NIH RESEARCH MATTERS: STRESS HORMONE CAUSES EPIGENETIC CHANGES

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Researchers found that chronic exposure to a stress hormone causes modifications to DNA in the brains of mice, prompting changes in gene expression. The new finding provides clues into how chronic stress might affect human behavior.

Reported by Harrison Wein, Ph.D.

http://www.nih.gov/researchmatters/september2010/09272010stress.htm

Submitted by Anna

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Advancing Drug Discovery for Schizophrenia

March 9 – 11, 2011
The New York Academy of Sciences
Presented by the New York Academy of Sciences
Early Bird Deadline: January 07, 2011
Poster Abstract Deadline: December 10, 2010

During the past decade there has been a marked decline in the number of novel drugs developed and approved for treatment of schizophrenia despite a significant investment in research and development by the pharmaceutical industry. The goal of this conference is to facilitate the translation of discoveries in basic neuroscience into the development of innovative pharmacological agents for the treatment of schizophrenia by convening and encouraging dialogue among clinical, translational and basic neuroscientists. Plenary sessions will include discussion of genetic and epigenetic approaches to studying schizophrenia; new molecular targets and approaches to small molecule therapeutics; and the relationship between genes, function, and clinical symptoms.

http://www.nyas.org/Events/Detail.aspx?cid=55938b51-f0d8-4d2b-aab7-de7436c96440

Submitted by Anna

RAPID ANTIDEPRESSANT WORKS BY BOOSTING BRAIN’S CONNECTIONS: SINGLE DOSE SPROUTS BUDDING SYNAPSES WITHIN HOURS IN RAT BRAIN

An experimental drug that lifts depression in hours likely works by rapidly stimulating connections between brain cells, a study in rats has revealed. The drug, called ketamine, quickly generated such synapses in a brain circuit implicated in human depression by triggering a key enzyme. “Discovery of this cellular mechanism helps point the way to development of a ketamine-like agent that could become a practical, rapid-acting treatment for depression,” said Dr. Ronald Duman, of Yale University, who led the research team supported by the National Institute of Mental Health (NIMH). Duman and his colleagues report on their findings in the August 20, 2010 issue of the journal Science. Science News: http://www.nimh.nih.gov/science-news/2010/rapid-antidepressant-works-by-boosting-brains-connections.shtml

$40 MILLION AWARDED TO TRACE HUMAN BRAIN’S CONNECTIONS—SOUPED-UP SCANNERS TO REVEAL INTRICATE CIRCUITRY IN HIGH RESOLUTION

The National Institutes of Health (NIH) awarded grants totaling $40 million to map the human brain’s connections in high resolution. Better understanding of such connectivity promises improved diagnosis and treatment of brain disorders. The grants are the first awarded under the Human Connectome Project. They will support two collaborating research consortia. The first will be led by researchers at Washington University, St. Louis, and the University of Minnesota, Twin Cities. The other will be led by investigators at Massachusetts General Hospital/Harvard University, Boston, and the University of California Los Angeles.
Press Release: http://www.nimh.nih.gov/science-news/2010/40-million-awarded-to-trace-human-brains-connections.shtml

Submitted by Anna

Autism and Schizophrenia: Family History May Not Always Be a Good Indicator

An international study led by University of Montreal scientists suggests family history may not be a good predictor of the presence of mutations predisposing to autism or schizophrenia.

The findings show how new or de novo gene mutations — alterations of the cell’s DNA — play a role in these devastating conditions. Published in the American Journal of Human Genetics, this study has implications for disease prevalence and severity.

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Montreal

Philip Awadalla et al. Direct Measure of the de novo Mutation Rate in Autism and Schizophrenia cohorts. American Journal of Human Genetics, 2010; DOI: 10.1016/j.ajhg.2010.07.019

http://www.sciencedaily.com/releases/2010/08/100826122610.htm

Submitted by Anna

Dopamine Connections May Link Creativity, Psychiatric Disorders

Roman philosopher Seneca once penned, “There is no great genius without a tincture of madness.” For centuries, philosophers and scientists have wondered about the nature of the relationship between creativity, a trait critical to genius, and psychiatric disorders like schizophrenia and bipolar disorder. A recent study in the journal PLoS One suggests that the density of a certain type of dopamine receptor on the thalamus, a brain area linked to passing sensory information to the cerebral cortex, may play a role.

Reported by Kayt Sukel
The DANA Foundation
http://www.dana.org/news/features/detail.aspx?id=28858

Submitted by Anna

Large Risk Schizophrenia Marker Revealed

A group of scientists has identified a genetic variant that substantially increases the risk for developing schizophrenia in Ashkenazi Jewish and other populations. The study, published on August 5th in the American Journal of Human Genetics, associates a deletion on chromosome 3 with increased incidence of schizophrenia.

Science Daily
http://www.sciencedaily.com/releases/2010/08/100805172951.htm
Story Source: The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Cell Press, via EurekAlert!, a service of AAAS.

Submitted by Anna

Scientists Identify Brain Region That May Give Rise to Schizophrenia

Schizophrenia is as mysterious as it is devastating. No one knows just what happens within the brain to cause the disease’s characteristic hallucinations, delusions and cognitive deficits. Now researchers have identified a small region in the hippocampus where an early increase in activity—before symptoms become marked—might represent the beginning of the disease process. The results could lead to new targets for drug treatment and new ideas for strategies to prevent the disease.

Schizophrenia is often preceded by a “prodromal” phase, when individuals begin to exhibit symptoms but fall short of the criteria for a psychiatric diagnosis. They might, for instance, withdraw socially, or hear their names in the sound of the wind rather than an outright hallucination. Some studies suggest that treatment—including medication—during these early stages may delay the onset of full schizophrenia, reduce its severity or prevent it altogether.

But not all prodromal individuals go on to develop the disease—just 35 percent within 2.5 years, says Thomas McGlashan, a professor of psychiatry at Yale University who works with such patients. In the face of this uncertainty, most clinicians believe the risks of side effects from treatment outweigh potential benefits and have adopted a conservative wait-and-see approach. “For the ‘false positives,’ which might be the majority, you’d be unnecessarily giving powerful agents that can have severe side effects,” McGlashan says.

To investigate why the prodromal phase progresses to schizophrenia in only one out of three patients, researchers from Columbia University used a high-resolution variant of functional magnetic resonance imaging (fMRI) to compare the brains of 18 people with established schizophrenia with 18 healthy controls. In the disease group, they found increased blood flow, suggesting higher levels of activity, in the orbitofrontal cortex and in a small section—the CA1 subfield—of the hippocampus. In the dorsolateral prefrontal cortex, meanwhile, blood flow decreased.

Reported by Carl Sherman
The DANA Foundation

http://www.dana.org/news/features/detail.aspx?id=23754

September 2009 issue of Archives of General Psychiatry

Submitted by Anna

Schizophrenia Drugs Raise the Volume of a Key Signaling System in the Brain

All the major groups of medications for schizophrenia turn up the volume of a brain signal known to be muted in individuals with this psychiatric disorder — a signal that also can be influenced by diet. “This is the first example of a common but specific molecular effect produced by all antipsychotic drugs in any biological system,” scientists note in the current edition of ACS Chemical Neuroscience.

Story Source: Adapted from materials provided by American Chemical Society, via EurekAlert!, a service of AAAS.

Journal Reference: Weeks et al. Antipsychotic Drugs Activate the C. elegans Akt Pathway via the DAF-2 Insulin/IGF-1 Receptor. ACS Chemical Neuroscience, 2010; 100325110757056 DOI: 10.1021/cn100010p

http://www.sciencedaily.com/releases/2010/05/100512112426.htm

Submitted by Anna

Children Bullied At School At High Risk Of Developing Psychotic Symptoms

Children who are bullied at school over several years are up to four times more likely to develop psychotic-like symptoms by the time they reach early adolescence.

Researchers at the University of Warwick found children who suffered physical or emotional bullying were twice as likely to develop psychotic symptoms by early adolescence, compared to children who are not bullied. However, if they experienced sustained bullying over a number of years that risk increases up to four times.

The research team, led by Professor Dieter Wolke, Professor of Developmental Psychology, followed 6,437 children from birth to 13 years.

The children took part in annual face-to-face interviews, psychological and physical tests. Parents were also asked to complete questionnaires about their child’s development. When they reached 13 years of age they were interviewed about experiences of psychotic symptoms in the previous six months.

Psychotic symptoms include hallucinations, delusions such as being spied on or bizarre thoughts such as one’s thoughts are being broadcast.

Professor Wolke said: “Our research shows that being victimised can have serious effects on altering perception of the world, such as hallucinations, delusions or bizarre thoughts where the person’s insight into why this is happening is reduced.”

“This indicates that adverse social relationships with peers is a potent risk factor for developing psychotic symptoms in adolescence and may increase the risk of developing psychosis in adulthood.”

Story Source from materials provided by University of Warwick.

Journal Reference: Schreier et al. Prospective Study of Peer Victimization in Childhood and Psychotic Symptoms in a Nonclinical Population at Age 12 Years. Archives of General Psychiatry, 2009; 66 (5): 527 DOI:10.1001/archgenpsychiatry.2009.23

http://www.sciencedaily.com/releases/2009/05/090503213612.htm

Submitted by Anna