IMR Press / FBE / Volume 7 / Issue 2 / DOI: 10.2741/730

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review
The role of trace elements, thiamin(e) in autism and autistic spectrum disorder
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1 Department of Chemistry, Cleveland State University, Cleveland OH USA
2 Gene Targeting Resource Center, The Rockefeller University, New York, NY USA
3 Pathology and Laboratory Medicine Service Department of Veteran Affairs Cleveland OH USA
4 Cleveland OH USA

*Author to whom correspondence should be addressed.

Academic Editor: Gjumrakch Aliev

Front. Biosci. (Elite Ed) 2015, 7(2), 263–277; https://doi.org/10.2741/730
Published: 1 January 2015
Abstract

There has been much research into autism or autistic spectrum disorder (ASD) and room for considerable conjecture regarding the etiology of these disorders remain. ASD is marked by a complex interaction between environmental factors and genetic predisposition, including epistasis. This manuscript argues that changes in oxidative metabolism, thiamine homeostasis, heavy metal deposition and cellular immunity have a role in the etiopathogenesis of autism and ASD. Recent evidence for abnormal thiol metabolism, marked by significant alteration in the deposition of several trace heavy metal species is provided here. We hypothesize that altered thiol metabolism from heavy metal toxicity, one of the key mechanisms for oxidative stress production, may be responsible for the biochemical alterations in transketolase, dysautonomia and abnormal thiamine homeostasis. It is unknown why these particular metals accumulate; but we suspect that children with ASD and forms of autism may have particular trouble excreting thiol-toxic heavy metal species. We maintain divalent cation accumulation is evidence of altered clearance, which leads to oxidative stress, offering intriguing component or possible mechanism for oxidative stress-mediated neurodegeneration in ASD patients.

Keywords
Heavy Metal
Copper
Iron
Mercury
Arsenic
Divalent Cation
Metal Transport
Autistic Spectrum Disorder
Mitochondria
vitamin B1
Thiamine
Transketolase
Oxidative Stress
Inflammation
Neurodegeneration
Review
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