loquacious creatures, and Kevin Mitchell would know. He oversees the care of about a million of them on Wilcox Farms properties in Washington State and Oregon. Mitchell says the birds have “patterns of speech” that reveal a lot about their well-being. They are usually noisiest in the morning—a robust concert of clucks, chortles and caws. “When I hear that, I know they are pretty healthy and happy,” Mitchell says. In the evenings when they’re preparing to roost, the chickens are much more mellow, cooing softly. When a hen lays an egg she celebrates with a series of staccato clucks, like drumbeats, culminating in a loud “buck-caw!” If chickens detect an aerial predator—say, by spotting the shadow of a hawk or eagle—they produce a short, high-pitched shriek. And they have a distinct warning for terrestrial threats: The repetitive clucking most people associate with chickens is in fact a ground predator alarm call. One morning many years ago Mitchell entered a chicken house and found it oddly calm and quiet. Instead of making the usual ruckus, the birds were murmuring and shuffling lethargically. He soon discovered that an automated lighting system had failed and the lights had not switched off the night before; the chickens were sleep-deprived. If he had only been able to eavesdrop on the flock, he might have known much sooner that something was amiss. Over the past five years, engineers and poultry scientists at The University of Georgia and Georgia Institute of Technology have been collaborating to help farmers like Mitchell make better use of the information latent in chicken chatter. © 2017 Scientific American

Keyword: Animal Communication; Language
Link ID: 24415 - Posted: 12.11.2017

By Catherine Offord Mantis shrimps are not the easiest animals to work with, as neuroanatomist Nicholas Strausfeld knows firsthand. Not least, there’s the challenge of capturing the crustaceans in the wild. Also known as stomatopods, mantis shrimps live in burrows in shallow seawater and have earned the descriptive nickname “thumb splitters,” thanks to their tendency to use their sharp, powerful claws to slash at prey and pursuers. “At low tide, you wade around and you try and catch these things,” says Strausfeld, who has plenty of experience chasing after the purple-spotted mantis shrimp (Gonodactylus smithii) with a small handheld net in the tropical waters around Lizard Island, Australia. “They’re incredibly fast—it’s very difficult.” For Strausfeld and other neurobiologists, however, all the trouble is well worth it, as these feisty little marine predators are yielding unique insight into the evolution of the arthropods—the most species-rich animal phylum on the planet, containing around 85 percent of all described animal species. “We knew [these shrimps] were very interesting,” says neuroanatomist Gabriella Wolff, previously a PhD student in Strausfeld’s lab at the University of Arizona and now a research associate at the University of Washington in Seattle. In addition to a complex visual system that receives inputs from independently moving eyes, “mantis shrimps have very advanced behaviors that we haven’t necessarily seen in other crustaceans so far.” Research has also suggested they are sophisticated navigators, regularly finding their way home from distant feeding sites. Plus, they recognize other individual mantis shrimps, and remember whether their interactions were confrontational or not. © 1986-2017 The Scientist

Keyword: Learning & Memory; Evolution
Link ID: 24414 - Posted: 12.11.2017

By Andy Coghlan Two gene variants have been found to be more common in gay men, adding to mounting evidence that sexual orientation is at least partly biologically determined. How does this change what we already knew? Didn’t we already know there were “gay genes”? We have known for decades that sexual orientation is partly heritable in men, thanks to studies of families in which some people are straight and some people are gay. In 1993, genetic variations in a region on the X chromosome in men were linked to whether they were heterosexual or homosexual, and in 1995, a region on chromosome 8 was identified. Both findings were confirmed in a study of gay and straight brothers in 2014. However, these studies didn’t home in on any specific genes on this chromosome. What’s new about the latest study? For the first time, individual genes have been identified that may influence how sexual orientation develops in boys and men, both in the womb and during life. Alan Sanders at North Shore University, Illinois, and his team pinpointed these genes by comparing DNA from 1077 gay and 1231 straight men. They scanned the men’s entire genomes, looking for single-letter differences in their DNA sequences. This enabled them to home in on two genes whose variants seem to be linked to sexual orientation. © Copyright New Scientist Ltd.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 24413 - Posted: 12.09.2017

By Ruth Williams Two studies in Science today—one that focuses on prenatal development in humans, the other on infancy to old age—provide insights into the extent of DNA sequence errors that the average human brain cell accumulates over a lifetime. Together, they reveal that mutations become more common as fetuses develop, and over a lifetime a person may rack up more than 2,000 mutations per cell. “I think these are both very powerful technical papers, and they demonstrate how single-cell sequencing . . . can reliably detect somatic changes in the genomes of human neurons,” says neuroscientist Fred Gage of the Salk Institute in La Jolla who was not involved in either study. “What’s cool about [the papers] is that they show two different ways that one can look at somatic mutations in single human neurons . . . and yet they get consistent results,” says neuroscientist Michael McConnell of the University of Virginia School of Medicine. Cells of the human body acquire mutations over time, whether because of errors introduced during DNA replication or damage incurred during transcription and other cellular processes. But, until recent technological developments enabled whole genome sequencing from the miniscule quantities of DNA found inside single cells or small clones of the same cell, investigating the nature and extent of such somatic mutations—and the resulting tissue mosaicism—was practically impossible. © 1986-2017 The Scientist

Keyword: Development of the Brain; Epigenetics
Link ID: 24412 - Posted: 12.09.2017

Michael Ruffolo When we talk about female representation in science, we’re rarely talking about test subjects. We tend to want more women behind the microscope, not under it. Neuroscience is one of the most skewed fields when it comes to testing on female physiology. One review found single-sex brain studies using male animals outnumbered those using females 6.7 to one. Aarthi Gobinath, a neuroscientist at the University of British Columbia, calls this a “hidden gap” in her field. She says there’s reason to question the assumption that the brains of males and females are identical, particularly in unique states like pregnancy. This is particularly true for early animal testing, where new drugs for depression and anxiety are first developed. “This leads to the ultimate outcome of our research not even benefiting males and females equally,” Gobinath said. Gobinath wanted to tackle the issue of sex bias by trying to understand what depression looks like in female rat brains, specifically looking at postpartum depression. Her research suggests our standard depression treatments don’t apply to new moms. VICE caught up with Gobinath to ask about her new study, which could have wide-ranging implications for humans of all sexes and genders. VICE: What do you mean when you say there’s “sex bias” in brain research? Aarthi Gobinath: So when I say "sex," what I mean is genetic sex, meaning XX or XY chromosomes. [Sex bias] is a bias toward using male subjects in research and then concluding from that research that what was true in that experiment will be true for both sexes without necessarily addressing that maybe it won’t be true for the female physiology.

Keyword: Sexual Behavior
Link ID: 24411 - Posted: 12.09.2017

By SHEILA KAPLAN Chris Beekman, whose company sells the dietary supplement Opiate Detox Pro, does not understand what all the fuss is about. “If it works, it works,” Mr. Beekman, the owner of NutraCore Health Products, said in an interview. “If it doesn’t, it doesn’t.” His customers, addicts trying to shake a dependence on opioids, can always get their money back, he said. Opiate Detox Pro’s label says, “Opioid addiction ease,” and the company’s website claims, “Our ingredients are the most effective on the market for treating withdrawal symptoms.” Mr. Beekman said he did not have scientific evidence to prove that the product worked, and would not be conducting research to buttress the company’s claims. “It’s just not going to happen,” he said, citing what he called the prohibitive cost of scientific studies and clinical trials. Peter Lurie thinks that is an unacceptable position from someone who sells supplements that purport to treat addiction. Dr. Lurie, a former Food and Drug Administration official, runs the nonprofit Center for Science in the Public Interest, which on Friday urged the F.D.A. and the Federal Trade Commission to crack down on businesses that target addicts with products that make unproven health claims. The F.D.A. has already zeroed in on another supplement, kratom, a botanical substance that has been promoted as a safe substitute for opioids and an adjunct to opioid use. Last month, the agency issued a public health advisory for kratom, warning that the product carried “deadly risks,” and linked about three dozen deaths to it. Earlier, the agency had ordered that kratom imports be seized and told companies to take it out of supplements. In general, the agency can fine companies that make and distribute them, or take other enforcement actions. In the past few weeks, reacting to other agency warnings, Amazon has stopped making available some products claiming to assist in opioid withdrawal. © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 24410 - Posted: 12.09.2017