By Lisa Feldman Barrett Jasanoff’s big message in “The Biological Mind” is you are not your brain. Or rather, you are not merely your brain — your body and the broader circumstances of your life also make you who you are. Jasanoff reminds us that the brain is not some mystical machine — it’s a gooey, bloody tangle of cells, dripping with chemicals. But we mythologize brains, creating false boundaries that divorce them from bodies and the outside world, blinding us to the biological nature of the mind. These divisions, Jasanoff contends, are why neuroscience has failed to make a real difference in anyone’s life. Unfortunately, the book’s own divisions between body versus brain, and nature versus nurture, reinforce the very dualisms that Jasanoff indicts. He gives examples of the ways our bodies and the world around us affect our thoughts, feelings and actions, but not how body and world become biologically embedded to constitute a mind. Missing is a discussion of how the workings of your body necessarily and irrevocably shape your brain’s structure and function, and vice versa. The artificial boundary between brain and world also goes largely unmentioned. In real life, the experiences we have from infancy onward impact the brain’s wiring. For example, childhood poverty and adversity fundamentally alter brain development, leaving an indelible mark that increases people’s risk of illness in adulthood. This is fascinating and profound stuff, but it mostly goes unexamined in Jasanoff’s book. Still, “The Biological Mind” is chock-full of fun facts that entertain. And best of all, it makes you think. I found myself debating with Jasanoff in my head as I read — surely a sign of a worthy book. © 2018 The New York Times Company

Keyword: Learning & Memory
Link ID: 25143 - Posted: 06.26.2018

By Elizabeth Gamillo Why does a wild rabbit flee when a person approaches it, but a domestic rabbit sticks around for a treat? A new study finds that domestication may have triggered changes in the brains of these—and perhaps other—animals that have helped them adapt to their new, human-dominated environment. The new study provides “specific and new insights” into the ongoing debate over the physiological factors shaping domestication and evolution, says Marcelo Sánchez-Villagra, a professor of paleobiology at the University of Zurich in Switzerland who was not involved with the work. The leader of the research team, animal geneticist Leif Andersson of Uppsala University in Sweden and Texas A&M University in College Station, thinks the process of domestication has led to changes in brain structure that allow the rabbit to be less nervous around humans. To find out, he and colleagues took MRI scans of the brains of eight wild and eight domestic rabbits and compared the results. The team found that the amygdala, a region of the brain that processes fear and anxiety, is 10% smaller in domesticated rabbits than in wild rabbits. Meanwhile, the medial prefrontal cortex, which controls responses to aggressive behavior and fear, is 11% larger in domesticated rabbits. The researchers also found that the brains of domesticated rabbits are less able to process information related to fight-or-flight responses because they have less white matter than their feral cousins do. White matter handles information processing. When a wild rabbit is in danger, more white matter is needed for faster reflexes and for learning what to be afraid of. © 2018 American Association for the Advancement of Science.

Keyword: Evolution; Emotions
Link ID: 25142 - Posted: 06.26.2018

Erika Engelhaupt The first scientific experiment on hormones took an approach that sounds unscientific: lopping off roosters’ testicles. It was 1848, and Dr. Arnold Berthold castrated two of his backyard roosters. The cocks’ red combs faded and shrank, and the birds stopped chasing hens. Then things got really weird. The doctor castrated two more roosters and implanted a testicle from each into the other’s abdomen. As Randi Hutter Epstein writes in a new book, each rooster “had nothing between his drumsticks but a lone testicle in his gut — yet he turned back into a full-fledged hen-chaser, red comb and all.” It was the first glimpse that certain body parts must produce internal secretions, as hormones were first known, and that these substances — and not just nerves — were important to the body’s control systems. Today, we know that hormones are chemical messengers shaping everything from sex and development to sleep, stress, mood, metabolism and behavior. Yet few of us know much about these powerful substances coursing through our bodies. That ignorance makes Aroused — titled for the Greek meaning of the word hormone — an invaluable guide. Epstein, a medical writer and M.D., tells the history of hormone research from that first rooster experiment, but cleverly moves back and forth through time, avoiding any hint of dry recitation. She explores the scientists who discovered and deciphered the effects of important hormones, as well as the personal stories of how people’s lives have been profoundly changed by these chemicals. |© Society for Science & the Public 2000 - 2018

Keyword: Hormones & Behavior
Link ID: 25141 - Posted: 06.26.2018

By Seth Mnookin In February 1981, a British psychiatrist named Lorna Wing published an academic paper highlighting a 1944 clinical account of “autistic psychopathy” by a recently deceased Austrian physician named Hans Asperger. It wasn’t an obvious piece of work to single out: As Wing acknowledged, Asperger’s study had received almost no attention from English-language researchers in the decades since publication. That was about to change. Wing argued that the disorder that Asperger had described was a unique syndrome, distinct from autism, and should be considered as one of “a wider group of conditions which have, in common, impairment of development of social interaction, communication and imagination.” Wing, whose daughter had been diagnosed with autism in the 1950s, understood from her own experience that this was a disorder with multiple gradations, which affected people across the full spectrum of intellectual abilities. But this was a radical notion: At the time, one of the dominant paradigms for understanding autism was that the condition was caused by “refrigerator mothers” — emotionally frigid women who were not warm enough to nurture developing children. It’s impossible to know why Wing chose to ground her report in Asperger’s rather flimsy research — his paper, after all, had referenced just four patients — rather than relying solely on her own, significantly more impressive work. (It is worth pointing out that then, as now, virtually all eponymous psychiatric conditions were named after men.) Whatever her motivation, Wing’s efforts were successful: “Asperger’s syndrome,” the term she proposed, soon entered the clinical vernacular. By the 1990s, it was recognized around the world as an accepted diagnosis — and autism was no longer viewed as a singular condition. © 2018 The New York Times Company

Keyword: Autism
Link ID: 25140 - Posted: 06.26.2018

By Marcus Woo Some laughs are genuine reactions to hilarity. Others are more contrived—fake, even. But, according to a new study, people can usually tell real laughs from fake ones, regardless of cultural differences. In the first cross-cultural experiment of its kind, researchers asked 884 people from 21 different cultures in six regions around the world, from Peru to South Korea, to listen to recordings of real, spontaneous laughter, and fake, “volitional” laughter recorded from college-aged, U.S. women. On average, nearly two-thirds of listeners in each culture could tell the difference, the team reports in a study accepted for publication in Psychological Science. Genuine chuckles were typically higher pitched and louder, analysis of the sound files revealed. Similar characteristics are seen in cries of pain and anguish, the researchers say, suggesting that laughing is a more emotional and primal response that emerged early in human evolution. A fake laugh, however, is a deliberate response that likely evolved later with speech, the team says. © 2018 American Association for the Advancement of Science.

Keyword: Emotions
Link ID: 25139 - Posted: 06.26.2018

By Austin Frakt One of the lighter moments along my journey to receiving a sleep apnea diagnosis was learning that “heroic snoring” is a clinical term. It sounds more like an oddball super power — snores that can be clearly heard through walls. Many of us have such a snorer in our lives, and some endure the disruption it causes nightly. We hardly need research to appreciate the difficulties this poses. Yet some studies on it have been done, and they document that snoring can lead to marital disruption, and that snorers’ bed partners can experience insomnia, headaches and daytime fatigue. But heroic (and less-than-heroic) snoring can also be a sign of an even deeper problem: obstructive sleep apnea, which is marked by a collapse of the upper airway leading to shallow breathing or breathing cessation that causes decreases in blood oxygen. Sleep apnea can be downright deadly, and not just for those who have it. It’s associated with a greater risk of depression, heart attacks, strokes and other cardiovascular conditions, as well as insulin resistance. As I learned, there’s no reason to meekly accept sleep apnea: There are many treatment options that can control it. The stakes are not small. In the last five years, crashes involving an Amtrak train in South Carolina, a Long Island Rail Road train, a New Jersey Transit train and a Metro-North train in the Bronx have resulted in multiple deaths, hundreds of injuries and tens of millions of dollars in property damage. Undiagnosed or untreated sleep apnea were blamed in each case. And these are far from the only sleep apnea-related accidents involving trains, buses, tractor-trailers and automobiles. Up to 30 percent of motor vehicle crashes are caused by sleepy drivers. Drivers with sleep apnea are nearly five times more likely to be involved in a motor vehicle accident than other drivers. One study found that 20 percent of American truck drivers admit to falling asleep at traffic lights. © 2018 The New York Times Company

Keyword: Sleep
Link ID: 25138 - Posted: 06.25.2018

Jennifer Ouellette Gerardo Ortiz remembers well the time in 2010 when he first heard his Indiana University colleague John Beggs talk about the hotly debated “critical brain” hypothesis, an attempt at a grand unified theory of how the brain works. Ortiz was intrigued by the notion that the brain might stay balanced at the “critical point” between two phases, like the freezing point where water turns into ice. A condensed matter physicist, Ortiz had studied critical phenomena in many different systems. He also had a brother with schizophrenia and a colleague who suffered from epilepsy, which gave him a personal interest in how the brain works, or doesn’t. Ortiz promptly identified one of the knottier problems with the hypothesis: It’s very difficult to maintain a perfect tipping point in a messy biological system like the brain. The puzzle compelled him to join forces with Beggs to investigate further. Ortiz’s criticism has beleaguered the theory ever since the late Danish physicist Per Bak proposed it in 1992. Bak suggested that the brain exhibits “self-organized criticality,” tuning to its critical point automatically. Its exquisitely ordered complexity and thinking ability arise spontaneously, he contended, from the disordered electrical activity of neurons. Bak’s canonical example of a self-organized critical system is a simple sandpile. If you drop individual grains of sand on top of a sandpile one by one, each grain has a chance of causing an avalanche. Bak and colleagues showed that those avalanches will follow a “power law,” with smaller avalanches occurring proportionally more frequently than larger ones. So if there are 100 small avalanches in which 10 grains slide down the side of the sandpile during a given period, there will be 10 larger avalanches involving 100 grains in the same period, and just one large avalanche involving 1,000 grains. When a huge avalanche collapses the whole pile, the base widens, and the sand begins to pile up again until it returns to its critical point, where, again, avalanches of any size may occur. The sandpile is incredibly complex, with millions or billions of tiny elements, yet it maintains an overall stability. All Rights Reserved © 2018

Keyword: Development of the Brain; Evolution
Link ID: 25137 - Posted: 06.25.2018

Paul Biegler explains. Mind-reading machines are now real, prising open yet another Pandora’s box for ethicists. As usual, there are promises of benefit and warnings of grave peril. The bright side was front and centre at the Society for Neuroscience annual meeting in Washington DC in November 2017. It was part of a research presentation led by Omid Sani from the University of Southern California. Sani and his colleagues studied six people with epilepsy who had electrodes inserted into their brains to measure detailed electrical patterns. It is a common technique to help neurosurgeons find where seizures start. The study asked patients, who can be alert during the procedure, to report their mood during scanning. That allowed the researchers to link the patients’ moods with their brainwave readings. Using sophisticated algorithms, the team claimed to predict patients’ feelings from their brainwaves alone. That could drive a big shift in the treatment of mental illness, say researchers. Deep brain stimulation (DBS), where electrodes implanted in the brain give circuits a regular zap, has been successful in Parkinson’s disease. It is also being trialled in depression; but the results, according to a 2017 report in Lancet Psychiatry, are patchy. Sani and colleagues suggest their discovery could bump up that success rate. A portable brain decoder may be available within a generation.

Keyword: Brain imaging
Link ID: 25136 - Posted: 06.25.2018

By Gretchen Reynolds The question of whether young children should use their heads on the soccer field has been a contentious one in recent years. In 2015, U.S. Youth Soccer, the organization that oversees most of the country’s leagues for children and teenagers, announced a ban on heading in games and practices by participants younger than 11, citing concerns that the play might contribute to concussions. In response, some soccer authorities pointed out that young players would be late to learn an essential soccer skill and that concussions from heading are rare in that age group regardless. Now a study presented last month at the annual convention of the American College of Sports Medicine may help quell doubts about the current regulations, which went into effect in 2016. According to studies of experienced adult soccer players, heading can generate impact forces almost equivalent to those of a helmet-to-helmet football tackle. But less attention has been directed at heading by young players and the attendant cognitive effects, if any. Last year, however, researchers in Puerto Rico gained permission to work with 30 boys and girls there, ages 9 to 11, who played in a local youth league. (Children this age are allowed to head in Puerto Rico.) The youngsters took a series of cognitive tests and were then outfitted with a specialized headband that recorded head movements and related impacts while they played. Most of the children wound up heading the ball at least once over the course of three games. Data from the headbands indicates their brains were subjected to acceleration forces ranging from 16 to 60 Gs. In adult players, 60 Gs during heading would be considered forceful enough to cause a concussion, although none of the children in the study received a concussion diagnosis. Most of the impacts were what researchers call “subconcussive,” or below the 60 G threshold. © 2018 The New York Times Company

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 25135 - Posted: 06.25.2018

Veronique Greenwood The question most of genetics tries to answer is how genes connect to the traits we see. One person has red hair, another blonde hair; one dies at age 30 of Huntington’s disease, another lives to celebrate a 102nd birthday. Knowing what in the vast expanse of the genetic code is behind traits can fuel better treatments and information about future risks and illuminate how biology and evolution work. For some traits, the connection to certain genes is clear: Mutations of a single gene are behind sickle cell anemia, for instance, and mutations in another are behind cystic fibrosis. But unfortunately for those who like things simple, these conditions are the exceptions. The roots of many traits, from how tall you are to your susceptibility to schizophrenia, are far more tangled. In fact, they may be so complex that almost the entire genome may be involved in some way, an idea formalized in a theory put forward last year. Starting about 15 years ago, geneticists began to collect DNA from thousands of people who shared traits, to look for clues to each trait’s cause in commonalities between their genomes, a kind of analysis called a genome-wide association study (GWAS). What they found, first, was that you need an enormous number of people to get statistically significant results — one recent GWAS seeking correlations between genetics and insomnia, for instance, included more than a million people. Second, in study after study, even the most significant genetic connections turned out to have surprisingly small effects. The conclusion, sometimes called the polygenic hypothesis, was that multiple loci, or positions in the genome, were likely to be involved in every trait, with each contributing just a small part. (A single large gene can contain several loci, each representing a distinct part of the DNA where mutations make a detectable difference.) All Rights Reserved © 2018

Keyword: Development of the Brain; Genes & Behavior
Link ID: 25134 - Posted: 06.25.2018

By Neuroskeptic Do scientists have a responsibility to make their work accessible to the public? “Public Engagement”, broadly speaking, means scientists communicating about science to non-scientists. Blogs are a form of public engagement, as are (non-academic) books. Holding public talks or giving interviews would also count as such. Recently, it has become fashionable to say that it is important for scientists to engage the public, and that this engagement should be encouraged. I agree completely: we do need to encourage it, and we need to overcome the old-fashioned view that it is somehow discreditable or unprofessional for scientists to fraternize with laypeople. However, some advocates of engagement go further than I’d like. It is sometimes said that every researcher actually has a responsibility to engage the public about the work that they do. Speaking about my own experience in neuroscience in the UK, this view is certainly in the air if not explicitly stated, and I think most researchers would agree. Public engagement and ‘broader impact’ sections now appear as mandatory sections of many grant applications, for instance. In my view, making public engagement a duty for all scientists is wrong. Quite simply, scientists are not trained to do public engagement, and it isn’t what they signed up to do when they chose that career. Some scientists (like me) want to do it anyway, and they should be encouraged (if I say so myself), but many don’t want to. Cajoling the latter into doing engagement is futile. A half-baked public engagement exercise helps no-one.

Keyword: Miscellaneous
Link ID: 25133 - Posted: 06.25.2018

By Sarah DeWeerdt, The Research on Autism and Development (RAD) Laboratory is located in a Tetris-like maze of brown wooden buildings, not far from the main campus of the University of California, San Diego. The lab itself is a nondescript warren of small beige rooms. But everything else about it is extraordinary. The first clue is a T-shirt one of the lab’s young interns wears on this sunny day in April, featuring the RAD Lab’s motto: “We play mind games.” One of the newer recruits, 20-year-old Naseem Baramki-Azar, sports a “Super Mario Bros.” shirt. A half-dozen other lab members huddle around computer screens displaying none of the usual fare of charts or spreadsheets: Instead, they’re hard at work making cartoon moles pop out of molehills, or fat spaceships careen toward the top of a computer screen. The lab’s director, Jeanne Townsend, and associate director, Leanne Chukoskie, periodically poke their heads in to check on the progress. The two women, a generation apart, are a study in contrasts. Townsend is reserved, with dark-framed square glasses; Chukoskie is a fast-talker with a California blond ponytail. But they finish each other’s sentences when they talk about their quest: to develop video games that can help children with autism. The project has stretched the two neuroscientists in unfamiliar directions. “I find myself doing a lot of computer science these days,” Chukoskie says. They are also fledgling entrepreneurs. Last year, they launched a startup, BrainLeap Technologies, also based in San Diego. That step, Chukoskie says, filled her with a mix of unenthusiastic “eh” and dread-filled “ugh.” Despite their discomfort, these two scientists are part of a growing cadre braving video-game development in search of novel therapies for autism. © 2018 American Association for the Advancement of Science

Keyword: Autism
Link ID: 25132 - Posted: 06.23.2018

by Katie Herzog • On Wednesday, Vox published an article entitled "How a Pseudopenis-packing Hyena Smashes the Patriarchy’s Assumptions: Lessons from Female Spotted Hyenas for the #MeToo Era." The piece, by Katherine J. Wu, a graduate student in microbiology and immunobiology, broadly explores how the spotted hyena could be used as a model for humankind. The bottom line: Humans get it wrong; hyenas get it right. "Unlike most other mammals," Wu writes, "spotted hyenas (Crocuta crocuta) live in matriarchal societies led by alpha females. In these clans throughout sub-Saharan Africa, females do the majority of the hunting, dictate the social structure, and raise cubs as single mothers. Even the highest-ranking male in the group is subservient to the most junior female. Accordingly, male spotted hyenas have evolved to be comparatively diminutive, weighing about 12 percent less than females—a feature uncommon even among matrilines." Sounds great. Unfortunately, it's not exactly true, according to Oliver Höner, a research scientist at the Leibniz Institute for Zoo and Wildlife and the co-founder of the Spotted Hyena Project, a research project based in Tanzania. A tweet by the Hyena Project was featured in Wu's article (much to Höner's chagrin), and when I saw him getting salty about Wu's work on Twitter, I reached out to ask what she got wrong. There was plenty in that paragraph alone. Höner says: © Index Newspapers LLC

Keyword: Sexual Behavior
Link ID: 25131 - Posted: 06.23.2018

Richard Harris One of the enduring mysteries of biology is why so much of the DNA in our chromosomes appears to be simply junk. In fact, about half of the human genome consists of repetitive bits of DNA that cut and paste themselves randomly into our chromosomes, with no obvious purpose. A study published Thursday finds that some of these snippets may actually play a vital role in the development of embryos. The noted biologist Barbara McClintock, who died in 1992, discovered these odd bits of DNA decades ago in corn, and dubbed them "jumping genes." (She won a Nobel prize for that finding in 1983.) McClintock's discovery stimulated generations of scientists to seek to understand this bizarre phenomenon. Some biologists have considered these weird bits of DNA parasites, since they essentially hop around our chromosomes and infect them, sometimes disrupting genes and leaving illness in their wake. But Miguel Ramalho-Santos, a biologist at the University of California, San Francisco, doesn't like that narrative. "It seemed like a waste of this real estate in our genome — and in our cells — to have these elements and not have them there for any particular purpose," Ramalho-Santos says. "So we just asked a very simple question: Could they be doing something that's actually beneficial?" He and his colleagues focused on a jumping gene called LINE-1; all told, copies of it make up a whopping 20 percent of our entire DNA. Ramalho-Santos' lab studies embryos, so the team wondered whether LINE-1 played any role in prompting a single fertilized egg to develop into an embryo. © 2018 npr

Keyword: Development of the Brain
Link ID: 25130 - Posted: 06.23.2018

By Sam Roberts Diana Hanbury King, a master teacher who helped generations of students struggling to read fluently, write and spell — and being stigmatized for it — because of an often undiagnosed learning disability called dyslexia, died on June 15 at her home in Lakeville, Conn. She was 90. The cause was complications from several falls, her son, Christopher, said. Ms. King, whose uncle was dyslexic, taught, tutored, founded camps and trained teachers in education programs that were replicated around the world. “The time to diagnose dyslexia is before the child has a chance to fail at reading,” she said. She was instrumental in transforming the popular perception of people with dyslexia from being backward or unteachable to being often highly intelligent despite their learning difficulties. Often they were endowed with keen powers of observation and original thinking, innate charm, a sense of balance and high energy. “We continue to see the tragedy of a bright child coming home from school in the second or third grade in tears — ‘I’m the dumbest kid in all of the second grade’ — and getting stomach aches before they go to school, and all of this totally unnecessary and totally preventable, ” Ms. King said in a videotaped interview with the International Dyslexia Association in 2013. “It drives me crazy.” She said that dyslexia affects as many as one in five people and can be detected by age 4. (A child’s saying “washerdisher,” for example, or “flutteryby” can be symptomatic.) But through intensive tutoring, she maintained — learning a few letters at a time, and integrating spelling and handwriting into their curriculum — students can pass standardized tests or even surpass their peers by the fourth grade. © 2018 The New York Times Company

Keyword: Dyslexia
Link ID: 25129 - Posted: 06.23.2018

By David Grimm The environment a laboratory animal lives in can have a dramatic impact on whether it’s a good model for human disease. A mouse that lives in a shoebox-size cage, for example, gets less exercise than its wild relatives, and thus may not be the best model for studying obesity. Enriched environments with bigger cages and more toys can help, says Garet Lahvis, but the best way to make animals good models is to take them out of the lab—and, in some cases, study them outside in the great wide world. This could be accomplished with cutting-edge electronics and remote sensors, says the behavioral neuroscientist at Oregon Health & Science University in Portland. He’s presenting his proposal today at the Behavior Genetics Association’s annual conference in Boston. Lahvis chatted with Science about what studying lab animals in the wild could look like, and why some researchers think it won’t happen. This interview has been edited for clarity and length. Required fields are indicated by an asterisk (*) Q: Why did you become interested in this idea? A: Our lab studies social behavior in mice. We’ve shown that mice have the capacity for empathy when they hear other mice getting an electrical shock, and that mice are gregarious—they like to hang out with each other. But we were studying them in these small, relatively sterile cages—not anything like they’d encounter in the wild. About 6 or 7 years ago, I started thinking, “How could it be normal for you to spend your entire life with only three other individuals in a small room? Are the mice we’re looking at really normal?” Once that door opened, I started to think about everything else that could go wrong with lab animal research. © 2018 American Association for the Advancement of Science.

Keyword: Animal Rights
Link ID: 25128 - Posted: 06.22.2018

By Emily Willingham Analysis of a Million-Plus Genomes Points to Blurring Lines Among Brain Disorders Brain scan of a 23-year-old schizophrenic man experiencing a hallucination. Credit: Getty Images Is lower academic achievement in early life tied to the same gene changes as an increased risk for Alzheimer’s in older age? That is one of dozens of possible deductions to be drawn from the largest genomic study of brain conditions ever conducted, research that obscures what often have been considered clear diagnostic borders. According to the findings, published June 22 in Science, conditions such as schizophrenia, major depressive disorder (MDD) and bipolar disorder share a suite of overlapping genetic variants rather than having distinct genetic signatures. In addition to the genetic links between educational attainment and Alzheimer’s risk, the results link neuroticism to anorexia nervosa, anxiety disorders, MDD and obsessive-compulsive disorder (OCD). Neurological disorders like Parkinson’s and multiple sclerosis, however, have few variants in common with each other or with psychiatric conditions. This mother lode of findings comes after a six-year delving into genomes representing more than a million people, a quest for unusual genetic signals that track with one or more of 42 disorders and traits. © 2018 Scientific American

Keyword: Schizophrenia; Genes & Behavior
Link ID: 25127 - Posted: 06.22.2018

Leah Rosenbaum Joel Dudley and his colleagues were searching through datasets for Alzheimer’s disease vulnerabilities to exploit in creating a treatment when they stumbled across a surprising correlation: Many of the brains they looked at had signs of herpesvirus infection. But those from people with Alzheimer’s disease had much higher levels of viral DNA than those from healthy people. In particular, the researchers found high levels of HHV-6 and HHV-7, two strains of herpesvirus associated with a common childhood illness called roseola, the team reports online June 21 in Neuron. “We had no intention of looking at viruses,” says Dudley, a biomedical informatics researcher at the Icahn School of Medicine at Mount Sinai in New York City, who gives a talk jokingly titled, “I went looking for drugs and all I found were these stupid viruses.” It is unclear whether the herpesviruses contribute to the development of Alzheimer’s, or if Alzheimer’s patients are just more susceptible to these viruses, which can remain latent in the body long after exposure. Genetic factors also influence a person’s risk of developing Alzheimer’s. The researchers did find that the viruses interacted with genes linked with Alzheimer’s disease, though the implications are still murky. |© Society for Science & the Public 2000 - 2018

Keyword: Alzheimers
Link ID: 25126 - Posted: 06.22.2018

By Catherine Offord An experimental gene therapy for Duchenne Muscular Dystrophy has showed better-than-expected results in a three-patient trial, according to preliminary data presented by Cambridge, Massachusetts–based biotech Sarepta Therapeutics on Tuesday (June 19). Company shares jumped 60 percent following the news that the treatment dramatically boosted levels of microdystrophin, a muscle-protecting protein designed by researchers, and reduced levels of an enzyme associated with the disease. “I have spent my life wanting to make a real change in this disease,” principal investigator Jerry Mendell of Nationwide Children’s Hospital in Columbus tells STAT News. “Finally, we may be there. I am very hopeful. This is an emotional time for people in the field.” Duchenne Muscular Dystrophy (DMD) is a rare genetic disorder caused by loss-of-function mutations in the dystrophin gene. An X-linked condition, the disease mostly affects boys, and usually manifests itself in the form of muscle weakness in children between the ages of 3 and 5. There is no cure for DMD, and although steroids can slow the progression of symptoms, the disease eventually causes life-threatening damage to the heart muscles. Few patients live beyond their 30s. The US Food and Drug Administration (FDA) approved the first drug for DMD, Sarepta’s oligonucleotide therapeutic Exondys 51 (eteplirsen), in 2016. But the therapy was only effective in around 15 percent of DMD patients—those with a specific genetic mutation—and produced just marginal improvements in dystrophin levels. More-recent, preclinical approaches are experimenting with CRISPR to correct DMD-causing point mutations. © 1986-2018 The Scientist

Keyword: Muscles; Genes & Behavior
Link ID: 25125 - Posted: 06.22.2018

by Lindsey Bever Koko, a beloved gorilla who learned to communicate with humans and then stole their hearts, has died. The Gorilla Foundation said the 46-year-old celebrity ape — a western lowland gorilla — died in her sleep earlier this week at the organization’s preserve in Northern California. The Gorilla Foundation, a nonprofit that works to study and protect great apes, said in a statement that Koko will be most remembered “as the primary ambassador for her endangered species.” “Koko touched the lives of millions as an ambassador for all gorillas and an icon for interspecies communication and empathy,” the statement said. “She was beloved and will be deeply missed.” The gorilla was born at the San Francisco Zoo on Independence Day in 1971, according to the Gorilla Foundation, and named Hanabi-ko, which means “fireworks child” in Japanese, though she was mainly known by her nickname, Koko. It was in San Francisco where the newborn gorilla met a budding psychologist, Francine “Penny” Patterson. By the next year, Patterson had started teaching the animal an adapted version of American Sign Language, which she dubbed “Gorilla Sign Language,” or GSL. Video footage from that time shows Patterson playing games with the young gorilla and trying to teach her a new way to communicate. © 1996-2018 The Washington Post

Keyword: Animal Communication; Language
Link ID: 25124 - Posted: 06.22.2018