Links for Keyword: Schizophrenia

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Scientists have reversed behavioral and brain abnormalities in adult mice that resemble some features of schizophrenia by restoring normal expression to a suspect gene that is over-expressed in humans with the illness. Targeting expression of the gene Neuregulin1, which makes a protein important for brain development, may hold promise for treating at least some patients with the brain disorder, say researchers funded by the National Institutes of Health. Like patients with schizophrenia, adult mice biogenetically-engineered to have higher Neuregulin 1 levels showed reduced activity of the brain messenger chemicals glutamate and GABA. The mice also showed behaviors related to aspects of the human illness. For example, they interacted less with other animals and faltered on thinking tasks. “The deficits reversed when we normalized Neuregulin 1 expression in animals that had been symptomatic, suggesting that damage which occurred during development is recoverable in adulthood,” explained Lin Mei, M.D., Ph.D.External Web Site Policy , of the Medical College of Georgia at Georgia Regents University, a grantee of NIH’s National Institute of Mental Health (NIMH). “While mouse models can’t really do full justice to a complex brain disorder that impairs our most uniquely human characteristics, this study demonstrates the potential of dissecting the workings of intermediate components of disorders in animals to discover underlying mechanisms and new treatment targets,” said NIMH Director Thomas R. Insel, M.D. “Hopeful news about how an illness process that originates early in development might be reversible in adulthood illustrates the promise of such translational research.” Schizophrenia is thought to stem from early damage to the developing fetal brain, traceable to a complex mix of genetic and environmental causes. Although genes identified to date account for only a small fraction of cases, evidence has implicated variation in the Neuregulin 1 gene. For example, postmortem studies have found that it is overexpressed in the brain's thinking hub, or prefrontal cortex, of some people who had schizophrenia. It codes for a chemical messenger that plays a pivotal role in communication between brain cells, as well as in brain development.

Related chapters from BP7e: 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: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 18186 - Posted: 05.23.2013

By Jeffrey A. Lieberman Like many psychiatrists, I have been amazed by the debates surrounding the DSM-5, the first major revision of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders in nearly twenty years, which was just released. Never before has a thick medical text of diagnostic nomenclature been the subject of so much attention. Although I was heartened to see more and more people discussing the real-world issues and challenges—for patients, families, clinicians and caregivers–within mental health care, for which the book offers an up-to-the-minute diagnostic GPS, I was also alarmed at the harsh criticism of the field of psychiatry and the APA. Consequently, I believe that as you read and watch this increased coverage, it’s important to understand the difference between thoughtful, legitimate debate, and the inevitable outcry from a small group of critics –made louder by social media and support from dubious sources —who have relentlessly sought to undermine the credibility of psychiatric medicine and question the validity of mental illness.. DSM-5 has ignited a broad dialogue on mental illness and opened up a conversation about the state of psychiatry and mental healthcare in this country. Critiques have ranged in focus from the inclusion of specific disorders in DSM-5, to the concern over a lack of biological measures which define them. Some have even questioned the entire diagnostic system, urging us to look with an eye focused on the impact to patients. These are the kinds of debate that I hope will continue long after DSM-5’s shiny cover becomes warn and wrinkled. Such meaningful discourse only fuels our ability to produce a manual that best serves those touched by mental illness. But there’s another type of critique that does not contribute to this goal. These are the groups who are actually proud to identify themselves as “anti-psychiatry.” © 2013 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18175 - Posted: 05.21.2013

Pregnant mothers’ exposure to the flu was associated with a nearly fourfold increased risk that their child would develop bipolar disorder in adulthood, in a study funded by the National Institutes of Health. The findings add to mounting evidence of possible shared underlying causes and illness processes with schizophrenia, which some studies have also linked to prenatal exposure to influenza. “Prospective mothers should take common sense preventive measures, such as getting flu shots prior to and in the early stages of pregnancy and avoiding contact with people who are symptomatic,” said Alan Brown, M.D., M.P.H, of Columbia University and New York State Psychiatric Institute, a grantee of the NIH’s National Institute of Mental Health (NIMH). “In spite of public health recommendations, only a relatively small fraction of such women get immunized. The weight of evidence now suggests that benefits of the vaccine likely outweigh any possible risk to the mother or newborn.” Brown and colleagues reported their findings online May 8, 2013 in JAMA Psychiatry. Although there have been hints of a maternal influenza/bipolar disorder connection, the new study is the first to prospectively follow families in the same HMO, using physician-based diagnoses and structured standardized psychiatric measures. Access to unique Kaiser-Permanente, county and Child Health and Development Study External Web Site Policy databases made it possible to include more cases with detailed maternal flu exposure information than in previous studies.

Related chapters from BP7e: 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: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 18154 - Posted: 05.14.2013

Heidi Ledford Nassir Ghaemi, director of the Mood Disorders Program at Tufts Medical Center in Boston, Massachusetts, has felt shackled by the Diagnostic and Statistical Manual of Mental Disorders (DSM), often called the bible of psychiatry. Some of his depressed patients occasionally show manic behaviour but do not fulfil the DSM’s criteria for a diagnosis of bipolar disorder. Ghaemi is interested in whether such patients might respond better to drugs for bipolar disorder than for depression. But his colleagues warned him against straying from the DSM when he applied for funding at the US National Institute of Mental Health (NIMH), because peer reviewers tended to insist on research that hewed to DSM categories. Ghaemi held off from applying. If NIMH director Thomas Insel has his way, Ghaemi and other mental-health researchers will no longer feel the weight of the DSM. “NIMH will be re-orienting its research away from DSM categories,” Insel wrote in a blog entry on 29 April. The latest edition, the DSM-5, will be unveiled on 22 May at the annual meeting of the American Psychiatric Association in San Francisco, California. Like many psychiatrists, Insel questions whether the DSM’s categories accurately reflect the way the brain works. He is pushing a project that aims to create a new framework that classifies mental-health disorders according to their biological roots. “Going forward, we will be supporting research projects that look across current categories — or sub-divide current categories — to begin to develop a better system,” Insel wrote. The blog post made waves in the media and rattled some psychiatric clinicians and researchers. But Insel says that he has been talking about the issue since 2008. “The word was just still not out there,” he says. Insel says that he has increasingly received complaints from grant applicants who have tried to follow his guidance, only to be shot down by peer reviewers for eschewing DSM scripture. © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18144 - Posted: 05.11.2013

by Claudia M Gold It seems that the National Institute of Mental Health (NIMH) may have dealt a death blow to the recently published Diagnostic and Statistical Manual of Mental Disorders (DSM 5) when the organization declared they would no longer fund research based on the DSM system of diagnosis. The views of NIMH director Thomas Insel were referenced in the recent New York Times article on the subject. His goal was to reshape the direction of psychiatric research to focus on biology, genetics and neuroscience so that scientists can define disorders by their causes, rather than their symptoms. I am no fan of the DSM system, which reduces complex experience to lists of symptoms; focusing on the "what" rather than the "why." However, the NIMH model has limits as well. There seems to be a wish to study mental illness in the same way we study cancer or diabetes. While I certainly have great respect for the complexity of the pancreas, or the process of malignant transformation of cells, trying to understand the brain/mind in an analogous way seems to be an unnecessary and even undesirable reduction of human experience. What is missing from both paradigms is recognition of the relational and historical context of being human. Fortunately there seems to be awareness that neither paradigm is complete. The Times article goes on to say: Dr. Insel is one of a growing number of scientists who think that the field needs an entirely new paradigm for understanding mental disorders, though neither he nor anyone else knows exactly what it will look like. © 2013 NY Times Co.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18143 - Posted: 05.11.2013

By James Gallagher Health and science reporter, BBC News Flu during pregnancy may increase the risk of the unborn child developing bipolar disorder later in life, research suggests. A study of 814 expectant women, published in JAMA Psychiatry, showed that infection made bipolar four times more likely. The overall risk remained low, but it echoes similar findings linking flu and schizophrenia. Experts said the risks were small and women should not worry. Bipolar leads to intense mood swings, which can last months, ranging from depression and despair to manic feelings of joy, overactivity and loss of inhibitions. Researchers at the Columbia University Medical Center identified a link between the condition, often diagnosed during late teens and twenties, and experiences in the womb. In their study looking at people born in the early 1960s, bipolar disorder was nearly four times as common in people whose mothers caught flu during pregnancy. The condition affects about one in 100 people. The lead researcher, Prof Alan Brown, estimated that influenza infection during pregnancy could lead to a 3-4% chance of bipolar disorder in the resulting children. However, in the vast majority of cases of bipolar disorder there would no history of flu. BBC © 2013

Related chapters from BP7e: 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: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 18135 - Posted: 05.09.2013

By PAM BELLUCK and BENEDICT CAREY Just weeks before the long-awaited publication of a new edition of the so-called bible of mental disorders, the federal government’s most prominent psychiatric expert has said the book suffers from a scientific “lack of validity.” The expert, Dr. Thomas R. Insel, director of the National Institute of Mental Health, said in an interview Monday that his goal was to reshape the direction of psychiatric research to focus on biology, genetics and neuroscience so that scientists can define disorders by their causes, rather than their symptoms. While the Diagnostic and Statistical Manual of Mental Disorders, or D.S.M., is the best tool now available for clinicians treating patients and should not be tossed out, he said, it does not reflect the complexity of many disorders, and its way of categorizing mental illnesses should not guide research. “As long as the research community takes the D.S.M. to be a bible, we’ll never make progress,” Dr. Insel said, adding, “People think that everything has to match D.S.M. criteria, but you know what? Biology never read that book.” The revision, known as the D.S.M.-5 and the first since 1994, has stirred unprecedented questioning from the public, patient groups and, most fundamentally, senior figures in psychiatry who have challenged not only decisions about specific diagnoses but the scientific basis of the entire enterprise. Basic research into the biology of mental disorders and treatment has stalled, they say, confounded by the labyrinth of the brain. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18128 - Posted: 05.07.2013

by Emily Underwood The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5)—slated for release this month—has lost a major customer before even going to print. Thomas Insel, director of the National Institute of Mental Health (NIMH), declared last week on his blog that the institution will no longer use the manual to guide its research. Instead, NIMH is working on a long-term plan to develop new diagnostic criteria and treatments based on genetic, physiologic, and cognitive data rather than symptoms alone. Insel's pronouncement is the most recent hit in a long barrage of criticism that has rained down upon the latest DSM revision process since it began over a decade ago. "While DSM has been described as a 'Bible' for the field," he wrote, "it is, at best, a dictionary, creating a set of labels and defining each." Although the manual's strength has been to standardize these labels, he wrote, "[t]he weakness is its lack of validity," and "[p]atients with mental disorders deserve better." Although Insel's blog was reported as a "bombshell," and "potentially seismic," NIMH's decision to scrap the DSM criteria has been public for several years, says Bruce Cuthbert, director of NIMH's Division of Adult Translational Research and Treatment Development. In 2010, the agency began to steer researchers away from the traditional categories of DSM by posting new guidance for grant proposals in five broad areas. Rather than grouping disorders such as schizophrenia and depression by symptom, the new categories focus on basic neural circuits and cognitive functions, such as those for reward, arousal, and attachment. © 2010 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18127 - Posted: 05.07.2013

By John Horgan What is mental illness? Schizophrenia? Autism? Bipolar disorder? Depression? Since the 1950s, the profession of psychiatry has attempted to provide definitive answers to these questions in the Diagnostic and Statistical Manual of Mental Disorders. Often called The Bible of psychiatry, the DSM serves as the ultimate authority for diagnosis, treatment and insurance coverage of mental illness. Now, in a move sure to rock psychiatry, psychology and other fields that address mental illness, the director of the National Institutes of Mental Health has announced that the federal agency–which provides grants for research on mental illness–will be “re-orienting its research away from DSM categories.” Thomas Insel’s statement comes just weeks before the scheduled publication of the DSM-V, the fifth edition of the Diagnostic and Statistical Manual. Insel writes: “While DSM has been described as a ‘Bible’ for the field, it is, at best, a dictionary, creating a set of labels and defining each. The strength of each of the editions of DSM has been ‘reliability’–each edition has ensured that clinicians use the same terms in the same ways. The weakness is its lack of validity. Unlike our definitions of ischemic heart disease, lymphoma, or AIDS, the DSM diagnoses are based on a consensus about clusters of clinical symptoms, not any objective laboratory measure. In the rest of medicine, this would be equivalent to creating diagnostic systems based on the nature of chest pain or the quality of fever. Indeed, symptom-based diagnosis, once common in other areas of medicine, has been largely replaced in the past half century as we have understood that symptoms alone rarely indicate the best choice of treatment. Patients with mental disorders deserve better.” © 2013 Scientific American

Related chapters from BP7e: 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: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 18120 - Posted: 05.06.2013

By Ferris Jabr This month the American Psychiatric Association (APA) will publish the fifth edition of its guidebook for clinicians, the Diagnostic and Statistical Manual of Mental Disorders, or DSM-5. Researchers around the world have eagerly anticipated the new manual, which, in typical fashion, took around 14 years to revise. The DSM describes the symptoms of more than 300 officially recognized mental illnesses—depression, bipolar disorder, schizophrenia and others—helping counselors, psychiatrists and general care practitioners diagnose their patients. Yet it has a fundamental flaw: it says nothing about the biological underpinnings of mental disorders. In the past, that shortcoming reflected the science. For most of the DSM's history, investigators have not had a detailed understanding of what causes mental illness. That excuse is no longer valid. Neuroscientists now understand some of the ways that brain circuits for memory, emotion and attention malfunction in various mental disorders. Since 2009 clinical psychologist Bruce Cuthbert and his team at the National Institute of Mental Health have been constructing a classification system based on recent research, which is revealing how the structure and activity of a mentally ill brain differs from that of a healthy one. The new framework will not replace the DSM, which is too important to discard, Cuthbert says. Rather he and his colleagues hope that future versions of the guide will incorporate information about the biology of mental illness to better distinguish one disorder from another. Cuthbert, whose project may receive additional funding from the Obama administration's planned Brain Activity Map initiative, is encouraging researchers to study basic cognitive and biological processes implicated in many types of mental illness. Some scientists might explore how and why the neural circuits that detect threats and store fearful memories sometimes behave in unusual ways after traumatic events—the kinds of changes that are partially responsible for post-traumatic stress disorder. Others may investigate the neurobiology of hallucinations, disruptions in circadian rhythms, or precisely how drug addiction rewires the brain. © 2013 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18101 - Posted: 05.01.2013

By LINDA LOGAN The last time I saw my old self, I was 27 years old and living in Boston. I was doing well in graduate school, had a tight circle of friends and was a prolific creative writer. Married to my high-school sweetheart, I had just had my first child. Back then, my best times were twirling my baby girl under the gloaming sky on a Florida beach and flopping on the bed with my husband — feet propped against the wall — and talking. The future seemed wide open. I don’t think there is a particular point at which I can say I became depressed. My illness was insidious, gradual and inexorable. I had a preview of depression in high school, when I spent a couple of years wearing all black, rimming my eyes in kohl and sliding against the walls in the hallways, hoping that no one would notice me. But back then I didn’t think it was a very serious problem. The hormonal chaos of having three children in five years, the pressure of working on a Ph.D. dissertation and a genetic predisposition for a mood disorder took me to a place of darkness I hadn’t experienced before. Of course, I didn’t recognize that right away. Denial is a gauze; willful denial, an opiate. Everyone seemed in league with my delusion. I was just overwhelmed, my family would say. I should get more help with the kids, put off my Ph.D. When I told other young mothers about my bone-wearying fatigue, they rolled their eyes knowingly and mumbled, “Right.” But what they didn’t realize was that I could scarcely push the stroller to the park, barely summon the breath to ask the store clerk, “Where are the Pampers?” I went from doctor to doctor, looking for the cause. Lab tests for anemia, low blood sugar and hypothyroidism were all negative. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18085 - Posted: 04.28.2013

Sunanda Creagh, The Conversation Testosterone may trigger a brain chemical process linked to schizophrenia but the same sex hormone can also improve cognitive thinking skills in men with the disorder, two new studies show. Scientists have long suspected testosterone plays an important role in schizophrenia, which affects more men than women. Men are also more likely to develop psychosis in adolescence, previous research has shown. A new study on lab rodents by researchers from Neuroscience Research Australia analysed the impact increased testosterone had on levels of dopamine, a brain chemical linked to psychotic symptoms of schizophrenia. The researchers found that testosterone boosted dopamine sensitivity in adolescent male rodents. “From these rodent studies, we hypothesise that adolescent increases in circulating testosterone may be a driver of increased dopamine activity in the brains of individuals susceptible to psychosis and schizophrenia,” said senior Neuroscience Research Australia researcher and author of the study, Dr Tertia Purves-Tyson, who is presenting her work at the International Congress on Schizophrenia Research in Florida. Dr Philip Mitchell, Scientia Professor and Head of the School of Psychiatry at the University of NSW, said the research was very interesting. © 2013 ScienceAlert Pty Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 18076 - Posted: 04.27.2013

David Adam David Kupfer is a modern-day heretic. A psychiatrist at the University of Pittsburgh in Pennsylvania, Kupfer, has spent the past six years directing the revision of a book commonly referred to as the bible of the psychiatric field. The work will reach a climax next month when the American Psychiatric Association (APA) unveils the fifth incarnation of the book, called the Diagnostic and Statistical Manual of Mental Disorders (DSM), which provides checklists of symptoms that psychiatrists around the world use to diagnose their patients. The DSM is so influential that just about the only suggestion of Kupfer's that did not meet with howls of protest during the revision process was to change its name from DSM-V to DSM-5. Although the title and wording of the manual are now settled, the debate that overshadowed the revision is not. The stark fact is that no one has yet agreed on how best to define and diagnose mental illnesses. DSM-5, like the two preceding editions, will place disorders in discrete categories such as major-depressive disorder, bipolar disorder, schizophrenia and obsessive–compulsive disorder (OCD). These categories, which have guided psychiatry since the early 1980s, are based largely on decades-old theory and subjective symptoms. The problem is that biologists have been unable to find any genetic or neuroscientific evidence to support the breakdown of complex mental disorders into separate categories. Many psychiatrists, meanwhile, already think outside the category boxes, because they see so many patients whose symptoms do not fit neatly into them. Kupfer and others wanted the latest DSM to move away from the category approach and towards one called 'dimensionality', in which mental illnesses overlap. According to this view, the disorders are the product of shared risk factors that lead to abnormalities in intersecting drives such as motivation and reward anticipation, which can be measured (hence 'dimension') and used to place people on one of several spectra. But the attempt to introduce this approach foundered, as other psychiatrists and psychologists protested that it was premature. © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18073 - Posted: 04.25.2013

By Daisy Yuhas Less than two hundred years ago, schizophrenia emerged from a tangle of mental disorders known simply as madness. Yet its diagnosis remains shrouded in ambiguity. Only now is the Diagnostics and Statistical Manual of Mental Disorders, psychiatrists’ primary guidebook, shedding the outdated, nineteenth-century descriptions that have characterized schizophrenia to this day. "There is substantial dissatisfaction with schizophrenia treated as a disease entity, it's symptoms are like a fever—something is wrong but we don't know what," says William Carpenter, a psychiatrist at the University of Maryland and chair of the manual’s Psychotic Disorder Workgroup. Psychiatrists may discover that this disorder is not a single syndrome after all but a bundle of overlapping conditions. © 2013 Scientific American,

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18022 - Posted: 04.11.2013

by Emily Underwood Hallucinations and paranoia aren't the only symptoms that make life difficult for people with schizophrenia. Problems with memory and other cognitive functions also interfere with daily tasks, such as remembering the way to the office or balancing a checkbook. Now, by dampening the activity of a small group of neurons deep within the mouse brain, researchers have produced cognitive deficits similar to those found in those with schizophrenia, a discovery that they say could potentially lead to new treatments for the disorder, which affects roughly 24 million people worldwide. There's an ongoing debate over how much mice can mirror human psychiatric diseases, ranging from autism to depression. Still, neuroscientists often turn to rodents to study specific features of these human conditions. One abnormality that researchers have observed in functional magnetic resonance imaging scans of the brains of people with schizophrenia is an unusually low level of activity from a specific group of neurons near the brain stem. Called the mediodorsal thalamus (MD), the region appears to work with the prefrontal cortex—an area associated with planning and decision-making—to carry out tasks that require us to remember and process multiple pieces of information at once. (Going to the kitchen to fetch something, while remembering what it was you needed, for example.) In the past, scientists have studied the effects of low brain activity in the MD by cutting it out in mice—an extreme measure that didn't accurately mimic the "mild" reduction in activity seen in schizophrenia, says Columbia University psychiatrist Joshua Gordon. To create a more realistic mouse model of low MD activity, the team devised a new method that uses a virus to embed into the surface of MD neurons receptors that block cellular activity in the presence of a compound called clozapine-N-oxide. The beauty of this approach is its "exquisite specificity," Gordon says—it targets only neurons in the MD, and you can control how many neurons get shut down. © 2010 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17935 - Posted: 03.23.2013

By Meghan Rosen Shushing neural chitchat in mouse brains can spark schizophrenia-like symptoms, a new study suggests. The findings are the first to demonstrate — at least in mice — that curbing communication among neurons in certain parts of the brain can cause some of the cognitive problems associated with schizophrenia. By muzzling neurons in the mediodorsal thalamus, or MD — a cell cluster that sends signals to the brain’s outer layer — researchers hindered mouse memory and learning in much the same way that schizophrenia seems to do in humans, scientists report March 20 in Neuron. Cognitive problems in schizophrenia have long been a mystery to scientists and a troubling symptom for people with the condition. The findings suggest that the problems stem from the thalamus, says neuropsychologist Neil Woodward of Vanderbilt University in Nashville, who was not involved with the new work. People with schizophrenia suffer from a range of debilitating symptoms: hallucinations, delusions and social disorders, says study coauthor Christoph Kellendonk of Columbia University. Patients also have problems with short-term memory and learning. Unlike other symptoms, these cognitive problems have been nearly impossible to treat. Brain imaging of people with schizophrenia had previously linked cognitive defects to changes in the MD — part of a walnut-sized chunk of gray matter snuggled above the brain stem. Normally, the MD relays information to and from the prefrontal cortex, the brain region behind the forehead that controls complex thought. In people with schizophrenia, the imaging showed, the MD is unusually quiet. © Society for Science & the Public 2000 - 2013

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 17929 - Posted: 03.23.2013

By NICHOLAS BAKALAR Compared with the rest of the population, people with mental illness may be at sharply increased risk of dying by homicide, a new study has found. Researchers used Swedish government registries to determine psychiatric diagnoses and causes of death among the entire adult population of 7.2 million from 2001 to 2008. There were 615 murders in the period, 141 of them of people with mental disorders. (The homicide rate in Sweden is about one-fifth that of the United States.) After controlling for age, education level, income and other factors, they found that people with mental illness were almost five times as likely to be a victim of murder as a person without a psychiatric diagnosis. The study appeared online last week in the journal BMJ. The risk was highest among those with substance use disorders — nine times that of the general population. Those with personality disorders had three times the risk, people with depression two and a half times, and those with anxiety or schizophrenia about twice the risk of being murdered, compared with people without mental illness. The lead author, Dr. Casey Crump, a clinical assistant professor of medicine at Stanford, said the findings were consistent with those from smaller studies done in the United States. Interestingly, he said, “these results extended to all the most common mental disorders.” Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17902 - Posted: 03.15.2013

By NICHOLAS BAKALAR Some studies have suggested that the risk factors for violence by people with mental illness are the same as those in the general population. But a new study finds that anger, coupled with psychotic delusions, may be the most significant factor in violence committed by people with mental illness. British researchers, writing online last week in JAMA Psychiatry, studied 458 patients ages 18 to 64 who had had a first episode of psychosis. Most patients were nonviolent, 26.4 percent were involved in minor violence, and 11.8 percent in violent acts using weapons or resulting in injury. Those who were violent were more likely to be younger men and to use illicit drugs, but they did not differ from the nonviolent in social class, unemployment or alcohol use. The researchers found no difference between violent and nonviolent patients with regard to feelings of elation, fear or anxiety. People with depression were less violent. But after adjusting for other health and socioeconomic variables, the researchers found that delusions accompanied by anger were present far more often among the violent patients. “If patients are not angry, the delusions themselves don’t cause a problem,” said the lead author, Dr. Jeremy W. Coid, a professor of psychiatry at Queen Mary University of London. “An area for future research is, ‘What do you need to do to make your patient safe again? Do you treat the delusions, the anger or both?’ ” Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 17892 - Posted: 03.12.2013

By GINA KOLATA The psychiatric illnesses seem very different — schizophrenia, bipolar disorder, autism, major depression and attention deficit hyperactivity disorder. Yet they share several genetic glitches that can nudge the brain along a path to mental illness, researchers report. Which disease, if any, develops is thought to depend on other genetic or environmental factors. Their study, published online Wednesday in the Lancet, was based on an examination of genetic data from more than 60,000 people worldwide. Its authors say it is the largest genetic study yet of psychiatric disorders. The findings strengthen an emerging view of mental illness that aims to make diagnoses based on the genetic aberrations underlying diseases instead of on the disease symptoms. Two of the aberrations discovered in the new study were in genes used in a major signaling system in the brain, giving clues to processes that might go awry and suggestions of how to treat the diseases. “What we identified here is probably just the tip of an iceberg,” said Dr. Jordan Smoller, lead author of the paper and a professor of psychiatry at Harvard Medical School and Massachusetts General Hospital. “As these studies grow we expect to find additional genes that might overlap.” The new study does not mean that the genetics of psychiatric disorders are simple. Researchers say there seem to be hundreds of genes involved and the gene variations discovered in the new study confer only a small risk of psychiatric disease. Steven McCarroll, director of genetics for the Stanley Center for Psychiatric Research at the Broad Institute of Harvard and M.I.T., said it was significant that the researchers had found common genetic factors that pointed to a specific signaling system. © 2013 The New York Times Company

Related chapters from BP7e: 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: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 17866 - Posted: 03.04.2013

by Emily Underwood No single cause has yet been discovered for schizophrenia, the devastating neuropsychiatric syndrome characterized by hallucinations, disordered thoughts, and other cognitive and emotional problems, typically beginning in early adulthood. Although schizophrenia runs in families, in many cases no genetic risk is apparent, leading many researchers to look for environmental explanations. Now, research in mice provides support for a long-held hypothesis: that the syndrome, and other neurological disorders, can emerge when multiple environmental insults such as prenatal infection and adolescent trauma combine. Environmental stressors such as infection and abuse were long ago shown to be risk factors for schizophrenia. Large studies of children whose mothers were infected with influenza during the last months of their pregnancy, for example, have a roughly twofold increase in risk of developing the syndrome compared with the general population. That doesn't explain why a few people who are exposed to an infection in the womb go on to develop schizophrenia while most don't, however, says Urs Meyer, a behavioral neurobiologist at the Swiss Federal Institute of Technology in Zurich and co-author of the study reported online today in Science. One long-held hypothesis, he says, is that early infection creates a latent vulnerability to schizophrenia that is only "unmasked" by later insults, such as physical injury or psychological trauma. Such stressors are thought to be particularly damaging during critical periods of brain development such as early puberty, he says. Although the "multiple-hit" hypothesis has been prominent in the literature for some time, it is difficult to test the idea with human epidemiology studies, he says. "You need huge, huge data sets to see anything." © 2010 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 17864 - Posted: 03.02.2013