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Several models have been put forward to explain the link between altered brain function and schizophrenia. [27] The prevailing model of schizophrenia is that of a neurodevelopmental disorder, and the underlying changes that occur before symptoms become evident are seen as arising from the interaction between genes and the environment. [126]
The dopamine hypothesis of schizophrenia or the dopamine hypothesis of psychosis is a model that attributes the positive symptoms of schizophrenia to a disturbed and hyperactive dopaminergic signal transduction. The model draws evidence from the observation that a large number of antipsychotics have dopamine-receptor antagonistic effects. The ...
The risk of enlarged ventricles on brain scan (associated with schizophrenia symptoms and biologically suggestive of Emil Kraepelin's dementia praecox) was greatly increased if the subjects had both a higher genetic load for schizophrenia and lower birthweight. The investigators suggested that in utero insults may specifically stress those with ...
'This will turn out to be the most important break in the disease,' the Broad Institute's director Eric Lander said.
Ketamine produces more similar symptoms (hallucinations, withdrawal) without observed permanent effects (other than ketamine tolerance). Both arylcyclohexamines have some(uM) affinity to D2 and as triple reuptake inhibitors. PCP is representative symptomatically, but does appear to cause brain structure changes seen in schizophrenia. [22]
The causes of schizophrenia that underlie the development of schizophrenia, a psychiatric disorder, are complex and not clearly understood.A number of hypotheses including the dopamine hypothesis, and the glutamate hypothesis have been put forward in an attempt to explain the link between altered brain function and the symptoms and development of schizophrenia.
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