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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 ...
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]
Brain-derived Neurotrophic Factor Individuals with schizophrenia have lower levels of brain-derived neurotrophic factor or BDNF. BDNF is responsible for promoting the proliferation, regeneration, and survival of neurons. It is also important for the regulation of cognitive function, something individuals with schizophrenia have trouble doing.
'This will turn out to be the most important break in the disease,' the Broad Institute's director Eric Lander said.
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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