Links for Keyword: Schizophrenia

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First genomic study of schizophrenia in African people turns up broken genes

Alison Abbott Researchers studying the biological basis of mental illness have conducted the first genomic analysis of schizophrenia in an African population, and have identified multiple rare mutations that occur more frequently in people with the condition. The mutations are mainly in genes that are important for brain development and the brain’s synapses, tiny structures that coordinate communication between neurons. The genes match those identified in other similar studies of schizophrenia — but nearly all previous research has been conducted in European or Asian populations. The latest work was published1 in Science on 31 January. This research is particularly important because Africa has represented a big gap in the populations that geneticists have studied, says psychiatric geneticist Andreas Meyer-Lindenberg, director of the Central Institute of Mental Health in Mannheim, Germany. He says that the work lends support to current hypotheses about the biological origins of schizophrenia, which can cause a range of symptoms including hallucinations, delusions and disordered thinking. Researchers think that each mutation might contribute a small amount to the overall risk of developing the condition, and that disruption to synapses could be crucial to the disease’s development. Over the past decade, as studies that use genome sequencing to identify the genetic basis of diseases have flourished, geneticists have come under increasing fire for failing to sample diverse populations, largely neglecting African people. Around 80% of participants in genetic studies are of European descent, and less than 3% are of African descent. © 2020 Springer Nature Limited

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: Development of the Brain
Link ID: 27016 - Posted: 02.04.2020

Schizophrenia study finds evidence of reduced links between brain cells

Hannah Devlin Science correspondent A groundbreaking brain-scanning technique has uncovered evidence that suggests schizophrenia is linked to a loss of connections between brain cells. Scientists had previously suspected a breakdown in the connections between neurons played a role in the condition, based on postmortem studies. The latest research, the first to find evidence for this in the brains of living people, could pave the way for new and better treatment. Prof Oliver Howes from the MRC London Institute of Medical Sciences, Imperial College London and King’s College London, who led the study, said: “Our current treatments for schizophrenia target only one aspect of the disease: the psychotic symptoms. “But the debilitating cognitive symptoms, such as loss of abilities to plan and remember, often cause much more long-term disability and there’s no treatment for them at the moment.” Howes believes the loss of connections, known as synapses, between brain cells, could be responsible for this broader array of symptoms. The study, published in Nature Communications, focused on measuring a protein found in synapses called SV2A, which has been shown to be a good marker of the overall density of connections in the brain. They used a tracer that binds to the protein and which emits a signal that can be picked up by a PET brain scan, which provided an indirect measure of the density of connections. The team scanned 18 adults with schizophrenia and compared them with 18 people without the condition. They found that levels of SV2A were significantly lower in the front of the brain – the region involved in planning – in people with schizophrenia. © 2020 Guardian News & Media Limited

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26964 - Posted: 01.15.2020

Glutamate Built the Brain—Can It Treat It, Too?

By Brooke N. Dulka Glutamate, arguably the most important chemical in your nervous system, is older than the brain itself. From a single cell bacterium, to mushrooms and plants, to you—every living thing on this planet relies on this tiny molecule for cellular communication. It is absolutely critical for everything we do. “The function of most, if not all, of the trillions of cells in the brain are regulated by glutamate,” neuroscientist David Baker explains to me. On November 1, 2019, neuroscientists gathered at the Harley-Davidson Museum in Milwaukee, WI to share their science. The chrome-laden motorcycle in the corner of the room was hard to ignore, but it was the presentation of Baker, a professor at Marquette University, that really caught my attention. Baker has dedicated his career to understanding how glutamate can treat disorders of the brain. Specifically, his hopes for targeting glutamate lie in a mechanism called system xc-. Glutamate is often called the “major excitatory neurotransmitter” within the brain. It is the brain’s “go” signal. Baker notes that glutamate receptors are found in every kind of brain cell, which means it is doing more than regulating the activity of neurons, it is regulating the brain’s support cells too. Glutamate is that widespread and important! But being almost everywhere increases the chances that something, somewhere, could go wrong. Thus, most disorders of the brain involve some degree of glutamate dysfunction. This includes disorders such as schizophrenia, depression, obsessive-compulsive disorder, Alzheimer’s disease and more. While one might think that this awareness provides neuroscientists with critical insights into treating disorders of the brain, actually the opposite has occurred. In fact, most psychiatric drugs weren’t even discovered through systematic drug development, as one might expect. More often than not, the drugs we commonly use today were serendipitous findings or accidental discoveries. Baker notes that almost none of the most commonly prescribed drugs for psychiatric disorders target glutamate. Given the importance of glutamate to nearly every brain function, there is a genuine, and well-reasoned, concern among both neuroscientists and psychiatrists that glutamatergic therapeutics will produce widespread impairments in the brain. © 2020 Scientific American

An Undercover Journey Into the Heart of Madness

By Christie Aschwanden When she was 24, Susannah Cahalan developed a sudden psychosis. She grew paranoid — convinced her apartment was infested with bedbugs, that people were spying on her, that her boyfriend was cheating. She started to believe she could age people with her mind. As she recounted in her 2013 bestseller, “Brain on Fire: My Month of Madness,” she received several misdiagnoses (bipolar disorder, schizoaffective disorder) before an alert doctor discovered the true culprit: autoimmune encephalitis. The moment her illness was deemed neurological, ”as in physical, in the body, real,” rather than psychiatric, “in the mind and therefore somehow less real,” the quality of her care drastically improved, Cahalan writes in her new book, “The Great Pretender.” Sympathy and understanding replaced the detached attitude that had defined her treatment as a mental patient, “as if a mental illness were my fault, whereas a physical illness was something unearned, something ‘real,’” she writes. Cahalan, a journalist, recovered from her brief psychosis, but the distinction between physical and mental illness continued to perplex her. “What does mental illness mean, anyway, and why would one affliction be more ‘real’ than another?” she asks. These questions form the backbone of “The Great Pretender.” The book centers on the work of David Rosenhan, a Stanford psychologist whose paper, “On Being Sane in Insane Places,” was an instant sensation when it was published in the journal Science in 1973. The paper begins with a question: “If sanity and insanity exist, how shall we know them?”

Having a Dog as a Child Is Tied to a Lower Risk of Schizophrenia as an Adult

By Nicholas Bakalar Living with a pet dog in childhood may be linked to a reduced risk of schizophrenia in adulthood. Researchers studied adult patients at Sheppard Pratt Health System in Baltimore, 396 with schizophrenia and 381 with bipolar disorder. They compared them with 594 healthy controls. The participants reported whether they had had a dog or a cat in the household when they were children and, if so, the first and most recent time they had contact with the animal. The findings appeared this month in PLOS One. More than half of the subjects had dogs, and about a third had cats before their 13th birthdays. After adjusting for other characteristics, the scientists found that exposure to a dog at any time in childhood was associated with a 24 percent reduced risk for schizophrenia. Those exposed to dogs at birth were 55 percent less likely to have schizophrenia than people who had not been exposed at all. There was no significant effect of exposure to cats, and no effect of either animal on the risk for bipolar disorder. “We don’t know the mechanism,” said the lead author, Dr. Robert H. Yolken, a professor of pediatrics at Johns Hopkins University in Baltimore, though he noted that the microbiome, or collection of gut bacteria, of people with schizophrenia is different from that of controls. “One possibility is that having a dog in the house causes a different microbiome and changes the likelihood of developing a psychiatric disorder,” he said. © 2019 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 26911 - Posted: 12.26.2019

Mental Illness Behind Bars: The Hard Lessons of Orleans Parish

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.

‘Mutating genes are key to treating schizophrenia’ says top neuroscientist

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

When Mental Illness Is Severe

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

A New Way to Think about Mental Illness

By Kristopher Nielsen Have you ever heard of a condition known as “general paresis of the insane”? Probably not. In the 19th century general paresis was one of the most commonly diagnosed mental disorders. Its symptoms included odd social behaviors, impaired judgment, depressed mood and difficulty concentrating. Around the turn of the 20th century, though, we figured what it really was—a form of late-stage syphilis infecting the brain and disrupting its function. A few decades later we discovered a highly effective treatment: penicillin. Although general paresis is now very rare, its example is still instructive. Any honest researcher will tell you we don’t currently have good explanations for most mental disorders. Depression, obsessive-compulsive disorder, schizophrenia—we don’t really know how these patterns of disrupted thought, behavior and emotion develop or why they stick around. Yet the hope remains that, much like with general paresis, we may soon discover the root causes of these illnesses, and this knowledge may tell us how to treat them. An example of this hope can be seen in the popular notion that a “chemical imbalance” causes depression. This might turn out to be true, but the truth is we don’t know. Some researchers are starting to think that for many mental disorders, such hope might be based on incorrect assumptions. Instead of having one root cause, as general paresis did, mental disorders might be caused by many mechanisms acting together. These mechanisms might be situated in the brain, but they could also be located in the body and even in the external environment, interacting with one another in a network to create the patterns of distress and dysfunction we currently recognize and label as varieties of mental illness. In this more complex view, patterns such as depression and generalized anxiety arise as tendencies in the human brain-body-environment system. Once the patterns are established, they are hard to change because the network continues to maintain them. © 2019 Scientific American

After Her Illness Was Misdiagnosed as Madness, Susannah Cahalan Tackles Madness in Medicine

By Emily Eakin Ten years ago, Susannah Cahalan was hospitalized with mysterious and terrifying symptoms. She believed an army of bedbugs had invaded her apartment. She believed her father had tried to abduct her and kill his wife, her stepmother. She believed she could age people using just her mind. She couldn’t eat or sleep. She spoke in gibberish and slipped into a catatonic state. Had it not been for an ingenious doctor brought in to consult on her case, Cahalan might well have ended up in a psychiatric ward. Instead, as she recounted in “Brain on Fire,” her best-selling 2012 memoir about her ordeal, she was eventually found to have a rare — or at least newly discovered — neurological disease: anti-NMDA-receptor autoimmune encephalitis. In plain English, Cahalan’s body was attacking her brain. She was only the 217th person in the world to be diagnosed with the disorder and among the first to receive the concoction of steroids, immunoglobulin infusions and plasmapheresis she credits for her recovery. Cahalan’s condition is what in medicine is called a “great pretender”: a disorder that mimics the symptoms of various disorders, confounding doctors and leading them astray. “The Great Pretender” also happens to be the title of Cahalan’s new book, which comes out on Tuesday. It, too, is a medical detective story, only this time at the heart of the mystery is not a patient or a disease but a member of the profession: David Rosenhan, a Stanford psychologist and the author of “On Being Sane in Insane Places,” a landmark 1973 study that, by questioning psychiatrists’ ability to diagnose mental illness, plunged the field into a crisis from which it has still not fully recovered. Cahalan, 34, learned about Rosenhan six years ago, while on tour for the paperback edition of “Brain on Fire.” She was inundated with letters, hundreds a week, from desperate patients and their families, convinced that they too might have a neurological condition masquerading as mental illness. She was haunted by the idea that sheer luck had allowed her to escape a similar fate. © 2019 The New York Times Company

Intensive DNA search yields 10 genes tied directly to schizophrenia

By Jocelyn Kaiser HOUSTON, TEXAS—Schizophrenia tends to run in families, which suggests it’s largely inherited. But a long-running search for genes underlying this severe psychiatric condition has yielded only indirect clues. Now, by scouring the DNA of tens of thousands of people, gene hunters have for the first time nabbed a handful of rare genes that, when mutated, appear to be direct contributors to the disease—and may shed light on what goes awry in a schizophrenia patient’s brain. “These are concrete genes with mutations with a clear molecular mechanism,” says Mark Daly of the Broad Institute in Cambridge, Massachusetts, and the University of Helsinki, who is principal investigator for a consortium that presented the work last week at the annual meeting of the American Society of Human Genetics (ASHG) here. “It was a fabulous talk,” says Jennifer Mulle of Emory University in Atlanta, who studies the genetics of psychiatric disorders. “We don’t understand anything about the biological pathways [in schizophrenia]. Now, these genes give us an avenue.” People with schizophrenia, which afflicts about 0.7% of the U.S. population, have a distorted sense of reality and confused thinking; they may have hallucinations and delusions. Some patients share similar genetic abnormalities, such as missing specific chunks of DNA, but how those gaps may contribute to disease isn’t known. © 2019 American Association for the Advancement of Science

Schizophrenia risk gene linked to cognitive deficits in mice

Researchers have discovered in mice how one of the few genes definitively linked to schizophrenia, called SETD1A, likely confers risk for the illness. Mice genetically engineered to lack a functioning version of the enzyme-coding gene showed abnormalities in working memory, mimicking those commonly seen in schizophrenia patients. Restoring the gene’s function corrected the working memory deficit. Counteracting the gene’s deficiencies also repaired neuronal circuit deficits in adult mice – suggesting clues for potential treatment strategies. A team of scientists led by Joseph Gogos, M.D., Ph.D., of Columbia University, New York City, reported on their research – supported by the National Institutes of Health – in Neuron. “You could call SETD1A a master regulator,” explained David Panchision Ph.D., of the NIH’s National Institute of Mental Health (NIMH), which co-funded the study. “This schizophrenia risk gene codes for an enzyme that influences the expression of many other genes. In mice, a hobbled version of SETD1A disrupted gene expression in a network harboring other genomic suspects in schizophrenia. Remarkably, the resulting abnormalities were reversible.” Researchers have identified both common and rare genetic variations that contribute to risk for schizophrenia. Mutant SETD1A is one of just a few rare genes known to unequivocally confer risk for schizophrenia. While common genetic variations linked to schizophrenia individually exert only tiny effects on risk, having just one mutant copy of SETD1A is sufficient to confer a large increase in disease risk. SETD1A plays a key role in epigenomic regulation – the switching on-and-off of genes in response to experience – a molecular process widespread in the brain. Mutations in SETD1A have primarily been found in people with schizophrenia, suggesting that this rare gene variation might hold important clues to the underlying disease process.

Social Mania

By Liz Eavey My brother Roland’s Facebook post set off a flurry of concern throughout his social network. He’d been assaulted, he wrote, by “old-world mentality Agent Smiths who are threatening our ability to bring natural plant-based Medicine and intelligent health care to the world.” In caps, he told his followers to ALERT THE PRESS AND BRING SIGNS OF PROTEST. The yogis sent positive vibes; the rebels cried fight the man; the good Samaritans offered to jump in their cars and rescue him. Except that Roland hadn’t exactly been assaulted. He’d been placed under an involuntary psychiatric hold and forcibly subdued in an emergency room at the same institution where he was training to become a psychiatrist. And, with that, four years ago, Facebook snitched our big family secret: Roland, the literary prodigy, the tenderhearted musician, the Ivy League grad, was bipolar. Roland — who read and approved this essay — is the effortlessly brilliant middle child who takes up a disproportionate amount of space in a room, with a booming voice and the charisma of a megachurch pastor. After college, he moved to Hollywood and landed, with zero experience or connections, a coveted job with an A-list director. Then, he decided to become a doctor, enrolling in a top-tier M.D./M.B.A. program. Everything about my brother is superlative, including his demons: crippling insomnia, legendary alcoholism and a chemical imbalance that has repeatedly imploded his life. I, the firstborn, am diplomatic and obedient, less concerned with standing out than blending in. Just 17 months apart, Roland and I constantly butted heads trying to assert our individuality growing up. In seventh grade, I wrote “An Older Sister’s Guide to Having Younger Brothers,” which began: “A smart idea, which would prevent use of this guide, would be to just not have younger brothers.” Yet, when we weren’t vying for sibling dominance, we were always looking out for each other. © 2019 The New York Times Company

Gene regulators work together for oversized impact on schizophrenia risk

Researchers have discovered that gene expression regulators work together to raise an individual’s risk of developing schizophrenia. Schizophrenia-like gene expression changes modeled in human neurons matched changes found in patients’ brains. The researchers, led by Kristen Brennand, of the Icahn School of Medicine at Mount Sinai, New York City, report on their findings in Nature Genetics. The work was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Genome-wide association studies have revealed at least 143 chromosomal sites associated with risk for schizophrenia. However, individually, each of these sites can explain only a small fraction of the risk. Even when the effects of disease-linked rare genetic variants are factored in, most of schizophrenia’s known high inheritance remains unexplained. One possible clue: more than 40% of the suspect chromosomal sites contain regulators, called expression quantitative trait loci, or eQTLs, that govern the expression of multiple genes. “Individually, these gene regulators have a modest effect on the brain. Working in concert, they exert different and more significant effects on the brain — effects that boost schizophrenia risk,” explained David Panchision, chief of the Developmental Neurobiology Program at NIMH. “Learning more about the downstream cellular and molecular effects of such synergy holds hope for advances in precision psychiatry and more personalized medicine.” To explore the role of these regulators, Brennand and colleagues studied them in induced neurons using a molecular modeling technology. This induced pluripotent stem cell method makes it possible to grow a person’s unique neurons in a petri dish using stem cells derived from their skin cells.

Interventions to Prevent Psychosis

By Jane E. Brody Tiffany Martinez was a 17-year-old college freshman when she began hearing voices, seeing shadowy figures and experiencing troubling, intrusive thoughts. Her friends at the University of Southern Maine, where she was majoring in psychology, noticed that she was acting strangely and urged her to get help. They most likely saved her from a crippling mental health crisis, prevented the derailment of her education and ultimately enabled her to become a psychiatric nurse practitioner who can help other young people avert a psychiatric crisis. Tiffany’s friends convinced her to go to the university’s health center, where she met with a nurse who had just attended an educational seminar about identifying the early signs of mental illness in young adults. The nurse suspected that Tiffany was at risk of developing a psychotic episode and referred her to the Portland Identification and Early Referral, or PIER, program at the Maine Health Center. The program was developed in 2001 by Dr. William R. McFarlane, a psychiatrist who suspected that if early intervention could reverse the course of diseases like cancer and heart disease, it should do likewise for psychosis. Despite conventional wisdom suggesting otherwise, he persevered in the belief that an impending psychotic break could be identified and prevented if it was recognized early and appropriate steps taken to head it off. Tiffany, who said her father had schizophrenia, was an early beneficiary of his vision and has become a poster child for what can be done to prevent a devastating, costly illness that afflicts up to 3 percent of the population. After the PIER program was extended to 25 school districts in and around Portland, there was a 35 percent decline in new hospital admissions for psychotic symptoms, Dr. McFarlane said. © 2019 The New York Times Company

Lithium: the gripping history of a psychiatric success story

Douwe Draaisma Some 70 years ago, John Cade, an Australian psychiatrist, discovered a medication for bipolar disorder that helped many patients to regain stability swiftly. Lithium is now the standard treatment for the condition, and one of the most consistently effective medicines in psychiatry. But its rise was riddled with obstacles. The intertwined story of Cade and his momentous finding is told in Lithium, a compelling book by US psychiatrist Walter Brown. Bipolar disorder, labelled manic-depressive illness until 1980, affects around 1 in 100 people globally. Without treatment, it can become a relentless cycle of emotional highs and lows. Suicide rates for untreated people are 10–20 times those in the general population. Fortunately, lithium carbonate — derived from the light, silvery metal lithium — can reduce that figure tenfold. Brown’s telling of Cade’s eventful life covers much of the same ground as Finding Sanity (2016), a rather hagiographic biography by Greg de Moore and Ann Westmore. What Brown does superbly well is to show that Cade made his discovery without access to advances in technology or to modern facilities — and almost despite them. His finding was the happy result of being forced to work with the simplest of means. During the Second World War, Cade was interred for more than three years in the notorious Japanese prisoner-of-war camp at Changi in Singapore. He was put in charge of the psychiatric section, where he began to note the decisive link between certain food deficiencies and diseases in his fellow prisoners. A lack of B vitamins, for instance, caused beriberi and pellagra.

Could air pollution contribute to psychiatric illness?

Natalie Parletta Poor air quality has been associated with higher rates of bipolar disorder and major depression in observational research involving more than 150 million people in the US and Denmark. The link was found to be more pronounced in Denmark, with research also suggesting that pollution exposure during childhood more than doubled the risk of schizophrenia and personality disorders. Genetic studies now reveal that genes only explain a small fraction of psychiatric illness onset. Therefore, researchers are exploring environmental factors in the search to comprehend the global increase in these complex disorders of brain function. “We were hoping to understand what aspects of human environments are driving psychiatric and neurological disease prevalence,” says senior author Andrey Rzhetsky from the University of Chicago, US. The findings are published in the journal PLOS ONE. The search thus far has focussed largely on family environments and childhood trauma, including prenatal influences. Other possible avenues include social circumstances, stressful life events, substance abuse, and emerging evidence for poor diet. Far less attention has been given to physical environments. Yet as the numerous adverse health impacts of air pollution have come to light, inspection of its potential role in neurological disorders has lagged.

'Lithium' Is A Homage To A Drug — And To The Renegade Side Of Science

Etelka Lehoczky Like any good story about a scientific discovery, Walter A. Brown's account of the history of lithium features plenty of improvisation, conjecture and straight-up kismet. Unlike many such stories, though, it also features a fair share of personal bias, senseless puttering and random speculation — on part of these scientific researchers. Brown, a practicing psychiatrist and university professor of more than 40 years, seems to have been drawn to write Lithium: A Doctor, A Drug and a Breakthrough as much because of lithium's fluky history and overlooked importance (for many years, he argues, it was "the Cinderella of psychiatric drugs") as by the profound impact it's had on countless sufferers of bipolar disorder and depression. Lithium is a homage, not just to a drug, but to the renegade side of science. Its heroes are researchers scattered around the globe, short on funding and frequently unaware of each other's work, without whom a commonly available substance would never have been recognized as a treatment for one of the most baffling psychiatric illnesses. By celebrating these men, Brown hopes to do a lot more than simply raise awareness about an underappreciated substance. He aims to demolish what remains of the myth that scientific progress is driven by rigorous dispassion. The story of lithium's use in medicine is certainly colorful, as is the history of the illness it's become known for. Brown doesn't stint on either tale. He goes all the way back to the first century to find a would-be description of manic depression by the Greek doctor Aretaeus of Cappadocia. These patients, Aretaeus wrote, "'laugh, play, dance night and day, and sometimes go openly to the market crowned, as if victors in some contest of skill,'" only to become "'torpid, dull and sorrowful.'" © 2019 npr

Can an Illusory World Help Treat Psychosis’s Real-World Delusions?

By Simon Makin Can an Illusory World Help Treat Psychosis's Real-World Delusions? Scenes of everyday living within a virtual-reality simulation attempt to lessen social anxiety for people with psychosis. Credit: University of Oxford/Oxford VR Many people with psychosis suffer from persecutory delusions—beliefs that terrible things will happen to them in everyday situations, such as people trying to harm them. The disorder causes social anxiety, which can be exacerbated by other symptoms, such as hearing voices. All of this makes ordinary activities such as shopping or going to the doctor challenging. Often a person just withdraws entirely from social contact. In a vicious cycle, the ensuing isolation and rumination can exacerbate other symptoms, including those causing the withdrawal. The idea behind a virtual-reality system called gameChange is to help patients learn to feel safer, allaying social anxiety by putting them in simulations of situations they fear in which their worst dread does not materialize. Last month, clinical psychologist Daniel Freeman of the University of Oxford and his colleagues launched a clinical trial of gameChange, the biggest such trial to date of a VR treatment for schizophrenia. It will enroll 432 people with psychosis from five National Health Service (NHS) centers across the U.K. Researchers will assess participants’ avoidance and distress in real-world situations, using an established measure, before and after treatment and then do so again six months later. The hope is that the treatment will reduce participants’ anxiety, which will, in turn, improve other symptoms, particularly persecutory delusions. Freeman co-founded an Oxford spin-off company, Oxford VR, to develop and commercialize the technology. And if the trial is successful, gameChange could be rolled out by the NHS. © 2019 Scientific American

One Family’s Ordeal With Schizophrenia

By Emily Anthes In 2002, Marin Sardy and her younger brother Tom traveled to a small Costa Rican town for what they hoped would be a low-key beach vacation. The siblings, both in their 20s, planned to spend a few weeks relaxing, learning to surf, and just generally enjoying each other’s company. Sardy reveals what it means to love someone who is mentally ill and how hard it is to truly understand another person’s mind. And then, one day, Tom began to complain about his face. His bones, he said, had detached from each other, and his jaw had separated from his head. He couldn’t get his face back into alignment, he told Sardy. He began to talk — excitedly and cryptically — about “building matrices” and his plans to swim from Alaska to Japan. His facial expressions turned blank. Sardy observed these developments with growing alarm. She and Tom had grown up with a mother whose life had been derailed by schizophrenia, and she was well acquainted with its signs and symptoms. “Memories unfurl inside as I watch Tom,” Sardy writes in her intimate, multigenerational memoir, “The Edge of Every Day: Sketches of Schizophrenia.” “It is as if I already know that doctors and medications and hospitals and our efforts will all fail him.” “The Edge of Every Day” is Sardy’s attempt to come to terms with a fundamentally mysterious disease and how its effects ripple throughout her family. It’s a deeply compassionate book about what it means to love someone who is mentally ill — about how hard it is to truly understand another person’s mind and the importance of continuing to try. Copyright 2019 Undark

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