The ultimate cause of schizophrenia remains to be found, but it clearly includes a significant genetic component with an estimated heritability up to 85%. This suggests that genes may act as a predisposing factor upon which a variety of environmental risk factors can exert their deleterious effects, determining the emergence of psychotic symptoms. A recently growing interest has re-arisen on perinatal brain infections, which may increase the risk for schizophrenia that can, in turn, be modified by hazardous genetic loading. This hypothesis is based on epidemiological evidence, which has shown a significant exposure of affected individuals to infections with different pathogens. Such results are supported by tests carried out on animals. Another possibility is that there may be a link between a primary maternal infection and the subsequent development of schizophrenia in offspring. It is also been hypothesized that maternal antibodies against microorganisms may damage the fetal neural tissue, the area which is later found to be affected by the lesion occurring in patients with schizophrenia. In the present chapter, we review recent evidence on the potential role of infectious agents in the etiology of schizophrenia and discuss possible implications on the future of diagnostic, preventive and therapeutic issues.
Keywords: Schizophrenia, infection, pathogen, influenza, herpes simplex, toxoplasmosis, genes, gene environment interactions, Microbial Agents, Psychosis, perinatal brain infections, neural tissue, dementia praecox, Psychiatrie, autointoxication, Psychiatry, psychopathology, typhoid fever, tuberculosis, diphtheria, malignant, encephalitis, neuropsychiatric, Toxoplasma gondii, Cytomegalovirus, Chlamydia, CNS, Epstein-Barr virus, rubella, HIV, IL-8, TNF, meningitis, stressors, Mumps, Human Herpes Simplex Virus Type 1, HSV-1, Human Herpes Virus Type 6, HHV-6, HSV-2, Glial dysfunctions, Ncam1, Rgs4
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