Science News About Schizophrenia

A small study suggests that people with certain genetic variants may be more susceptible to extreme weight gain if they take certain antipsychotic medications.

For the first time, scientists have tracked the activity, across the lifespan, of an environmentally responsive regulatory mechanism that turns genes on and off in the brain’s executive hub. Among key findings of the study by National Institutes of Health scientists: genes implicated in schizophrenia and autism turn out to be members of a select club of genes in which regulatory activity peaks during an environmentally-sensitive critical period in development.

Researchers continue to make progress in the NIMH Recovery After an Initial Schizophrenia Episode (RAISE) Project, which seeks to intervene at the earliest stages of illness in order to prevent long term disability. Recent refinements to the two RAISE studies will ensure that RAISE continues efficiently, and generates results that will be relevant to consumers and health care policy makers.

Patients experiencing cardiovascular or metabolic side effects while taking an antipsychotic medication may fare better if they switch to a different medication provided they are closely monitored, according to an NIMH-funded study.

Scientists are eyeing a rare genetic glitch for clues to improved treatments for some people with schizophrenia – even though they found the mutation in only one third of 1 percent of patients.

Scientists have discovered a compound that restores the capacity to form new memories in aging rats, likely by improving the survival of newborn neurons in the brain’s memory hub. The research, funded in part by the National Institutes of Health, has turned up clues to a neuroprotective mechanism that could lead to a treatment for Alzheimer’s disease.

Few youths with early-onset schizophrenia who are treated with antipsychotic medications for up to a year appear to benefit from their initial treatment choice over the long term, according to results from an NIMH-funded study. The study was published online ahead of print May 4, 2010, in the Journal of the American Academy of Child and Adolescent Psychiatry.

The strongest known recurrent genetic cause of schizophrenia impairs communications between the brain’s decision-making and memory hubs, resulting in working memory deficits, according to a study in mice.

NIMH is launching a long-term project aimed at ultimately improving treatment and prevention by studying classification of mental illness, based on genetics and neuroscience in addition to clinical observation. The Research Domain Criteria (RDoC) project is not intended to replace psychiatry’s existing diagnostic system for practitioners and will proceed in an independent direction, said Bruce Cuthbert, Ph.D., Director of the NIMH Division of Adult Translational Research, who is directing the effort. By taking a fresh look – without preconceived categories – the project aims to improve the validity of classification for researchers.

Deleting one type of neurotransmitter receptor in a specific population of brain cells can induce schizophrenia-like behavior in mice, but only when the receptor is deleted early in development, according to a study by NIMH intramural scientists. The work provides strong support for previous observations implicating these receptors in psychosis; further, the mice provide a model of how psychotic symptoms can arise from a disruption in neuronal development, consistent with observations of how schizophrenia emerges in humans.

Researchers recently announced discovery of a new class of molecules that holds promise for blocking the clumps of protein that clog the brain in Alzheimer’s disease. The new findings are the latest made possible by the NIH Roadmap Molecular Libraries initiative, which employs high-tech robots and molecular genetics to speedily screen molecules for their biological effects. The discovery required testing nearly 300,000 compounds – a task thought insurmountable just a decade ago.

When and where in the brain a gene turns on holds clues to its possible role in disease. For example, a recent study found that forms of a gene associated with schizophrenia are over-expressed in the fetal brain, adding to evidence implicating this critical developmental period.

Even when we’re not doing much of anything, our brain’s cortex, or outer mantle, is bustling with activity. In fact, scientists for the first time have detected “avalanches” of cortex activity in awake monkeys at rest.

A gene called DISC1, (for “disrupted in schizophrenia”) has been a leading contender among possible genetic causes since it was implicated in schizophrenia in a large Scottish clan two decades ago. The DISC1 gene codes for a protein important for brain development, as well as for mood and memory – functions that are disturbed in schizophrenia. However, until now there have been few clues as to how DISC1 might increase risk for the chronic mental disorder.

The National Institute of Mental Health (NIMH) is launching a large-scale research project to explore whether using early and aggressive treatment, individually targeted and integrating a variety of different therapeutic approaches, will reduce the symptoms and prevent the gradual deterioration of functioning that is characteristic of chronic schizophrenia.

A trio of genome-wide studies – collectively the largest to date – has pinpointed a vast array of genetic variation that cumulatively may account for at least one third of the genetic risk for schizophrenia. One of the studies traced schizophrenia and bipolar disorder, in part, to the same chromosomal neighborhoods.

A study on schizophrenia has implicated machinery that maintains the flow of potassium in cells and revealed a potential molecular target for new treatments. Expression of a previously unknown form of a key such potassium channel was found to be 2.5 fold higher than normal in the brain memory hub of people with the chronic mental illness and linked to a hotspot of genetic variation.

The first large-scale study of its kind in twins has turned up evidence that we inherit instructions for the turning on and off of genes via mechanisms beyond the traditional sequence differences in the genetic code. Moreover, the results suggest that early random errors in replicating these instructions may trump environmental influences in shaping us.

With a mandate to use innovative, multidisciplinary research approaches to address important mental health questions, four newly funded centers have begun investigations of schizophrenia, brain development, and adolescent mood disorders.

Numerous biological, psychological, and social factors are likely to play a role in the high rates of smoking in people with psychiatric disorders, according to the report of an expert panel convened by the National Institute of Mental Health. The report reviews current literature and identifies research needed to clarify these factors and their interactions, and to improve treatment aimed at reducing the rates of illness and mortality from smoking in this population.

The first study of its kind to pinpoint environment-triggered genetic changes in schizophrenia has been launched with $9.8 million in funding from NIMH. The five-site study seeks telltale marks in the genome that hold clues to how nurture interacts with nature to produce the illness.

An analysis of studies on antipsychotics reveals multiple differences among the newer, second-generation antipsychotics as well as the older medications, and suggests the current classification system blurs important differences, rendering it unhelpful.

Growth of the brain’s long distance connections, called white matter, is stunted and lopsided in children who develop psychosis before puberty, NIMH researchers have discovered.

Certain atypical antipsychotic medications may raise the risk for heart disease in people with schizophrenia, according to an analysis of data from the NIMH-funded Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study.

A new NIMH-funded grant will examine ways to control the metabolic side effects associated with the use of the newer atypical antipsychotic medications in children with schizophrenia or bipolar disorder.

If, as the song laments, our get up and go fades as we get older, it may stem from aging-related changes in a brain reward circuit.

Mice genetically engineered to have an over active version of a human gene, like their human counterparts, gain in emotional mettle under stress, but at a cost of less efficient thinking, NIMH scientists have discovered.

Two newer atypical antipsychotic medications were no more effective than an older conventional antipsychotic in treating child and adolescent schizophrenia and may lead to more metabolic side effects, according to a new study funded by the National Institutes of Health’s National Institute of Mental Health (NIMH).

Childhood bedwetting occurred twice as often in adults with schizophrenia than in their unaffected brothers and sisters, according to a new study from researchers at NIMH.

People with schizophrenia bear an “increased burden” of rare deletions and duplications of genetic material, genome-wide, say researchers supported in part by the National Institute of Mental Health (NIMH), a component of the National Institutes of Health (NIH).

Some atypical antipsychotics may be more likely than others to cause metabolic and cardiovascular side effects, according to recent analyses using data from the NIMH-funded Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE).

Antipsychotic medications can reduce the risk of violence among people with schizophrenia, but the newer atypical antipsychotics are no more effective in doing so than older medications, according to a recent analysis of data from the NIMH-funded Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE).

Schizophrenia may occur, in part, because brain development goes awry during adolescence and young adulthood, when the brain is eliminating some connections between cells as a normal part of maturation, results of a study suggest. The new report appears online July 8, 2008 in Molecular Psychiatry.

An NIMH initiative to fill the gap between advances in basic cognitive neuroscience and practical clinical applications for patients with schizophrenia is the topic of the July 1, 2008 issue of Biological Psychiatry.

New mouse strains engineered to express human genes related to mental disorders are being developed under a recently-launched grant program from NIMH’s Division of Neuroscience and Basic Behavioral Science.

NIMH has recently awarded a grant to study whether an intensive computerized training program can help prevent those at high risk of developing schizophrenia from having a first psychotic episode and improve adaptive functioning. The program is based on principles of brain development and resilience and an understanding of the processes that go awry in schizophrenia.

People with schizophrenia have high rates of rare genetic deletions and duplications that likely disrupt the developing brain, according to studies funded in part by the National Institutes of Health.

An NIMH study using an emerging imaging technology has discovered faulty wiring in the brains of people with Williams Syndrome, a rare genetic disorder that affects some aspects of thinking.

New research adds to evidence of potentially better molecular targets in the brain to treat depression and other mental disorders, according to NIMH-funded scientists.

Youth who are going to develop psychosis can be identified before their illness becomes full-blown 35 percent of the time if they meet widely accepted criteria for risk, but that figure rises to 65 to 80 percent if they have certain combinations of risk factors, the largest study of its kind has shown. Knowing what these combinations are can help scientists predict who is likely to develop the illnesses within two to three years with the same accuracy that other kinds of risk factors can predict major medical diseases, such as diabetes.

Two new NIMH grants are aimed at determining the most accurate methods of measuring how well community-dwelling people with schizophrenia are faring. Results of the project are meant to provide scientists who conduct future research on the effectiveness of treatments with tools that will reflect the truest possible picture of daily-life outcomes.

Different variations in the same gene influence how well different ethnic groups, and people within the same ethnic group, respond to various antipsychotic medications, report NIMH-funded researchers. If confirmed, their findings could one day help clinicians predict which medication is most likely to help a patient, based on his or her genetic makeup.

Forms of a gene known to increase risk for schizophrenia may create an imbalance in brain pathways for dopamine, suggests a recent study by NIMH scientists.

Schizophrenia may occur, in part, because of a problem in an intermittent on/off switch for a gene involved in making a key chemical messenger in the brain, scientists have found in a study of human brain tissue.

Two gene variants implicated in schizophrenia interact to degrade the brains ability to process information, NIMH researchers have discovered.

Some people with schizophrenia who become violent may do so for reasons unrelated to their current illness, according to a new study analyzing data from the Clinical Antipsychotic Trials for Intervention Effectiveness (CATIE).

Patients with schizophrenia taking antipsychotic medications experience a small improvement in thinking and reasoning skills (neurocognition), but no one medication appears to be better than the others in improving these skills during the first two crucial months of treatment, according to the latest results from the NIMH-funded Clinical Antipsychotic Trials for Intervention Effectiveness (CATIE).

Two new studies from the Clinical Antipsychotic Trials for Intervention Effectiveness (CATIE) provide more insights into comparing treatment options, and to what extent antipsychotic medications help people with schizophrenia learn social, interpersonal and community living skills.

Most people inherit a version of a gene that optimizes their brain’s thinking circuitry, yet also appears to increase risk for schizophrenia, a severe mental illness marked by impaired thinking, scientists at the National Institutes of Health’s (NIH) National Institute of Mental Health (NIMH) have discovered.

A gene implicated in schizophrenia in adults has now also been linked to schizophrenia in children for the first time, strengthening evidence that the gene plays a role in the disease.