Chapter 16. None

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By Michael Price Contrary to popular lore that portrays chimpanzees as having “super strength,” studies have only found modest differences with humans. But our closest relatives are slightly stronger by several measures, and now a study comparing the muscle fibers of different primates reveals a potential explanation: Humans may have traded strength for endurance, allowing us to travel farther for food. To determine why chimpanzees are stronger than humans—at least on a pound-for-pound basis—Matthew O’Neill, an anatomy and evolution researcher at the University of Arizona College of Medicine in Phoenix, and colleagues biopsied the thigh and calf muscles of three chimps housed at the State University of New York at Stony Brook. They dissected the samples into individual fibers and stimulated them to figure out how much force they could generate. Comparing their measurements to known data from humans, the team found that, at the individual fiber level, muscle output was about the same. Given that different fibers throughout the muscle might make a difference, the researchers conducted a more thorough analysis of tissue samples from pelvic and hind limb muscles of three chimpanzee cadavers from various zoos and research institutes around the United States. Previous studies in mammals have found that muscle composition between trunk, forelimb, and hind limb muscles is largely the same, O’Neill says, so he’s confident the samples are representative across most of the chimp’s musculature. The team used a technique called gel electrophoresis to break down the muscles into individual muscle fibers, and compared this breakdown to human muscle fiber data. © 2017 American Association for the Advancement of Science.

Keyword: Muscles; Evolution
Link ID: 23782 - Posted: 06.27.2017

Carl Zimmer Mark D. Zabel wants to set some fires. Dr. Zabel and his colleagues are developing plans to burn plots of National Park Service land in Arkansas and Colorado. If the experiments turn out as the researchers hope, they will spare some elk and deer a gruesome death. Across a growing swath of North America, these animals are dying from a mysterious disorder called chronic wasting disease. It’s caused not by a virus or bacterium, but a deformed protein called a prion. When ingested, prions force normal proteins in the animal’s body to become deformed as well. Over the course of months, prions can gradually wreck the animal’s nervous system, ultimately killing it. This year is the 50th anniversary of the discovery of chronic wasting disease. In the September issue of Microbiology and Molecular Biology Reviews, Dr. Zabel, an immunologist at Colorado State University, and his former graduate student Aimee Ortega survey what scientists have learned about the slow-spreading plague. It makes for ominous reading. “There’s a lot that we still don’t know and don’t understand about the disease,” Dr. Zabel said in an interview. Once chronic wasting disease gets a foothold, it can spread relentlessly. It’s now documented in 24 states, and continues to expand into new ranges. In some herds, as many as half of the animals carry prions. It’s only been in recent years that scientists have gained crucial clues to how the disease spreads. Direct contact, it turns out, isn’t the only way that the prions get from one animal to another. © 2017 The New York Times Company

Keyword: Prions
Link ID: 23781 - Posted: 06.27.2017

Frances Perraudin A 90-tonne machine that will allow cancer patients to receive state-of-the-art high-energy proton beam therapy on the NHS for the first time is to be installed at a hospital in Manchester. The cyclotron delivers a special type of radiotherapy currently only available overseas. The NHS has been paying for patients to travel abroad for the treatment since 2008. A 90-metre (300ft) crane will be used to lower the machine into position at the Christie hospital on Thursday. It will sit in a bunker reinforced with 270 timber, steel and concrete posts. Proton beam therapy targets certain cancers very precisely, increasing success rates and reducing side-effects. It causes less damage to healthy tissue surrounding the tumour and is particularly appropriate for certain cancers in children, who are more at risk of lasting damage because their organs are still growing. The treatment came to national attention in 2014 when a police search was mounted after the parents of five-year-old Ashya King took him out of hospital against doctors’ wishes and travelled to the continent. The couple hoped to secure proton beam therapy to treat their son’s brain tumour, but doctors argued that the treatment would not increase the boy’s chances of recovery. © 2017 Guardian News and Media Limited

Keyword: Miscellaneous
Link ID: 23777 - Posted: 06.27.2017

By Diana Kwon Across the animal kingdom, nearly all creatures sleep or display sleep-like states. The roundworm, Caenorhabditis elegans, does not sleep in a typical day-night cycle like humans and many other animals. Instead, these worms catch most of their z’s while transitioning from one larval stage to another, during a period called lethargus. When these creatures fall asleep, most of their neurons become inactive spontaneously, suggesting that sleep—at least in worms—is a passive state of the brain, according to a study published today (June 22) in Science. “The condition between sleep to wakefulness is probably one of the most drastic changes that our brains undergo,” says Manuel Zimmer, a neuroscientist at the Research Institute of Molecular Pathology at the Vienna Biocenter in Austria. “How a brain can switch between such drastically different states is not really understood.” To investigate this process, Zimmer and colleagues examined the brains of C. elegans. These worms do indeed have primitive brains, yet their nervous system comprises only 302 neurons, making it much easier to tackle than, say, the human brain, with billions of neurons, or even the fly brain, which has around 100,000 nerve cells. Using transgenic worms engineered with a fluorescent indicator that becomes active in response to high calcium levels in neurons (a proxy for neural activity), the researchers imaged the C. elegans brain during the transitions between sleep and wake states by adjusting oxygen levels. Because these soil-dwelling creatures live among low levels of oxygen (10 percent), atmospheric oxygen concentrations (21 percent) induce hyperactivity and wakefulness. © 1986-2017 The Scientist

Keyword: Sleep
Link ID: 23775 - Posted: 06.26.2017

Andrea Hsu Intuitively, we tend to think of forgetting as failure, as something gone wrong in our ability to remember. Now, Canadian neuroscientists with the University of Toronto are challenging that notion. In a paper published Wednesday in the journal Neuron, they review the current research into the neurobiology of forgetting and hypothesize that our brains purposefully work to forget information in order to help us live our lives. I spoke with Blake Richards, one of the co-authors of the paper, who applies artificial intelligence theories to his study of how the brain learns. He says that in the AI world, there's something called over-fitting — a phenomenon in which a machine stores too much information, hindering its ability to behave intelligently. He hopes that greater understanding of how our brains decide what to keep and what to forget will lead to better AI systems that are able to interact with the world and make decisions in the way that we do. We hear a lot about the study of memory. Is the study of forgetting a relatively new thing? Within psychology, there's a long history of work examining forgetting. So that's not a new field of study. But the neuroscientists — those of us who work with the biology of how the brain works — have not really examined forgetting much in the past. Generally, the focus for the last few decades in neuroscience has been the question of how do the cells in our brains change themselves in order to store information and remember things. It's only been in the last few years that there's been an upswing in scientific studies looking at what's happening inside our brains at the cellular level that might actually produce forgetting. © 2017 npr

Keyword: Learning & Memory
Link ID: 23771 - Posted: 06.24.2017

By Sam Wong People who have had amputations can control a virtual avatar using their imagination alone, thanks to a system that uses a brain scanner. Brain-computer interfaces, which translate neuron activity into computer signals, have been advancing rapidly, raising hopes that such technology can help people overcome disabilities such as paralysis or lost limbs. But it has been unclear how well this might work for people who have had limbs removed some time ago, as the brain areas that previously controlled these may become less active or repurposed for other uses over time. Ori Cohen at IDC Herzliya, in Israel, and colleagues have developed a system that uses an fMRI brain scanner to read the brain signals associated with imagining a movement. To see if it can work a while after someone has had a limb removed, they recruited three volunteers who had had an arm removed between 18 months and two years earlier, and four people who have not had an amputation. While lying in the fMRI scanner, the volunteers were shown an avatar on a screen with a path ahead of it, and instructed to move the avatar along this path by imagining moving their feet to move forward, or their hands to turn left or right. The people who had had arm amputations were able to do this just as well with their missing hand as they were with their intact hand. Their overall performance on the task was almost as good as of those people who had not had an amputation. © Copyright New Scientist Ltd.

Keyword: Robotics
Link ID: 23770 - Posted: 06.24.2017

By Chris Brown, Chris Corday, All it took was a single beer for Murray's Shaw life to unravel. The moment came on a bike holiday in January 2016 in San Diego while he was with some friends from the Vancouver area. After almost 20 years sober, the community college instructor from New Westminster, B.C., cracked open a cold one at the end of a long ride. Fourteen months later, he died alone in a hotel room in Vancouver's Downtown Eastside. Fentanyl overdose was the coroner's conclusion. "He wasn't making a choice with a rational mind. He was depressed and he was battling this impulse to use," said his wife, Sasha Wood, who offered to tell her husband's story to CBC News in the hopes it might help other families dealing with substance abuse issues. Fentanyl has become a scourge across the country, but B.C. has been hit the hardest: an average of four people have died of drug overdose every day in 2017. Wood said the events that led to Shaw's death illustrate much that's wrong with how the Canadian health care system treats those with an addiction. 'I just thought he could stop' Shaw had problems with alcohol in his 20s and got into trouble with the law. But Wood, 49, says he sought treatment and turned his life around. He stopped drinking completely, went to university and worked toward a PhD. ©2017 CBC/Radio-Canada.

Keyword: Drug Abuse
Link ID: 23769 - Posted: 06.24.2017

By KATIE THOMAS Nolan and Jack Willis, twins from upstate New York, and just 10 other boys took part in a clinical trial that led to the approval last fall of the very first drug to treat their rare, deadly muscle disease. Now the Willis boys are again test cases as a different type of medical question comes to the fore: whether insurers will cover the controversial drug, Exondys 51, which can cost more than $1 million a year even though it’s still unclear if it works. The boys’ insurer, Excellus BlueCross BlueShield, refused to cover the cost of the drug because the twins, who are 15, can no longer walk. Their disease, Duchenne muscular dystrophy, overwhelmingly affects boys and causes muscles to deteriorate, killing many of them by the end of their 20s. “I’m cycling between rage and just sadness,” their mother, Alison Willis Hoke, said recently, on the day she learned that an appeal for coverage had been denied. For now, the company that sells the drug, Sarepta Therapeutics, is covering the treatment’s costs, but Mrs. Hoke does not know how long that will last. The desperation in Mrs. Hoke’s voice reflects a sobering reality for families of boys with the disease since their elation last fall over the drug’s approval. Because the Food and Drug Administration overruled its own experts — who weren’t convinced the Exondys 51 had shown sufficiently good results — and gave the drug conditional approval, many insurers are now declining to cover it or are imposing severe restrictions that render patients ineligible. The story of Exondys 51 raises complex and emotionally charged questions about what happens when the F.D.A. approves an expensive drug based on a lower bar of proof. In practice, health insurers have taken over as gatekeeper in determining who will get the drug. © 2017 The New York Times Company

Keyword: Muscles; Movement Disorders
Link ID: 23768 - Posted: 06.23.2017

By Kat McGowan Doctors at Zuckerberg San Francisco General Hospital could not figure out what was wrong with the 29-year-old man sitting before them. An otherwise healthy construction worker from Nicaragua, the patient was suffering from a splitting headache, double vision and ringing in his ears. Part of his face was also numb. The cause could have been anything—from an infection to a stroke, a tumor or some kind of autoimmune disease. The Emergency Department (ED) staff took a magnetic resonance imaging scan of the man’s brain, performed a spinal tap and completed a series of other tests that did not turn up any obvious reason for the swelling in his brain—a condition that is formally known as encephalitis. Most likely, it was some kind of infection. But what kind? Nineteen standard tests are available to help clinicians try to pin down the source of encephalitis, but they test for the presence of only the most common infections; more than 60 percent of cases go unsolved each year. Physicians looked in the patient’s cerebrospinal fluid (which surrounds the brain and protects it) for evidence of Lyme disease, syphilis and valley fever, among other things. Nothing matched. So the S.F. General ED staff settled on the most likely culprit as a diagnosis: a form of tuberculosis (TB) that causes brain inflammation but cannot always be detected with typical tests. Doctors gave the man a prescription for some steroids to reduce the swelling plus some anti-TB drugs and sent him home. © 2017 Scientific American,

Keyword: Miscellaneous
Link ID: 23767 - Posted: 06.23.2017

Jon Hamilton Thanks to Sigmund Freud, we all know what it means to dream about swords, sticks and umbrellas. Or maybe we don't. "For 100 years, we got stuck into that Freudian perspective on dreams, which turned out to be not scientifically very accurate," says Robert Stickgold, a sleep researcher and associate professor of psychiatry at Harvard Medical School. "So it's only been in the last 15 to 20 years that we've really started making progress." Today, most brain scientists reject Freud's idea that dreams are highly symbolic representations of unconscious (and usually sexual) desire. That dream umbrella, they say, is probably just an umbrella. But researchers are still trying to figure out what dreams do represent, and what their purpose is. "There's not really a solid theory about why dreaming is there," says Benjamin Baird, a postdoctoral fellow at the Center for Sleep and Consciousness at the University of Wisconsin ­– Madison. "It's a big mystery." We all have a future self, a version of us that is better, more successful. It can inspire us to achieve our dreams, or mock us for everything we have failed to become. In this episode of the NPR podcast Invisibilia, hosts Alix Spiegel and Hanna Rosin talk to a woman who believes she can connect with her younger self in dreams. © 2017 npr

Keyword: Sleep
Link ID: 23765 - Posted: 06.23.2017

By Sharon Begley, STAT To anyone who’s aware that efforts to develop Alzheimer’s drug treatments have met failure after failure, and to have therefore decided that prevention is the only hope, a U.S. panel of experts issued a sobering message on Thursday: Don’t count on it. From physical activity to avoiding high blood pressure to brain training, a 17-member committee assembled by the National Academies of Sciences concluded, no interventions are “supported by high-strength evidence.” Instead, some high-quality studies found that one or another intervention worked, but other equally rigorous studies found they didn’t. 1. Cognitive training The evidence for programs aimed at boosting reasoning, problem-solving, memory, and speed of processing does include randomized trials that reported benefits from brain training, but the report calls that evidence “low to moderate strength.” One problem: There seemed to be benefits for two years, but not after five or 10. Results in other randomized studies were even more equivocal. There are also data from studies that are less rigorous, leading the committee to conclude that brain training (computer-based or not) can delay or slow age-related cognitive decline—but not Alzheimer’s. 2. Controlling blood pressure Evidence that this helps is weaker still. © 2017 Scientific American

Keyword: Alzheimers
Link ID: 23763 - Posted: 06.23.2017

Researchers have identified structural changes in two genes that increase the risk of developing Tourette syndrome, a neurological disorder characterized by involuntary motor and vocal tics. The study, published in the journal Neuron, was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Our study is the tip of the iceberg in understanding the complex biological mechanisms underlying this disorder. With recent advancements in genetic research, we are at the cusp of identifying many genes involved in Tourette syndrome,” said Jeremiah Scharf, M.D., Ph.D., assistant professor of neurology and psychiatry at Harvard Medical School and Massachusetts General Hospital, Boston, and co-corresponding author of the study. The research was part of an international collaboration co-led by Dr. Scharf; Giovanni Coppola, M.D., professor of psychiatry and neurology at the University of California, Los Angeles; Carol Mathews, M.D., professor of psychiatry at the University of Florida in Gainesville; and Peristera Paschou, Ph.D., associate professor in the department of biological sciences at Purdue University, West Lafayette, Indiana. The scientific team conducted genetic analyses on 2,434 individuals with Tourette syndrome and compared them to 4,093 controls, focusing on copy number variants, changes in the genetic code resulting in deletions or duplications in sections of genes. Their results determined that deletions in the NRXN1 gene or duplications in the CNTN6 gene were each associated with an increased risk of Tourette syndrome. In the study, approximately 1 in 100 people with Tourette syndrome carried one of those genetic variants.

Keyword: Tourettes; Genes & Behavior
Link ID: 23761 - Posted: 06.22.2017

Parkinson’s disease is commonly thought of as a movement disorder, but after years of living with the disease, approximately 25 percent of patients also experience deficits in cognition that impair function. A newly developed research tool may help predict a patient’s risk for developing dementia and could enable clinical trials aimed at finding treatments to prevent the cognitive effects of the disease. The research was published in Lancet Neurology and was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This study includes both genetic and clinical assessments from multiple groups of patients, and it represents a significant step forward in our ability to effectively model one of the most troublesome non-motor aspects of Parkinson’s disease,” said Margaret Sutherland, Ph.D., program director at the NINDS. For the study, a team of researchers led by Clemens Scherzer, M.D., combined data from 3,200 people with Parkinson’s disease, representing more than 25,000 individual clinical assessments and evaluated seven known clinical and genetic risk factors associated with developing dementia. From this information, they built a computer-based risk calculator that may predict the chance that an individual with Parkinson’s will develop cognitive deficits. Dr. Scherzer is head of the Neurogenomics Lab and Parkinson Personalized Medicine Program at Harvard Medical School and a member of the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital, Boston.

Keyword: Parkinsons
Link ID: 23759 - Posted: 06.22.2017

By Matthew Hutson Artificial neural networks, computer algorithms that take inspiration from the human brain, have demonstrated fancy feats such as detecting lies, recognizing faces, and predicting heart attacks. But most computers can’t run them efficiently. Now, a team of engineers has designed a computer chip that uses beams of light to mimic neurons. Such “optical neural networks” could make any application of so-called deep learning—from virtual assistants to language translators—many times faster and more efficient. “It works brilliantly,” says Daniel Brunner, a physicist at the FEMTO-ST Institute in Besançon, France, who was not involved in the work. “But I think the really interesting things are yet to come.” Most computers work by using a series of transistors, gates that allow electricity to pass or not pass. But decades ago, physicists realized that light might make certain processes more efficient—for example, building neural networks. That’s because light waves can travel and interact in parallel, allowing them to perform lots of functions simultaneously. Scientists have used optical equipment to build simple neural nets, but these setups required tabletops full of sensitive mirrors and lenses. For years, photonic processing was dismissed as impractical. Now, researchers at the Massachusetts Institute of Technology (MIT) in Cambridge have managed to condense much of that equipment to a microchip just a few millimeters across. © 2017 American Association for the Advancement of Science

Keyword: Robotics
Link ID: 23758 - Posted: 06.21.2017

Ian Sample Science editor Older men tend to have “geekier” sons who are more aloof, have higher IQs and a more intense focus on their interests than those born to younger fathers, researchers claim. The finding, which emerged from a study of nearly 8,000 British twins, suggests that having an older father may benefit children and boost their performance in technical subjects at secondary school. Researchers in the UK and the US analysed questionnaires from 7,781 British twins and scored them according to their non-verbal IQ at 12 years old, as well as parental reports on how focused and socially aloof they were. The scientists then combined these scores into an overall “geek index”. Magdalena Janecka at King’s College London said the project came about after she and her colleagues had brainstormed what traits and skills helped people to succeed in the modern age. “If you look at who does well in life right now, it’s geeks,” she said. Drawing on the twins’ records, the scientists found that children born to older fathers tended to score slightly higher on the geek index. For a father aged 25 or younger, the average score of the children was 39.6. That figure rose to 41 in children with fathers aged 35 to 44, and to 47 for those with fathers aged over 50. The effect was strongest in boys, where the geek index rose by about 1.5 points for every extra five years of paternal age. The age of the children’s mothers seemed to have almost no effect on the geek index. © 2017 Guardian News and Media Limited

Keyword: Epigenetics; Development of the Brain
Link ID: 23757 - Posted: 06.21.2017

By Karl Gruber Birds, fish, and even humans have shattered barriers when it comes to mating rituals, from which partner initiates the courting to which one picks up the check at a fancy restaurant. But things are a bit simpler for frogs, as males and females stick to clearly defined roles: Males serenade the females, and females pick their favorite males to mate. Now, a new study suggests that the smooth guardian frog of Borneo (Limnonectes palavanensis) is an exception to that rule. During the mating season, the female frogs sing to the males in an attempt to win them over—a reversal of the normal process. In fact, if you see a single frog surrounded by a bunch of serenading croakers, called a “lek,” it’s most likely a lucky male being courted by a chorus of females. Males occasionally belt out “advertisement calls” to let females know that they are available. After mating, it’s the males who stay behind to care for the eggs, even taking tadpoles to small ponds after they hatch. This is the first known example of role reversal in singing frogs, scientists write in a recent issue of Behavioral Ecology and Sociobiology. It may even represent the first case of full-blown sex role reversal, which would also require that males do the mate choosing. Researchers are working on that now, but they say that—judging by the high rate of female serenading—males may be the picky ones. © 2017 American Association for the Advancement of Science.

Keyword: Sexual Behavior
Link ID: 23755 - Posted: 06.21.2017

By SAM QUINONES COVINGTON, KY. — Not long ago, I visited a Narcotics Anonymous meeting where men with tattoos and short-cropped hair sat in a circle and talked out their errors. One had lived under an overpass, pimping his girlfriend’s daughter for cash to buy heroin. As the thought brought him to tears, his neighbor patted his shoulder. Others owned to stealing from grandparents, to losing jobs and children. Soon, most in the room — men with years of street addiction behind them — were wiping their eyes. What made the meeting remarkable, however, was not the stories, but where it was taking place. Unit 104 is a 70-man pod in Kenton County Detention Center in northern Kentucky, across the Ohio River from Cincinnati. The unit, and an equivalent one for women, is part of a new approach to jail made necessary by our nationwide epidemic of opiate addiction. Drug overdoses are now the leading cause of death among Americans under 50. As the country has awakened to that epidemic, a new mantra has emerged: “We can’t arrest our way out of this,” accompanied by calls for more drug-addiction treatment. Yet the opiate epidemic has swamped our treatment-center infrastructure. Only one in 10 addicts get the treatment they need, according to a 2016 surgeon general’s report. New centers are costly to build, politically difficult to find real estate for and beyond the means of most uninsured street addicts, anyway. So where can we quickly find cheap new capacity for drug treatment accessible to the street addict? Jail is one place few have thought to look. Jails typically house inmates awaiting trial or serving up to a year for a misdemeanor crime. Many inmates are drug addicts. They vegetate for months, trading crime stories in an atmosphere of boredom and brutality. Any attempt at treatment is usually limited to a weekly visit by a pastor or an Alcoholics Anonymous volunteer. When inmates are released, they’re in the clothes they came in with, regardless of the weather, and have no assistance to re-enter the real world. This kind of jail has always been accepted as an unavoidable fixed cost of government. © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 23754 - Posted: 06.20.2017

By Michael Price Whether it’s giving to charity or helping a stranger with directions, we often assist others even when there’s no benefit to us or our family members. Signs of such true altruism have been spotted in some animals, but have been difficult to pin down in our closest evolutionary relatives. Now, in a pair of studies, researchers show that chimpanzees will give up a treat in order to help out an unrelated chimp, and that chimps in the wild go out on risky patrols in order to protect even nonkin at home. The work may give clues to how such cooperation—the foundation of human civilization—evolved in humans. “Both studies provide powerful evidence for forms of cooperation in our closest relatives that have been difficult to demonstrate in other animals besides humans,” says Brian Hare, an evolutionary anthropologist at Duke University in Durham, North Carolina, who was not involved with the research. In the first study, psychologists Martin Schmelz and Sebastian Grüneisen at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, trained six chimps at the Leipzig Zoo to play a sharing game. Each chimp was paired with a partner who was given a choice of four ropes to pull, each with a different outcome: give just herself a banana pellet; give just the subject a pellet; give both of them pellets; or forgo her turn and let her partner make the decision instead. © 2017 American Association for the Advancement of Science.

Keyword: Evolution
Link ID: 23753 - Posted: 06.20.2017

By Timothy Revell Feeling sad? Soon your dolls will be able to tell. To demonstrate the power of a new chip that can run artificially intelligent algorithms, researchers have put it in a doll and programmed it to recognise emotions in facial images captured by a small camera. The doll can recognise eight emotions in total, including surprise and happiness, all while running on a small battery and without doing any processing in the cloud. The total cost of putting the new chip together is just €115 – an indicator of how easy it is becoming to give devices basic AI abilities. “In the near future, we will see a myriad of eyes everywhere that will not just be watching us, but trying to help us,” says project leader Oscar Deniz at the University of Castilla-La Mancha in Ciudad Real, Spain. Recent advances in AI mean we already have algorithms that can recognise objects, lip-read, make basic decisions and more. It’s only a matter of time before these abilities make their way on to little cheap chips like this one, and then put into consumer devices. “We will have wearable devices, toys, drones, small robots, and things we can’t even imagine yet that will all have basic artificial intelligence,” says Deniz. © Copyright New Scientist Ltd.

Keyword: Emotions
Link ID: 23752 - Posted: 06.20.2017

/ By Joshua C. Kendall Dr. Joshua A. Gordon, the new director of the National Institute of Mental Health, took office in the final year of Barack Obama’s presidency. But he has this much in common with Obama’s successor: He has little patience for incremental reforms. As Gordon defines it, the job involves both advocating for the mental health needs of Americans and developing science to guide policymakers and clinicians. A 49-year-old psychiatrist who made his reputation as a brilliant researcher of mice with mutations that mimic human mental disorders, Gordon is convinced that radical changes are needed in the treatment of illnesses like schizophrenia. In an interview in his office at the NIMH campus in Bethesda, Maryland, he lamented that while modest improvements have been made in patient care over the last few decades, we don’t know enough about the brain to “even begin to imagine what the transformative treatments of tomorrow will be like.” Few psychiatrists would disagree that change is overdue. Take depression: Current approaches, which employ drugs like Prozac or cognitive-behavioral therapy, or a combination of the two, can relieve major symptoms in only some patients. The hope is that “precision medicine” — treatments targeted to the specific biological makeup of the patient — can do for psychiatry what scientists like Gordon’s Nobel Prize-winning mentors J. Michael Bishop and Harold E. Varmus did for cancer treatment a generation ago. Unfortunately, as Gordon is well aware, mental illness is particularly challenging in this regard. In contrast to many types of cancer, where one genetic mutation can cause unregulated cell growth, psychiatric diseases rarely stem from any single faulty gene; instead, they are typically rooted in a complex interplay of genetic, environmental, and cultural factors. Copyright 2017 Undark

Keyword: Depression; Schizophrenia
Link ID: 23751 - Posted: 06.17.2017