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. 2008:1:99-103.
doi: 10.4137/cpath.s1143. Epub 2008 Sep 18.

The pathogenesis of autism

Affiliations

The pathogenesis of autism

Timothy John Watts. Clin Med Pathol. 2008.

Abstract

Autism is well known as a complex developmental disorder with a seemingly confusing and uncertain pathogenesis. The definitive mechanisms that promote autism are poorly understood and mostly unknown, yet available theories do appear to focus on the disruption of normal cerebral development and its subsequent implications on the functional brain unit. This mini-review aims solely to discuss and evaluate the most prominent current theories regarding the pathogenesis of autism. The main conclusion is that although there is not a clear pathway of mechanisms directed towards a simple pathogenesis and an established link to autism on the symptomatic level; there are however several important theories (neural connectivity, neural migration, excitatory-inhibitory neural activity, dendritic morphology, neuroimmune; calcium signalling and mirror neurone) which appear to offer an explanation to how autism develops. It seems probable that autism's neurodevelopmental defect is 'multi-domain' in origin (rather than a single anomaly) and is hence distributed across numerous levels of study (genetic, immunopathogenic, etc.). A more definitive understanding of the pathogenesis could facilitate the development of better treatments for this complex psychiatric disorder.

Keywords: autism; dendritic; mirror neurone; neural migration; neuroimmune.

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References

    1. Araghi-Niknam M, Fatemi SH. Levels of Bcl-2 and P53 are altered in superior frontal and cerebellar cortices of autistic subjects. Cell Mol Neurobiol. 2003;23:945–52. - PMC - PubMed
    1. Aschner M, Allen JW, Kimelberg HK, et al. Glial cells in neurotoxicity development. Annu Rev Pharmacol Toxicol. 1999;39:151–73. - PubMed
    1. Ashwood P, van de Water J. Is autism an autoimmune disease? Autoimmun Rev. 2004;3:557–62. - PubMed
    1. Ashwood P, Wills S, Van de Water J. The immune response in autism: a new frontier for autism research. J Leukoc Biol. 2006;80:1–15. - PubMed
    1. Boeckers TM, Bockmann J, Kreutz MR, Gundelfinger ED. ProSAP/Shank proteins—a family of higher order organizing molecules of the postsynaptic density with an emerging role in human neurological disease. J Neurochem. 2002;81:903–10. - PubMed

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