Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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By Lenny Bernstein Comedian Robin Williams was grappling with severe depression when he committed suicide Monday, and on Thursday we learned that he also was in the early stages of Parkinson's disease. Sadly, the two conditions are often found together. In a 2012 study conducted by the National Parkinson Foundation, 61 percent of 5,557 Parkinson's patients surveyed reported that they also suffered from depression, with symptoms that ranged from mild to severe. Both conditions are associated with a shortage of dopamine, a neurotransmitter that helps regulate movement and control the brain's pleasure center. "Dopamine is a feel-good chemical. If you are low in dopamine, you are not going to feel so good," said Joyce Oberdorf, president and CEO of the National Parkinson Foundation. "There are [also] other neurotransmitters that can be low." A separate study published Friday found that newly-diagnosed Parkinson's patients have higher rates of depression, anxiety, fatigue, and apathy than a control group of people without Parkinson's. Researchers from the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania found that 13.9 percent of patients had symptoms of depression when they were diagnosed with Parkinson's, a proportion that rose to 18.7 percent after 24 months. Just 6.6 percent of people without the disease had depression, and that dropped to just 2.4 percent after 24 months. Despite their depressive symptoms, most of the Parkinson's patients who also had that condition were not treated with anti-depressants at any point in the two-year study. The findings were published in the journal Neurology.
By Rebecca Boyle Like a dog wagging its tail in anticipation of treats to come, dolphins and belugas squeal with pleasure at the prospect of a fish snack, according to a new study. It’s the first direct demonstration of an excitement call in these animals, says Peter Madsen, a biologist at Aarhus University in Denmark who was not involved in the study. To hunt and communicate, dolphins and some whale species produce a symphony of clicks, whistles, squeaks, brays, and moans. Sam Ridgway, a longtime marine biologist with the U.S. Navy’s Marine Mammal Program, says he heard distinctive high-pitched squeals for the first time in May 1963 while training newly captured dolphins at the Navy’s facility in Point Mugu, California. “We were throwing fish in, and each time they would catch a fish, they would make this sound,” he says. He describes it as a high-pitched “eeee,” like a child squealing in delight. Ridgway and his collaborators didn’t think much of the sound until later in the 1960s, when dolphins trained to associate a whistle tone with a task or behavior also began making it. Trainers teach animals a task by rewarding them with a treat and coupling it with a special noise, like a click or a whistle. Eventually only the sound is used, letting the animal know it will get a treat later. The whistle was enough to provoke a victory squeal, Ridgway says. Meanwhile, beluga whales would squeal after diving more than 600 meters to switch off an underwater speaker broadcasting tones. “As soon as the tone went off, they would make this same sound,” Ridgway says, “despite the fact that they’re not going to get a reward for five minutes.” He also heard the squeal at marine parks in response to trainers’ whistles. © 2014 American Association for the Advancement of Science.
Greta Kaul It was a rainy day, and earthworms wriggled out of the ground and began to arrange themselves on the pavement as Julian Plumadore walked to his community college zoology class in 1991. They spelled out messages only he could read. "I was very frightened to be a custodian of that kind of cosmic information and be able to do absolutely nothing about it," Plumadore said. Other times, there were voices - demons screaming - telling him he was going to hell. Plumadore was eventually diagnosed as having schizoaffective disorder, a psychosis that combines the hallucinations of schizophrenia with a mood disorder like depression. People with psychotic disorders, of which schizophrenia is the most severe, have hallucinations, like the voices Plumadore was hearing, that are divorced from reality. Now, a Stanford researcher suggests that the voices he experienced might have been different if he had grown up somewhere other than the U.S. If he were from India, he might have heard family members telling him to do household chores. If he were from Ghana, he might have heard the voice of God guiding him. For a study published in June, Tanya Luhrmann, a Stanford anthropologist, and other researchers interviewed 60 people who met the criteria for schizophrenia: 20 from in and around San Mateo, 20 from India and 20 from Ghana. Though the patients heard both positive and negative voices no matter where they were from, those in India and in Ghana tended to have less negative experiences than Americans: They could more often identify who was talking to them and had less violent hallucinations. Though the study isn't conclusive, Luhrmann believes the differences in voice-hearing between cultures may be a clue into how social expectations and environment shape the way people hear those imaginary voices. © 2014 Hearst Communications, Inc.
Hearing voices is an experience that is very distressing for many people. Voices – or “auditory verbal hallucinations” – are one of the most common features of schizophrenia and other psychiatric disorders. But for a small minority of people, voice-hearing is a regular part of their lives, an everyday experience that isn’t associated with being unwell. It is only in the past 10 years that we have begun to understand what might be going on in “non-clinical” voice-hearing. Most of what we know comes from a large study conducted by Iris Sommer and colleagues at UMC Utrecht in the Netherlands. In 2006 they launched a nationwide attempt to find people who had heard voices before but didn’t have any sort of psychiatric diagnosis. From an initial response of over 4,000 people, they eventually identified a sample of 103 who heard voices at least once a month, but didn’t have psychosis. Their voice-hearing was also not caused by misuse of drugs or alcohol. Twenty-one of the participants were also given an MRI scan. When this group was compared with voice-hearers who did have psychosis, many of the same brain regions were active for both groups while they were experiencing auditory hallucinations, including the inferior frontal gyrus (involved in speech production) and the superior temporal gyrus (linked to speech perception). Subsequent studies with the same non-clinical voice-hearers have also highlighted differences in brain structure and functional connectivity (the synchronisation between different brain areas) compared with people who don’t hear voices. These results suggest that, on a neural level, the same sort of thing is going on in clinical and non-clinical voice-hearing. We know from first-person reports that the voices themselves can be quite similar, in terms of how loud they are, where they are coming from, and whether they speak in words or sentences. © 2014 Guardian News and Media Limited
The news of Robin Williams’s suicide has brought mental health into the spotlight this week. According to data from the Massachusetts Violent Death Reporting System at the department of public health, the number of deaths per year as a result of suicide in the state has increased 4 percent per year since 2003. The rate increased from 424 suicides in 2003 to a peak of 600 in 2010, before dropping back down to 588. That’s 8.9 suicides per 100,000, a total of 4,500 deaths for this preventable public health problem. There are many biological, sociological, and psychological risk factors that can increase an individual’s risk for committing suicide. But did you know that poor sleep could be a major factor pushing people over the edge, even if they aren’t depressed? We all know the feeling that when we’re under slept, we aren’t quite ourselves, but according to the Substance Abuse and Mental Health Services Administration, sleep complaints are actually one of the top 10 warning signs for suicide. A study published today in JAMA Psychiatry is the first research of its kind to draw a correlation between poor sleep habits and an increased risk for death by suicide by controlling for signs of depression. Stanford University School of Medicine researchers have found that over a 10 year observation period, people with poor sleep quality and no other depressive symptoms demonstrated a 1.2 times greater risk for death by suicide.
By EDWARD LARKIN and IRENE HURFORD PHILADELPHIA — A FEW months ago, a patient came to our hospital, seeking help. One of us, Edward, was on the team that treated him. He was pleasant, if slightly withdrawn, and cogent. He was a college graduate in his 20s and had recently been fired from his job as a high school math teacher, because of unexpected absences. He had come to believe that government agents were conspiring against him, and he had taken to living out of a truck and sleeping in different parking lots. By the time he came to us, he was exhausted. A diagnosis became clear: he had schizophrenia. We admitted him to the hospital, and after a few days, with his symptoms under control, we released him. Unfortunately, we prescribed a medication for him that could cause significant, permanent harm, instead of an equally effective drug with milder side effects — all because he was uninsured. Schizophrenia, which affects 1 percent of the population and emerges in the late teens to early 20s, is deeply misunderstood. People who suffer from it are often suspected of being dangerous, but this is not usually the case, and antipsychotic drugs are very effective. Our patient was exactly the kind of person who, with the right treatment, could have weakened the stigma surrounding schizophrenia. Antipsychotic drugs fall into two classes: the older ones, like Haldol, and newer ones, like Abilify and Latuda. Both classes are equally effective at treating some of the worst symptoms of schizophrenia, specifically the hallucinations, delusions and paranoia that cause social alienation. (They’re not effective for treating “negative symptoms,” like low motivation.) But the older drugs can cause a multitude of serious side effects, including a potentially devastating one called tardive dyskinesia. This condition involves unsettling, animalistic smacking and wagging of the lips and tongue. At its extreme, it can affect the entire body. It occurs in 20 percent or more of patients who take the drugs long-term, and it tends to start so mildly that patients can’t identify it in time to stop taking the drugs. It is often irreversible. © 2014 The New York Times Company
Link ID: 19950 - Posted: 08.13.2014
By MICHAEL CIEPLY and BROOKS BARNES LOS ANGELES — Peering through his camera at Robin Williams in 2012, the cinematographer John Bailey thought he glimpsed something not previously evident in the comedian’s work. They were shooting the independent film “The Angriest Man in Brooklyn,” and Mr. Williams was playing a New York lawyer who, facing death, goes on a rant against the injustice and banality of life. His performance, Mr. Bailey said Tuesday, was a window into the “Swiftian darkness of Robin’s heart.” The actor, like his character, was raging against the storm. That defiance gave way on Monday to the personal demons that had long tormented Mr. Williams. With his suicide at age 63, Mr. Williams forever shut the window on a complicated soul that was rarely visible through the cracks of an astonishingly intact career. Given his well-publicized troubles with depression, addiction, alcoholism and a significant heart surgery in 2009, Mr. Williams should have had a résumé filled with mysterious gaps. Instead, he worked nonstop. At the very least — if his life had followed the familiar script of troubled actors — there would have been whispers of on-set antics: lateness, forgotten lines, the occasional flared temper. Not so with Mr. Williams. “He was ready to work, he was the first one on the set,” said Mr. Bailey, speaking of Mr. Williams’s contribution to “The Angriest Man in Brooklyn,” of which he was the star. “Robin was always 1,000 percent reliable,” said a senior movie agent, speaking on the condition of anonymity to conform to the wishes of Mr. Williams’s family. “He was almost impossibly high functioning.” As Hollywood struggled on Tuesday to understand how Mr. Williams — effervescent in the extreme — could take his own life, authorities released details of his death. A clothed Mr. Williams hanged himself with a belt from a door frame in his bedroom in Tiburon, Calif., according to Lt. Keith Boyd, assistant deputy chief coroner for Marin County. © 2014 The New York Times Company
Link ID: 19948 - Posted: 08.13.2014
By Lenny Bernstein, Lena H. Sun and Sandhya Somashekhar Suicides are the 10th-leading cause of death in the United States and eighth among people in the 55- to 64-year-old age group. Comedian Robin Williams, who died Monday of an apparent suicide, was 63. In 2010, 38,364 people died this way. Many suicides are the result of undiagnosed or untreated depression, often masked by self-medicating behaviors such as alcohol and drug use. Though we don’t yet know the exact circumstances of Williams’s death, we do know that he long battled addictions to cocaine and alcohol and, according to his publicist, was struggling with “severe depression.” But unlike many people, Williams had the resources and the motivation to seek treatment, at least for his addictions. According to this report, he had undergone rehab at the famed Hazelden Addiction Treatment Center in Minnesota two months ago, and had sought treatment in 2006 when he began drinking again after 20 years of sobriety. How, then, do we explain the death of someone who appeared to recognize the danger he faced and was trying to address it? Here are some thoughts: • Suicides are often impulsive acts: People who kill themselves are not thinking clearly, have trouble solving problems and weigh risks differently from us, Jill Harkavy-Friedman, vice president of research for the American Foundation for Suicide Prevention, told To Your Health in March. If thwarted in their first attempt, they often do not try again immediately, she said.
|By Nathan Collins Time zips by when you're having fun and passes slowly when you're not—except when you are depressed, in which case your time-gauging abilities are pretty accurate. Reporting in PLOS ONE, researchers in England and Ireland asked 39 students—18 with mild depression—to estimate the duration of tones lasting between two and 65 seconds and to produce tones of specified lengths of time. Happier students overestimated intervals by 16 percent and produced tones that were short by 13 percent, compared with depressed students' 3 percent underestimation and 8 percent overproduction. The results suggest that depressive realism, a phenomenon in which depressed people perceive themselves more accurately (and less positively) than typical individuals, may extend to aspects of thought beyond self-perception—in this case, time. They speculate that mindfulness treatments may be effective for depression, partly because they help depressed people focus on the moment, rather than its passing. © 2014 Scientific American
Helen Shen Most people gradually recover from trauma, but a small fraction of individuals develop post-traumatic stress disorder (PTSD) — prompting scientists to look for the biological underpinnings of this extreme response to traumatic situations such as warfare, car accidents and natural disasters. Research published on 11 August in Proceedings of the National Academy of Sciences identifies up to 334 genes that may be involved in vulnerability to post-traumatic stress in rats1. Most animal studies of stress use intense stimuli such as electric shocks, designed to produce large, group differences between exposed and unexposed animals. But Nikolaos Daskalakis and his colleagues tried a subtler approach to elicit a wide range of individual responses in rats that had all experienced the same trauma — more closely mimicking the variability of human responses to disturbing events. "We wanted to capture the differences between a susceptible individual and one that is not susceptible to the same experience," says Daskalakis, a neuroendocrinologist at the Icahn School of Medicine at Mount Sinai in New York. The researchers exposed around 100 rats to soiled cat litter — which evokes a feared predator — and tested the animals one week later for lingering effects of the trauma. About one-quarter of the exposed animals were classified as 'extreme' responders, showing high levels of anxiety and startling easily on hearing loud noises. Another quarter of the animals were 'minimal' responders, and exhibited anxiety levels similar to those of non-exposed rats. © 2014 Nature Publishing Group
By Emily Underwood The early signs of Creutzfeldt-Jakob disease (CJD)—a rare, incurable brain disorder caused by infectious, misshapen proteins called prions—are difficult to interpret. At first, people may simply feel depressed and can undergo personality changes or bouts of psychosis. By the time memory failure, blindness, and coma set in, typically within a year of infection, death is usually imminent. Now, researchers report that a simple nasal swab may help physicians detect the disease far more accurately and earlier than current methods. Finding simple, noninvasive diagnostic tests is “one of the holy grails” for CJD and other prion diseases, says biochemist Byron Caughey of the National Institute of Allergy and Infectious Diseases’ Rocky Mountain Laboratories in Hamilton, Montana, who helped lead the new work. Although there’s no cure for CJD, early diagnosis is important because it can help rule out other, treatable disorders, and it allows medical personnel to take precautions that prevent the disease from spreading to others through exposure to brain tissue or spinal fluid, he says. Researchers made a major stride toward better diagnostic methods in 2010, when Caughey and other researchers first described a new technique called the RT-QuIC test. The test requires removing cerebrospinal fluid (CSF) from patients by means of a spinal tap, putting samples into a bath of normally shaped prion proteins, and agitating the solution to encourage any abnormal prion “seeds” in the tissue to latch onto the regular proteins. If even trace amounts of pathogenic protein are present, they rapidly use the normal proteins to create millions of insoluble, fibrous amyloid strands. Researchers believe that these amyloid aggregates, also seen in other neurodegenerative diseases such as Alzheimer’s disease, ultimately cause CJD by interfering with or killing off neurons en masse. After death, the brains of people affected by CJD are so badly damaged that they often resemble Swiss cheese or sponges. © 2014 American Association for the Advancement of Science.
Link ID: 19926 - Posted: 08.07.2014
By Sandhya Somashekhar The first time Jeremy Clark met his 18-year-old client, the teenager was sitting in his vice principal’s office, the drawstrings of his black hoodie pulled tight. Jacob had recently disclosed to his friends on Facebook that he was hearing voices, and their reaction had been less than sympathetic. So Clark was relieved when a beaming Jacob showed up on time for their next meeting, at a comic book shop. As the pair bantered about “Star Wars” and a recent Captain America movie, however, Clark picked up troubling signs: Jacob said he was “detaching” from his family, often huddling alone in his room. As the visit ended, Clark gave the teen a bear hug and made a plan. “Let’s get together again next week,” he said. The visit was part of a new approach being used nationwide to find and treat teenagers and young adults with early signs of schizophrenia. The goal is to bombard them with help even before they have had a psychotic episode — a dramatic and often devastating break with reality that is a telltale sign of the disease. The program involves an intensive two-year course of socialization, family therapy, job and school assistance, and, in some cases, antipsychotic medication. What makes the treatment unique is that it focuses deeply on family relationships, and occurs early in the disease, often before a diagnosis. So far, the results have been striking: In Portland, Maine, where the treatment was pioneered, the rate of hospitalizations for first psychotic episodes fell by 34 percent over a six-year period, according to a March study. And just last month, a peer-reviewed study published in the journal Schizophrenia Bulletin found that young people undergoing the treatment at six sites around the country were more likely to be in school or working than adolescents who were not in the program. The research was funded by a $17 million grant from the Robert Wood Johnson Foundation.
|By Tori Rodriguez and Victoria Stern A growing number of people are seeking alternatives to antidepressant medications, and new research suggests that acupuncture could be a promising option. One new study found the traditional Chinese practice to be as effective as antidepressants, and a different study found that acupuncture may help treat the medications' side effects. In acupuncture, a practitioner inserts needles into the skin at points of the body thought to correspond with specific organs (right). Western research suggests the needles may activate natural painkillers in the brain; in traditional Chinese medicine, the process is believed to improve functioning by correcting energy blocks or imbalances in the organs. A study published last fall in the Journal of Alternative and Complementary Medicine found that electroacupuncture—in which a mild electric current is transmitted through the needles—was just as effective as fluoxetine (the generic name of Prozac) in reducing symptoms of depression. For six weeks, patients underwent either electroacupuncture five times weekly or a standard daily dose of fluoxetine. The researchers, the majority of whom specialize in traditional Chinese medicine, assessed participants' symptoms every two weeks and tracked their levels of glial cell line–derived neurotrophic factor (GDNF), a neuroprotective protein. Previous studies have found lower amounts of GDNF among patients with major depressive disorder, and in other research levels of the protein rose after treatment with antidepressant medication. © 2014 Scientific American,
Link ID: 19920 - Posted: 08.06.2014
By Caelainn Hogan A simple blood test could determine a person’s risk of suicide and provide a future tool of prevention to stem suicide rates. In a study published online Wednesday in the American Journal of Psychiatry, researchers say they have discovered a genetic indicator of a person’s vulnerability to the effects of stress and anxiety and, therefore, the risk of suicidal thoughts or attempts. The Johns Hopkins researchers looked at how a group of chemicals known as methyls affect the gene SKA2, which modifies how the brain reacts to stress hormones. If the gene’s function is impaired by a chemical change, someone who is stressed won’t be able to shut down the effect of the stress hormone, which would be like having a faulty brake pad in a car for the fear center of the brain, worsening the impact of even everyday stresses. Researchers studied about 150 postmortem brain samples of healthy people and those with mental illness, including some who had committed suicide. They found that those who died by suicide had significantly higher levels of the chemical that altered the SKA2 gene. As a result of the gene’s modification, it was not able to “switch off” the effect of the stress hormone. The researchers then tested sets of blood samples from more than 325 participants in the Johns Hopkins Center for Prevention Research study to see whether they could determine those who were at greater risk of suicide by the same biomarker. They were able to guess with 80 to 90 percent accuracy whether a person had thoughts of suicide or made an attempt by looking at the single gene, while accounting for age, gender and levels of stress or anxiety.
By ANNA NORTH What does it mean to be lonely? It’s tempting to equate the feeling with a dearth of social interaction, but some people are now saying that it’s more complicated than that — and that true loneliness might be dangerous. In a story at Medium, Robin Marantz Henig busts some common loneliness myths. Lonely people aren’t necessarily weird or uncool: Ms. Henig cites a study of Ohio State undergrads showing that “those who called themselves lonely had just as much ‘social capital’ — defined by physical attractiveness, height, weight, socioeconomic status, and academic achievement — as their non-lonely peers.” And they may not be actually alone: “The students at Ohio State who were lonely belonged to as many clubs and had as many roommates as those who were ‘socially embedded.’ And while some studies indicate that living alone puts people at greater risk for loneliness, living with a spouse is not necessarily any protection.” Rather, loneliness may be psychological. The lonely, writes Ms. Henig, are more likely than others “to feel put upon and misunderstood” in social situations, to see “social danger even where none might exist.” She writes: “People grow lonely because of the gloomy stories they tell themselves. And, in a cruel twist, the loneliness itself can further distort their thinking, making them misread other people’s good intentions, which in turn causes them to withdraw to protect themselves from further rejection — and causes other people to keep them at arm’s length.” This distancing can have a physical impact; Ms. Henig argues that loneliness deserves further study, in part because it may increase the risk of high blood pressure, sleep problems and Alzheimer’s disease. © 2014 The New York Times Company
|By Fikri Birey What’s the difference between you and a rat? The list is unsurprisingly long but now, we can cross a universal human experience — feelings of regret — off of it. A new study shows for the first time that rats regret bad decisions and learn from them. In addition to existentialist suggestions of a rat’s regret — and what that takes away from, or adds to, being “human” — the study is highly relevant to basic brain research. Researchers demonstrated that we can tap into complex internal states of rodents if we hone in on the right behavior and the right neurons. There is a significant literature on what brain regions are representative of certain states, like reward predictions and value calculations, but the study, powered by a novel behavioral test, is able to put together such discrete behavioral correlates into a “rat” definition of regret. Finding better animal models of human behavior constitute a long-standing challenge in neuroscience: It has been difficult to authentically recapitulate mental states in animal models of neuropsychiatric disorders: For example, an attempt to model depression in rodents can often go no further than relatively coarse approximations of the core symptoms like guilt or sadness, which often translates to behaviors like social avoidance or anhedonia in rodents. The inability to efficiently approach the questions of mental abnormalities is a major problem. Depression is currently ranked as the leading cause of disability globally, and it’s estimated that by 2020, depression will lead 1.5 million people to end their lives by suicide. Now, thanks to a simple yet well-conceived series of experiments by Steiner and Redish, a compound behavior like regret is fully open to investigation. The investigators use a spatial decision-making set-up called “Restaurant Row”: an arena with four zones where four different flavors of food (banana, cherry, chocolate or unflavored) are introduced in sequence. © 2014 Scientific American
By Smitha Mundasad Health reporter, BBC News Scientists say a part of the brain, smaller than a pea, triggers the instinctive feeling that something bad is about to happen. Writing in the journal PNAS, they suggest the habenula plays a key role in how humans predict, learn from and respond to nasty experiences. And they question whether hyperactivity in this area is responsible for the pessimism seen in depression. They are now investigating whether the structure is involved in the condition. Animal studies have shown that the habenula fires up when subjects expect or experience adverse events, But in humans this tiny structure (less than 3mm in diameter) has proved difficult to see on scans. Inventing a technique to pinpoint the area, scientists at University College London put 23 people though MRI scanners to monitor their brain activity. Participants were shown a range of abstract pictures. A few seconds later, the images were linked to either punishment (painful electric shocks), reward (money) or neutral responses. For some images, a punishment or reward followed each time but for others this varied - leaving people uncertain whether they were going to feel pain or not. And when people saw pictures associated with shocks the habenula lit up. And the more certain they were a picture was going to result in a punishment, the stronger and faster the activity in this area. Scientists suggests the habenula is involved in helping people learn when it is best to stay away from something and may also signal just how bad a nasty event is likely to be. BBC © 2014
By CATHERINE SAINT LOUIS “This has happened before,” she tells herself. “It’s nowhere near as bad as before, and it will pass.” Robbie Pinter’s 21-year-old son, Nicholas, is upset again. He yells. He obsesses about something that can’t be changed. Even good news may throw him off. So Dr. Pinter breathes deeply, as she was taught, focusing on each intake and release. She talks herself through the crisis, reminding herself that this is how Nicholas copes with his autism and bipolar disorder. With these simple techniques, Dr. Pinter, who teaches English at Belmont University in Nashville, blunts the stress of parenting a child with severe developmental disabilities. Dr. Pinter, who said she descends from “a long line of the most nervous women,” credits her mindfulness practice with giving her the tools to cope with whatever might come her way. “It is very powerful,” she said. All parents endure stress, but studies show that parents of children with developmental disabilities, like autism, experience depression and anxiety far more often. Struggling to obtain crucial support services, the financial strain of paying for various therapies, the relentless worry over everything from wandering to the future — all of it can be overwhelming. “The toll stress-wise is just enormous, and we know that we don’t do a really great job of helping parents cope with it,” said Dr. Fred R. Volkmar, the director of Child Study Center at Yale University School of Medicine. “Having a child that has a disability, it’s all-encompassing,” he added. “You could see how people would lose themselves.” But a study published last week in the journal Pediatrics offers hope. It found that just six weeks of training in simple techniques led to significant reductions in stress, depression and anxiety among these parents. © 2014 The New York Times Company
By Emily Underwood The Broad Institute, a collaborative biomedical research center in Cambridge, Massachusetts, has received a $650 million donation from philanthropist and businessman Ted Stanley to study the biological basis of diseases such as schizophrenia and bipolar disorder. The largest donation ever made to psychiatric research, the gift totals nearly six times the current $110 million annual budget for President Barack Obama’s Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative. Stanley has already given Broad $175 million, and the $650 million will be provided as an annual cash flow on the order of tens of millions each year, with the remainder to be given after Stanley’s death. The gift accompanies a paper published online today in Nature from researchers at Broad and worldwide, which identifies more than 100 areas of the human genome associated with schizophrenia, based on samples from almost 37,000 people with schizophrenia and about 113,000 without the disease. Researchers are likely to find hundreds of additional genetic variations associated with the disease as the number of patients sampled grows, says psychiatrist Kenneth Kendler of the Virginia Institute for Psychiatric and Behavioral Genetics in Richmond, a co-author on the study. Identifying the variants themselves is unlikely to lead directly to new drug targets, Kendler says. Instead, the hope is that researchers at Broad and elsewhere will be able to use those data to reveal clusters of genetic variation, like placing pins on a map, he says. © 2014 American Association for the Advancement of Science.
Sara Reardon Broad population studies are shedding light on the genetic causes of mental disorders. Researchers seeking to unpick the complex genetic basis of mental disorders such as schizophrenia have taken a huge step towards their goal. A paper1 published in Nature this week ties 108 genetic locations to schizophrenia — most for the first time. The encouraging results come on the same day as a US$650-million donation to expand research into psychiatric conditions. Philanthropist Ted Stanley gave the money to the Stanley Center for Psychiatric Research at the Broad Institute in Cambridge, Massachusetts. The institute describes the gift as the largest-ever donation for psychiatric research. “The assurance of a very long life of the centre allows us to take on ambitious long-term projects and intellectual risks,” says its director, Steven Hyman. The centre will use the money to fund genetic studies as well as investigations into the biological pathways involved in conditions such as schizophrenia, autism and bipolar disorder. The research effort will also seek better animal and cell models for mental disorders, and will investigate chemicals that might be developed into drugs. The Nature paper1 was produced by the Psychiatric Genomics Consortium (PGC) — a collaboration of more than 80 institutions, including the Broad Institute. Hundreds of researchers from the PGC pooled samples from more than 150,000 people, of whom 36,989 had been diagnosed with schizophrenia. This enormous sample size enabled them to spot 108 genetic locations, or loci, where the DNA sequence in people with schizophrenia tends to differ from the sequence in people without the disease. “This paper is in some ways proof that genomics can succeed,” Hyman says. © 2014 Nature Publishing Group