The study is the first time scientists have been able to move from genetic studies to a biological insight
into schizophrenia risk, says geneticist David Goldstein of Columbia University.
Not exact matches
In addition to stressful life events, trauma and family history of
schizophrenia and, the calculator takes
into account five other factors to determine an individual's level of
risk.
A Johns Hopkins University team this week reported inserting a disrupted human gene, the
schizophrenia risk factor DISC1,
into lab mice, causing them to exhibit the brain asymmetry characteristic of
schizophrenia as well as agitation in open spaces and trouble finding hidden food — traits reminiscent of the restlessness, impaired sense of smell and depressionlike symptoms schizophrenics suffer, Reuters reports.
«No link found between subcortical brain volumes, genetic
risk for
schizophrenia: Proof - of - concept study provides roadmap for future research
into possible associations between brain volume measures, known genetic
risk factors.»
Dr. Coyle's Laboratory for Psychiatric and Molecular Neuroscience takes advantage of insights
into recently identified genes that confer
risk for
schizophrenia and related disorders and translates them
into genetic mouse models to determine how these mutations affect brain changes as well as function, neurochemistry, and behavior.
«The findings also provide insight
into which cognitive abilities put individuals at
risk of developing
schizophrenia and demonstrate that control carriers provide an opportunity to study cognitive abnormalities without the confounding effects of psychosis or medication.»
These Danish researchers followed 207 high -
risk subjects (children of mothers with
schizophrenia) and 104 low -
risk subjects (children of parents with no psychiatric illness) from adolescence
into adulthood.
Though PLEs and internalising and externalising psychopathology in middle childhood all constitute replicated antecedents of
schizophrenia, our data indicate that internalising and externalising psychopathology experienced only during childhood is not associated with increased
risk for PLEs in adolescence, whereas psychopathology that persists from childhood
into adolescence or is incident in adolescence confers increased
risk for later PLEs [28].