Autism spectrum disorders are early-onset chronic conditions of qualitatively impaired social interaction and reciprocal communication with an estimated prevalence rate of 0.6%. Autism is heterogeneous in phenotype and comorbidity. Its precise etiology remains largely an enigma, but twin and family studies indicate substantial hereditary fundamentals. In this report, we briefly review the progress of molecular genetic, environmental and (auto-)immunologic research in autism and similar conditions. At the present time, idiopathic autism is assumed to be an oligogenic epistatic disorder. In a minority of cases, some Mendelian syndromes and other medical conditions as well as exogenous and immune mechanisms may also cause or trigger autism. A standard epidemiologic vulnerability model has been proposed to integrate possible major and minor risks of different origin.

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