Etiopathogenesis of autism spectrum disorders: Fitting the pieces of the puzzle together. Ivan Gentile, Emanuela Zappulo, Roberto Militerni, Antonio Pascotto, Guglielmo Borgia, Carmela Bravaccio Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy. Electronic address: . Medical Hypotheses (MED HYPOTHESES) Publisher: Elsevier ISSN: 1532-2777 Medical Hypotheses (Impact Factor: 1.05). 04/2013; DOI:10.1016/j.mehy.2013.04.002 Source: PubMed ABSTRACT Autism spectrum disorders (ASD) are disorders of the central nervous system characterized by impairments in communication and social reciprocity. Despite thousands of studies on this topic, the etiopathogenesis of these disorders remains unclear, apart from a general belief that they derive from an interaction between several genes and the environment. Given the mystery surrounding the etiopathogenesis of ASD it is impossible to plan effective preventive and treatment measures. This is of particular concern due to the progressive increase in the prevalence of ASD, which has reached a figure as high as 1:88 children in the USA. Here we present data corroborating a novel unifying hypothesis of the etiopathogenesis of ASD. We suggest that ASD are disorders of the immune system that occur in a very early phase of embryonic development. In a background of genetic predisposition and environmental predisposition (probably vitamin D deficiency), an infection (notably a viral infection) could trigger a deranged immune response which, in turn, results in damage to specific areas of the central nervous system. If proven, this hypothesis would have dramatic consequences for strategies aimed at preventing and treating ASD. To confirm or refute this hypothesis, we need a novel research approach, which unlike former approaches in this field, examine the major factors implicated in ASD (genetic, infections, vitamin D deficiency, immune system deregulation) not separately, but collectively and simultaneously.
Posted on: Fri, 21 Mar 2014 08:34:48 +0000
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