By John Williams Credit...Sonny Figueroa/The New York Times Let’s get right to the overwhelming question: What does it mean to experience something? Chances are that when you recount a great meal to a friend, you don’t say that it really lit up your nucleus of the solitary tract. But chances are equally good, if you adhere to conventional scientific and philosophical wisdom, that you believe the electrical activity in that part of your brain is what actually accounts for the sensation when you dine. In “Out of My Head,” the prolific British writer Tim Parks adds to the very long shelf of books about what he calls the “deep puzzle of minute-by-minute perception.” The vast majority of us — and this is undoubtedly for the best, life being hard enough — don’t get tripped up by the ontological mysteries of our minute-to-minute perceiving. We just perceive. But partly because it remains a stubborn philosophical problem, rather than a neatly explained scientific one, consciousness — our awareness, our self-awareness, our self — makes for an endlessly fascinating subject. And Parks, though not a scientist or professional philosopher, proves to be a companionable guide, even if his book is more an appetizer than a main course. He wants “simply” to ask, he writes, whether “we ordinary folks” can say anything useful about consciousness. But he also wants to poke skeptically at the “now standard view of conscious experience as something locked away in the head,” the “dominant internalist model which assumes the brain is some kind of supercomputer.” “Out of My Head” was inspired, in large part, by the theories of Riccardo Manzotti, a philosopher, roboticist and friend of Parks with whom the author has had “one of the most intense and extended conversations of my life.” (A good chunk of that conversation appeared as a 15-part dialogue on the website of The New York Review of Books, whose publishing arm has released “Out of My Head.”) © 2019 The New York Times Company

Keyword: Consciousness
Link ID: 26842 - Posted: 11.22.2019

Jon Hamilton When we hear a sentence, or a line of poetry, our brains automatically transform the stream of sound into a sequence of syllables. But scientists haven't been sure exactly how the brain does this. Now, researchers from the University of California, San Francisco, think they've figured it out. The key is detecting a rapid increase in volume that occurs at the beginning of a vowel sound, they report Wednesday in Science Advances. "Our brain is basically listening for these time points and responding whenever they occur," says Yulia Oganian, a postdoctoral scholar at UCSF. The finding challenges a popular idea that the brain monitors speech volume continuously to detect syllables. Instead, it suggests that the brain periodically "samples" spoken language looking for specific changes in volume. The finding is "in line" with a computer model designed to simulate the way a human brain decodes speech, says Oded Ghitza, a research professor in the biomedical engineering department at Boston University who was not involved in the study. Detecting each rapid increase in volume associated with a syllable gives the brain, or a computer, an efficient way to deal with the "stream" of sound that is human speech, Ghitza says. And syllables, he adds, are "the basic Lego blocks of language." Oganian's study focused on a part of the brain called the superior temporal gyrus. "It's an area that has been known for about 150 years to be really important for speech comprehension," Oganian says. "So we knew if you can find syllables somewhere, it should be there." The team studied a dozen patients preparing for brain surgery to treat severe epilepsy. As part of the preparation, surgeons had placed electrodes over the area of the brain involved in speech. © 2019 npr

Keyword: Language; Hearing
Link ID: 26841 - Posted: 11.21.2019

Alejandra Manjarrez Typically, the worm Caenorhabditis elegans falls asleep after it experiences stress or hours of swimming. In a recent study, scientists observed another sleep trigger: being confined to a microfluidic chamber. As such devices are widely used to analyze different worm behaviors, the authors caution that the sleep induction could interfere with data interpretation. The results were published November 6 in Nature Communications. “In our field, microfluidic chambers have become very commonly used, and they are valuable tools for precise environmental control and for neural imaging . . . but what this study highlights is that we are significantly impacting the physiology and behavior of these animals by confining them in such a way,” says Cheryl Van Buskirk, a geneticist at California State University in Northridge. Van Buskirk studies sleep and stress response in worms, but she was not involved in this research. The team first observed this behavior while developing a technique to make electrical measurements of individual cells in worms placed in microfluidic chambers. They noticed that the muscle cells of these animals would not show any activity during some periods of time. Inactivity, however, is not always equivalent to sleep. “There are specific criteria for sleep, so we actually spent a good deal of the [latest] paper testing those specific criteria,” says Daniel Gonzales, who participated in this study as a graduate student at Rice University in Houston, but has now moved to Purdue University in Indiana. They tested, for example, whether this behavior was reversible, if it was associated with a decreased response to stimuli, and if the worms took on a stereotypical sleep posture. They found that, in addition to fulfilling these criteria, this microfluidics-induced quiescence was also regulated by neurons previously reported to control sleep in C. elegans. © 1986–2019 The Scientist.

Keyword: Sleep
Link ID: 26840 - Posted: 11.21.2019

By Nick Chrastil In May of 2016, not long after his release from a psychiatric hospital, Colby Crawford, a 23-year old black man, was booked into the Orleans Justice Center (OJC) — a new $150-million-dollar jail opened a year earlier to replace the crumbling and now shuttered Orleans Parish Prison complex, and touted as a symbol of a more progressive approach to incarceration in New Orleans. Ten months later, he was dead. Colby Crawford was diagnosed with schizophrenia, bipolar disorder, and substance use disorder. A lawsuit argues that his death at Orleans Parish jail was in part due to a profound lack of treatment for his mental illness. Visual: Courtesy of the Crawford family. Prior to Crawford’s incarceration, he had been diagnosed with schizophrenia, bipolar disorder, and substance use disorder. A psychiatrist at OJC noted that he was prone to “seeing spirits and ghosts, insomnia, anxiety, paranoia, and bad dreams,” and prescribed an antipsychotic and anticonvulsant. A month after Crawford’s arrest on allegations that he hit his mother and sister, he was transferred about an hour outside of New Orleans to a state prison called the Elayn Hunt Correctional Center — the one place he received adequate mental health care while incarcerated, according to a wrongful death suit filed by his mother. But two months later, Crawford was transferred back to OJC and placed in “disciplinary segregation” for 20 days. Upon release back into the general population, he deteriorated. He stopped taking his medications consistently and started hearing voices and seeing spirits. He couldn’t sleep and got in fights. Jail records cited in the complaint show that medical staff was aware of Crawford’s declining condition. He requested to be moved to a psychiatric tier. He never was.

Keyword: Schizophrenia
Link ID: 26839 - Posted: 11.21.2019

By Nicholas Bakalar People who never learned to read and write may be at increased risk for dementia. Researchers studied 983 adults 65 and older with four or fewer years of schooling. Ninety percent were immigrants from the Dominican Republic, where there were limited opportunities for schooling. Many had learned to read outside of school, but 237 could not read or write. Over an average of three and a half years, the participants periodically took tests of memory, language and reasoning. Illiterate men and women were 2.65 times as likely as the literate to have dementia at the start of the study, and twice as likely to have developed it by the end. Illiterate people, however, did not show a faster rate of decline in skills than those who could read and write. The analysis, in Neurology, controlled for sex, hypertension, diabetes, heart disease and other dementia risk factors. “Early life exposures and early life social opportunities have an impact on later life,” said the senior author, Jennifer J. Manly, a professor of neuropsychology at Columbia. “That’s the underlying theme here. There’s a life course of exposures and engagements and opportunities that lead to a healthy brain later in life.” “We would like to expand this research to other populations,” she added. “Our hypothesis is that this is relevant and consistent across populations of illiterate adults.” © 2019 The New York Times Company

Keyword: Language; Alzheimers
Link ID: 26838 - Posted: 11.21.2019

By Knvul Sheikh Shortly after the birth of her first son, Monika Jones learned that he had a rare neurological condition that made one side of his brain abnormally large. Her son, Henry, endured hundreds of seizures a day. Despite receiving high doses of medication, his little body seemed like a rag doll as one episode blended into another. He required several surgeries, starting when he was 3 1/2 months old, eventually leading to a complete anatomical hemispherectomy, or the removal of half of his brain, when he turned 3. The procedure was first developed in the 1920s to treat malignant brain tumors. But its success in children who have brain malformations, intractable seizures or diseases where damage is confined to half the brain, has astonished even seasoned scientists. After the procedure, many of the children are able to walk, talk, read and do everyday tasks. Roughly 20 percent of patients who have the procedure go on to find gainful employment as adults. Now, research published Tuesday in the journal Cell Reports suggests that some individuals recover so well from the surgery because of a reorganization in the remaining half of the brain. Scientists identified the variety of networks that pick up the slack for the removed tissue, with some of the brain’s specialists learning to operate like generalists. “The brain is remarkably plastic,” said Dorit Kliemann, a cognitive neuroscientist at the California Institute of Technology, and the first author of the study. “It can compensate for dramatic loss of brain structure, and in some cases the remaining networks can support almost typical cognition.” The study was partially funded by a nonprofit organization that Mrs. Jones and her husband set up to advocate for others who need surgery to stop seizures. The study’s findings could provide encouragement for those seeking hemispherectomies beyond early childhood. © 2019 The New York Times Company

Keyword: Development of the Brain; Laterality
Link ID: 26837 - Posted: 11.20.2019

Jef Akst From a small inflatable boat in the Rangiroa atoll in French Polynesia, Pamela Carzon got her first glimpse of the “strange” trio of marine mammals she’d been told about: a bottlenose dolphin mother (Tursiops truncatus), her seven-month-old calf, and another young cetacean that was slightly smaller and looked to be not a bottlenose dolphin at all, but a melon-headed whale (Peponocephala electra). It was April 2015, and Carzon and a colleague at the Marine Mammal Study Group of French Polynesia, a nongovernmental organization dedicated to whale and dolphin conservation, were out for the NGO’s annual photo-ID survey, very much hoping to find animals that a former collaborator had seen while diving in the region the previous November. “[T]he sea was very calm, and there were many dolphins around,” Carzon, also a PhD student at the Center for Island Research and Environmental Observatory (CRIOBE) in French Polynesia and the École Pratique des Hautes Études in Paris, recalls in an email to The Scientist. “It took us maybe two minutes to spot them: the dark calf was easy to spot among the bottlenose dolphins.” The mother, dubbed ID#TP25 by the researchers, was known to tolerate divers and boats, and that April day she approached the inflatable with both calves. Carzon grabbed her underwater camera and slipped into the water. “I was able to get good underwater footage and to sex both calves,” she says. ID#TP25’s natural calf was a female; the second calf was male. “I also noticed that both were ‘gently’ pushing each other [in order] to remain under the adult female’s abdomen” in so-called infant position. Continued observation over the following months revealed that the dolphin mom was nursing the foreign calf, whose species ID remains to be confirmed with genetic testing, and otherwise treated him as one of her own. © 1986–2019 The Scientist.

Keyword: Sexual Behavior
Link ID: 26836 - Posted: 11.20.2019

By Michele C. Hollow As soon as James Griffin gets off the school bus he tells his mom, “Go dance, go dance.” James is 14 and has autism, and his speech is limited. He’s a participant in a program for children on the autism spectrum at the University of Delaware that is studying how dance affects behavior and verbal, social and motor skills. One afternoon while dancing, he spun around, looked at his mother, smiled and shouted, “I love you.” His mom, Rachelan Griffin, said she had waited his whole life to hear him say those words. “I think that the program is a big part of that, because he was dancing when he said it,” she said. According to Anjana Bhat, an associate professor in the department of physical therapy at the University of Delaware, “Parents report that their children with autism enjoy musical activities and show more positive interactions with others through greater eye contact, smiling and speaking after engaging in a dance and music program.” James is one of about a dozen children on the autism spectrum who meet individually with Dr. Bhat’s graduate and undergraduate students for the dance study, which also uses yoga and musical activities. Some children also participated in robotic therapy, in which a humanoid robot helps them learn to follow dance moves. “Across many different studies we find that social skills like smiling and verbalization are substantially higher when children with autism engage in socially embedded movements versus sedentary games like checkers or building a Lego set,” Dr. Bhat said. © 2019 The New York Times Company

Keyword: Autism
Link ID: 26835 - Posted: 11.20.2019

By Laura Sanders Bulging stomachs often take the blame for ending holiday indulging. But bulging guts might be the real appetite killer, a study in mice suggests. The results, published November 14 in Cell, could point out new ways to treat obesity, or even help explain how gastric bypass surgeries limit eating. Those procedures result in food moving faster through the stomach into the intestines, stretching the gut in a way that might signal fullness, the authors speculate. Zachary Knight, a neuroscientist at the University of California, San Francisco, and colleagues identified and studied nerve cells in mice’s intestines that sense mechanical stretching. To simulate full intestines, the team activated these nerve cells with light and chemicals. As a result, the mice ate less food. Physically stretching the mice’s intestines with a salty liquid or a diuretic also caused the mice to eat less. Different stretch-sensing cells in the stomach also curbed mice’s appetites, but to a lesser extent, the researchers found. These nerve cell endings relay messages up the vagus nerve (SN: 11/13/15), which then zips signals to the brain. These messages about intestinal stretching help influence the eat-or-not decision, researchers suspect. L. Bai et al. Genetic identification of vagal sensory neurons that control feeding. Cell. Vol. 179, November 14, 2019, p. 1129. doi: 10.1016/j.cell.2019.10.031 © Society for Science & the Public 2000–2019.

Keyword: Obesity
Link ID: 26834 - Posted: 11.20.2019

By Kim Tingley We humans spend a third of our lives asleep, oblivious to our surroundings and temporarily paralyzed. It’s a vulnerability that would seem to diminish our odds of survival, so evolutionarily speaking it must also somehow confer tremendous benefits. Yet our best guesses about what those benefits are tend to come from observing what happens when sleep is curtailed. As far as we know, all animals sleep in some way; deprive most of them of it for long enough, and they will die, but exactly why is unclear. In 2015, the American Academy of Sleep Medicine and the Sleep Research Society published a joint statement, based on a comprehensive review of research, saying that “sleeping less than seven hours per night on a regular basis” — which is the case for an estimated 35 to 40 percent of Americans during the workweek — is associated with adverse health outcomes. These include weight gain and obesity, diabetes, hypertension, heart disease and stroke, depression, impaired immune function, increased pain, greater likelihood of accidents and “increased risk of death.” The National Institutes of Health reported last year that sleep deficits may increase the beta-amyloid proteins in the brain linked with Alzheimer’s disease. But when it comes to “what sleep is, how much you need and what it’s for,” says Louis Ptacek, a professor of neurology at the University of California, San Francisco, “we know almost nothing — other than it’s bad not to get enough of it.” Indeed, says David Dinges, one of the statement’s authors and a professor of psychiatry at the University of Pennsylvania, “All of this makes it really tough to send out simple messages to the public about when you should sleep and how much you should sleep.” Scientists believe that there are two separate but interrelated internal systems that regulate sleep. The first is the circadian system that tells our body when to sleep. Medicine already knows a great deal about how it works: Approximately every 24 hours, the suprachiasmatic nucleus, a small region in the hypothalamus, orchestrates physiological changes to prepare us for sleep, like lowering body temperature and releasing dopamine. But the second system — the one that tells our body the amount of sleep it needs — is still mysterious. One way to elucidate it would be to find genes that govern how long or deeply people sleep and observe where those genes are active. This fall, Ptacek, Ying-Hui Fu and other colleagues announced, in the journals Neuron and Science Translational Medicine, the discovery of two genetic mutations that seem to cause certain people to sleep far less than average. This brought the number of genes known to be involved in sleep duration to just three. © 2019 The New York Times Company

Keyword: Sleep
Link ID: 26833 - Posted: 11.19.2019

By R. Douglas Fields Neuroscientists have always presumed that learning and memory depend on strengthening or weakening the connection points between neurons (synapses), increasing or decreasing the likelihood that the cell is going to pass along a message to its neighbor. But recently some researchers have started pursuing a completely different theory that does not involve changing the strength of synaptic transmission; in fact, it does not even involve neurons. Instead other types of brain cells, called glia, are responsible. A new study from the University of Toronto, published on-line this week in the journal Neuron furnishes support for this theory. It provides evidence that the basic act of learning whether one’s environs are safe or not, a behavior common to all animals, depends on glial cells that form the fatty sheath called myelin—electrical insulation that covers nerve fibers. The new theory postulates that establishing indelible memories that can be recalled long after sensory input or training on a task involves an interaction between glia and peculiar brain waves produced during sleep. “The role of myelin in cognitive functions has been largely neglected, an omission elegantly rectified by this paper,” says myelin researcher Bernard Zalc, at the Sorbonne Université in Paris, commenting on this new study. Traditionally researchers who study the myelin insulation on nerve fibers, called axons, have focused on diseases, such as multiple sclerosis, in which the fatty sheath is damaged. In multiple sclerosis, neural transmission fails, causing wide-ranging disabilities. Much like the plastic coating on a copper wire, myelin was understood to be vital for neural transmission but inert and irrelevant to information processing and memory storage. © 2019 Scientific American

Keyword: Learning & Memory
Link ID: 26832 - Posted: 11.19.2019

Robin McKie Major psychological disorders such as schizophrenia will continue to affect humans because men and women are continually generating genetic mutations that disrupt brain development. This will be the key conclusion of Professor Sir Michael Owen, director of Cardiff University’s centre for neuropsychiatric genetics and genomics, when he gives the annual Darwin Lecture at the Royal Society of Medicine this week. Understanding such conditions at an evolutionary level will be crucial to developing treatments, Owen believes. Thirty years ago, the new technology of DNA analysis raised hopes that schizophrenia – a condition that can track through families – would soon reveal links to one or two specific genes, said Owen. Treatments might then be relatively easy to develop, it was thought. Instead scientists found that hundreds of genes, each having a tiny effect, dictate whether or not a person will be susceptible to the condition. Characterised by profound behavioural changes, hallucinations, and delusions, these transformations in behaviour can have profound consequences, he added. For example, men with schizophrenia have – on average – only a quarter as many children as males in the general population while women with the condition have about half as many as unaffected females. That low reproduction rate should have had one clear result, Owen told the Observer last week. “Schizophrenia cases should have declined and disappeared long ago as those affected were out bred by those unaffected. This has not happened. A steady level of 1% people continue to be affected.” © 2019 Guardian News & Media Limited

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26831 - Posted: 11.19.2019

Ashley P. Taylor Autoimmune diseases tend to ease up during pregnancy, and for women with multiple sclerosis, physicians have documented fewer relapses of the condition while women are pregnant compared to before and after having a baby. Anecdotally, many MS patients also feel better when they’re expecting. Researchers believe that this happens because during pregnancy, the body reins in its immune response so as to not reject the fetus—and in doing so counteracts autoimmune diseases. But as to how exactly this all works, scientists are uncertain. “Obviously, everybody would love to understand why it happens because if you could bottle that property of pregnancy, perhaps you could use it therapeutically,” Adrian Erlebacher, a reproductive immunologist at the University of California, San Francisco, tells The Scientist. To investigate why this happens in pregnant women with multiple sclerosis (MS), Stefan Gold, a neuroscientist at the Institute of Neuroimmunology and Multiple Sclerosis at the Universitätsklinikum Hamburg-Eppendorf, in Hamburg, Germany, and colleagues examined T cell populations in 11 MS patients before, during, and after pregnancy and in 12 women without MS during and after pregnancy. They categorized the T cells into different groups based on a genetic analysis of the cells’ receptors. In the first trimester, they found, MS patients’ T cells were dominated by just a few types, called clones, each with a different T cell receptor. Between the first and third trimesters, those dominant clones declined in abundance, and T cells became more evenly distributed across the different populations, Gold says. In women without MS, the pregnancy-associated changes in the T cell repertoire were not significant. Gold and his colleagues reported their results in Cell Reports on October 22. © 1986–2019 The Scientist.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26830 - Posted: 11.19.2019

By Jane E. Brody There‌ are‌ ‌some‌ ‌crimes‌ ‌that‌ ‌are‌ almost‌ ‌impossible‌ ‌to‌ ‌forget. ‌ ‌ For‌ me, ‌they‌ ‌include‌ ‌the‌ ‌death‌ ‌in‌ ‌1999‌ ‌of‌ ‌Kendra‌ ‌Webdale, ‌an‌ ‌aspiring‌ ‌young‌ ‌journalist‌ ‌who‌ ‌was‌ ‌pushed‌ ‌in‌ ‌front‌ ‌of‌ ‌a‌ ‌New‌ ‌York‌ ‌subway‌ ‌train‌ ‌by‌ ‌a‌ ‌29-year-old‌ ‌man‌ ‌with‌ ‌schizophrenia‌ ‌who‌ ‌had‌ ‌stopped‌ ‌taking‌ ‌his‌ ‌medication. ‌That‌ ‌same‌ ‌year, ‌two‌ ‌mentally‌ ‌ill‌ ‌teenage‌‌‌ ‌boys‌ ‌massacred‌ ‌12‌ ‌students‌ ‌and‌ ‌one‌ ‌teacher‌ ‌at‌ ‌Columbine‌ ‌High‌ ‌School‌ ‌in‌ ‌Colorado. ‌ ‌ Thirteen‌ ‌years‌ ‌later, ‌a‌ ‌seriously‌ ‌emotionally‌ ‌disturbed‌ ‌20-year-old‌ ‌man‌ ‌murdered‌ ‌20‌ ‌young‌ ‌children‌ ‌and‌ ‌six‌ ‌adults‌ ‌at‌ ‌Sandy‌ ‌Hook‌ ‌Elementary‌ ‌School‌ ‌in‌ ‌Connecticut. ‌This‌ ‌year, ‌a‌ ‌homeless‌ ‌24-year-old‌ ‌man‌ ‌bludgeoned‌ ‌four‌ ‌men‌ ‌to‌ ‌death‌ ‌while‌ ‌they‌ ‌slept‌ ‌on‌ ‌the‌ ‌streets‌ ‌of‌ ‌my‌ ‌city. ‌ ‌ Although‌ ‌New York is now far‌ ‌safer‌ ‌than‌ ‌when‌ ‌I‌ ‌was‌ ‌a‌ ‌child‌ ‌in‌ ‌the‌ ‌1940s‌ ‌and‌ ‌’50s‌ ‌who‌ ‌walked‌ ‌to‌ ‌and‌ ‌from‌ ‌school‌ ‌unescorted, ‌like‌ ‌most‌ ‌big‌ ‌cities, ‌it still‌ ‌harbors‌ ‌untold‌ ‌numbers‌ ‌of‌ ‌men‌ ‌and‌ ‌women‌ ‌with‌ ‌known‌ ‌or‌ ‌undiagnosed‌ ‌severe‌ ‌mental‌ ‌illness‌ ‌that‌ ‌can‌ ‌and‌ ‌should‌ ‌be‌ ‌treated‌ ‌before‌ ‌yet‌ ‌another‌ ‌personal‌ ‌or‌ ‌societal‌ ‌tragedy‌ ‌occurs. ‌ ‌ What, ‌I‌ ‌wondered, ‌is‌ ‌or‌ ‌can‌ ‌be‌ ‌done‌ ‌to‌ ‌help‌ ‌them‌ ‌and‌ ‌avert‌ ‌further‌ ‌disasters? ‌ ‌ Contrary‌ ‌to‌ ‌politically‌ ‌motivated‌ ‌claims, ‌I‌ ‌learned‌ ‌that‌ ‌people‌ ‌with‌ ‌serious‌ ‌mental‌ ‌ills‌ ‌are‌ ‌not‌ ‌necessarily‌ ‌prone‌ ‌to‌ ‌commit‌ ‌violent‌ acts‌ ‌ — ‌they‌ ‌are‌ ‌far‌ ‌more‌ ‌likely‌ ‌to‌ ‌become‌ ‌‌victims‌‌ ‌of‌ ‌crime. ‌Rather, ‌the‌ ‌issue‌ ‌is‌ ‌that‌ ‌treatments‌ ‌known‌ ‌to‌ ‌be‌ ‌effective‌ ‌are‌ ‌underfunded‌ ‌or‌ ‌wrongly‌ ‌dismissed‌ ‌as‌ ‌ineffective‌ ‌or‌ ‌too‌ ‌dangerous; ‌basic‌ ‌research‌ ‌in‌ ‌university‌ ‌and‌ ‌government‌ ‌laboratories‌ ‌into‌ ‌new‌ ‌and‌ ‌better‌ ‌drugs‌ ‌is‌ ‌limited‌ ‌and‌ ‌also‌ ‌underfunded; ‌and‌ ‌pharmaceutical‌ ‌companies‌ ‌have‌ ‌shown‌ ‌little‌ ‌interest‌ ‌in‌ ‌developing‌ ‌and‌ ‌testing‌ ‌treatments‌ ‌for‌ ‌severe‌ ‌mental‌ ‌illness. ‌ ‌ Also‌ ‌at‌ ‌issue‌ ‌is‌ ‌that, ‌as‌ ‌was‌ true‌ for‌ ‌cancer‌ ‌until‌ ‌recently, ‌acknowledgment‌ ‌of‌ ‌mental‌ ‌illness‌ ‌carries‌ ‌a‌ ‌stigma‌ ‌that‌ ‌impedes‌ ‌its‌ ‌early‌ ‌recognition, ‌when‌ ‌it‌ ‌can‌ ‌be‌ ‌most‌ ‌effectively‌ ‌treated‌ ‌or‌ ‌reversed. ‌ ‌ © 2019 The New York Times Company

Keyword: Schizophrenia; Aggression
Link ID: 26829 - Posted: 11.18.2019

Lorenz Wagner Henry Markram, the neuroscientist behind the billion-dollar Blue Brain Project to build a supercomputer model of the brain, has set the goal of decoding all disturbances of the mind within a generation. This quest is personal for him. The driving force behind his grand ambition has been his son Kai, who suffers from autism. Raising Kai made Henry Markram question all that he thought he knew about neuroscience, and then inspired his groundbreaking research that would upend the conventional wisdom about autism, leading to his now-famous theory of the Intense World Syndrome. When Kai was first diagnosed, his father consulted studies and experts. He knew as much about the human brain as almost anyone but still felt as helpless as any parent confronted with this condition in his child. What’s more, the scientific consensus that autism was a deficit of empathy didn’t mesh with Markram’s experience of his son. He became convinced that the disorder, which has seen a 657 percent increase in diagnoses over the past decade, was fundamentally misunderstood. Bringing his world-class research to bear on the problem, he devised a radical new theory of the disorder: People like Kai don’t feel too little; they feel too much. Their senses are too delicate for this world. The following is an extract condensed from "The Boy Who Felt Too Much: How a Renowned Neuroscientist Changed Our View of Autism Forever," by Lorenz Wagner, just out from Arcade Publishing, which tells this remarkable story. The car was coasting. Kai heard the wheels crunch as it drew to a halt outside his house. The car door opened, and a young man hopped out. He popped the hood and disappeared beneath it. “You’ve got to be kidding me!” he fumed. © 2019 Salon.com, LLC

Keyword: Autism
Link ID: 26828 - Posted: 11.18.2019

An exciting new study out of the University of Toronto shows that the brain lights up when you think things. “I mean it’s incredible,” said neuroscientist Dr. Prya Laghara. “We now have the technology to put someone into an fMRI, tell them to think things, and then watch their brain light up.” In order to prove this, Dr. Laghara recruited undergraduate students, put them in fMRIs, and then asked them to think things. “I told them to think about anything, anything at all, and no matter what they thought about their brains lit up.” When asked whether her study had any methodological issues, Dr. Laghara scoffed. “We ran this study with 2000 undergraduate participants over the course of three years. In every condition, with every participant, their brain lit up when they thought things.” “My colleagues all over the world are replicating this study, and so far nobody has been able to refute the hypothesis that the brain lights up when you think things. It’s an incredibly robust finding.” Thanks to this breakthrough in neuroscience, the University of Toronto is taking the next decade’s stem cell research funds and using them to purchase ten fMRIs. Copyright Simplosion 2019

Keyword: Brain imaging
Link ID: 26827 - Posted: 11.18.2019

By Susana Martinez-Conde The many evils of social media notwithstanding, millions of users agree that some of its most delightful aspects include viral illusions and cute cat videos. The potential for synergy was vast in retrospect—but only realized in 2013, when Rasmus Bååth, a cognitive scientist from Lund University in Sweden, blended both elements in a YouTube video of his kitten attacking a printed version of Akiyoshi Kitaoka’s famous “Rotating Snakes” illusion. The clip, which has been viewed more than 6 million times as of this writing, led to subsequent empirical research and an internet survey of cat owners, where 29% of respondents answered that their pets reacted to the Rotating Snakes. The results, published in the journal Psychology in 2014, indicated—though not conclusively—that cats experience illusory motion when they look at the Rotating Snakes pattern, much as most humans do. Now, a team of researchers from University of Padova, Italy, Queen Mary University of London in the UK, and the Parco Natura Viva—Garda Zoological Park in Bussolengo, Italy, has collected additional evidence that cats—in this case, big cats—find the Rotating Snakes Illusion fascinating. Advertisement Intrigued by the earlier study on house cats, Christian Agrillo of the University of Padova and his collaborators set out to determine whether lions at Parco Natura Viva were similarly susceptible to motion illusions, as well as explore the possibility that such patterns might serve as a source of visual enrichment for zoo animals. Their findings were published last month in Frontiers in Psychology. © 2019 Scientific American,

Keyword: Vision; Evolution
Link ID: 26826 - Posted: 11.18.2019

By Neuroskeptic | Many people may be living life without a particular brain region – and not suffering any ill-effects. In a new paper in Neuron, neuroscientists Tali Weiss and colleagues discuss five women who appear to completely lack olfactory bulbs (OB). According to most neuroscience textbooks, no OB should mean no sense of smell, because the OB is believed to be a key relay point for olfactory signals. As Wikipedia puts it: The olfactory bulb transmits smell information from the nose to the brain, and is thus necessary for a proper sense of smell. Scent molecules activate olfactory receptors and signals travel up the olfactory nerves to the olfactory bulb, and then on to the rest of the brain via the olfactory tract. From Wikipedia. However, remarkably, Weiss et al.’s five women seem to have entirely normal sense of smell despite lacking any visible OBs on brain MRI scans. On both subjective and objective measures of olfactory function, these women showed no abnormalities. MRIs showing normal development of olfactory bulbs (A) compared to two women with no visible olfactory bulbs but normal sense of smell (B) & (D) and one woman with no sense of smell (C). From Weiss et al. Fig 1 Weiss et al. came across two of the women serendipitously while carrying out MRI scans for an unrelated project. The other 3 were found among healthy controls in the Human Connectome Project MRI dataset.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 26825 - Posted: 11.18.2019

Regina Denney's 17-year-old son Brian called her in a panic; he couldn't stop throwing up. It was April 7, 2018 and the Indianapolis teen asked her to take him to the emergency room — but doctors there couldn't figure out what was wrong. He was severely dehydrated and constantly vomiting. "As we're sitting there talking, another doctor happens to walk by our room and she pokes her head in and she says, 'Do you smoke marijuana?'" Denney said. "And he said yes. And she said, 'Does it get better with hot showers or hot baths?' And he said yes." Brian Smith Jr. was diagnosed with a rare condition called cannabinoid hyperemesis syndrome (CHS). When his lab results came back, his mother said the teen's kidneys were shutting down and his liver wasn't functioning properly. "It was just crazy," Denney said. "They were able to rehydrate him. And [the results] improved. So they released him the next day, but didn't give us any information about what CHS was, what causes it, what to look for." He was a heavy cannabis smoker and his mother convinced him to stop, at least until they could see a gastroenterologist 45 days later. Denney said he still had symptoms leading up to that appointment and thought if they were related to his cannabis use, he would have been symptom free. So he started smoking again. What they didn't know was CHS can present symptoms weeks or months after stopping cannabis use. By October, Denney said her son had lost more than 40 pounds. "You could see his bones. He looked sick," she said. "It's torture." ©2019 CBC/Radio-Canada

Keyword: Drug Abuse
Link ID: 26824 - Posted: 11.16.2019

Ruth Williams Throughout the animal kingdom, there are numerous examples of neurons that respond to multiple stimuli and faithfully transmit information about those various inputs. In the mouse, for example, there are certain neurons that respond to both temperature and potentially damaging touch. In the fruit fly, there are neurons that sense light, temperature, pain, and proprioceptive stimuli—those arising as a result of body position and movement. And in C. elegans, two sensory neurons, known as PVD neurons, that run the length of the body on either side are thought to regulate proprioception as well as responses to harsh touch and cold temperature. Scientists have now figured out how a single PVD neuron can relay two different stimuli: while harsh touch results in typical firing of the neuron—an impulse that travels the length of the cell—proprioception causes a localized response in one part of the cell with no apparent involvement of the rest. The findings are reported today (November 14) in Developmental Cell. “[The] paper illustrates that different parts of the neuron do different things,” says neuroscientist Scott Emmons of Albert Einstein College of Medicine who did not participate in the research, “and that just makes the whole system much more complex to interpret,” he says. To examine how a single neuron interprets distinct inputs and drives corresponding behaviors, neuroscientist Kang Shen of Stanford University and colleagues focused on PVD neuron–regulated escape behavior when a worm is poked with a wire and the worm’s normal wiggling motion as it responds to proprioceptive stimuli. © 1986–2019 The Scientist

Keyword: Pain & Touch; Development of the Brain
Link ID: 26823 - Posted: 11.16.2019