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Schizophrenia is thought to have a heritable component in some people, but many people who appear to carry schizophrenia-associated genes may not develop the disease. [13] Research has shown that schizophrenia is a polygenic disorder and that genetic vulnerability to schizophrenia is highly multifactorial , caused by the interactions of several ...
The epigenetics of schizophrenia is the study of how inherited epigenetic changes are regulated and modified by the environment and external factors and how these changes influence the onset and development of, and vulnerability to, schizophrenia. Epigenetics concerns the heritability of those changes, too.
The question of how schizophrenia could be primarily genetically influenced, given that people with schizophrenia have lower fertility rates, is a paradox. It is expected that genetic variants that increase the risk of schizophrenia would be selected against, due to their negative effects on reproductive fitness .
Risk factors for mental illness include psychological trauma, adverse childhood experiences, genetic predisposition, and personality traits. [7] [8] Correlations between mental disorders and substance use are also found to have a two way relationship, in that substance use can lead to the development of mental disorders and having mental disorders can lead to substance use/abuse.
Schizophrenia is a somewhat rare disease affecting approximately 3.2 million Americans in the United States. Also, in an average year, about 100,000 individuals will be diagnosed with schizophrenia. [18] In 2010, there were approximately 397,200 hospitalizations for schizophrenia in the United States.
However, linkage analysis and genome-wide association studies have found few reproducible risk factors. [1] Heterogeneity is an important factor to consider when dealing with genetics. Two types of heterogeneity have been identified in association with psychiatric genetics: causal and clinical.
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.
The glutamate hypothesis of schizophrenia models the subset of pathologic mechanisms of schizophrenia linked to glutamatergic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of glutamatergic signaling via NMDA receptors .
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