Although there may be genetic or developmental components to autism, the evidence in this current review of the brain findings in autism clearly indicates the reality of brain injury in Autism Spectrum Disorders (ASD); moreover, the brain injury symptoms which characterize autism closely correspond to those seen in sub-acute mercury (Hg) intoxication. The evidence presented in this paper is consistent with Hg being identified as either causal or contributory, working synergistically with other compounds or pathogens in producing the brain pathology observed in those diagnosed with ASD.
Their review article is published in Acta Neurobiologiae Experimentalis (2012; 72 (2): 113-153). This peer-reviewed journal is published by Nencki Institute of Experimental Biology in Warsaw, Poland.
Janet K. Kern, David A. Geier, Tapan Audhya, Paul G. King, Lisa K. Sykes, and Mark R. Geier
Evidence of parallels between mercury intoxication and the brain pathology in autism
Acta Neurobiol Exp (Wars) 2012; 72 (2): 113-153
The purpose of this review is to examine the parallels between the effects mercury intoxication on the brain and the brain pathology found in autism spectrum disorder (ASD). This review finds evidence of many parallels between the two, including: (1) microtubule degeneration, specifically large, long-range axon degeneration with subsequent abortive axonal sprouting (short, thin axons); (2) dentritic overgrowth; (3) neuroinflammation; (4) microglial/astrocytic activation; (5) brain immune response activation; (6) elevated glial fibrillary acidic protein; (7) oxidative stress and lipid peroxidation; (8) decreased reduced glutathione levels and elevated oxidized glutathione; (9) mitochondrial dysfunction; (10) disruption in calcium homeostasis and signaling; (11) inhibition of glutamic acid decarboxylase (GAD) activity; (12) disruption of GABAergic and glutamatergic homeostasis; (13) inhibition of IGF-1 and methionine synthase activity; (14) impairment in methylation; (15) vascular endothelial cell dysfunction and pathological changes of the blood vessels; (16) decreased cerebral/cerebellar blood flow; (17) increased amyloid precursor protein; (18) loss of granule and Purkinje neurons in the cerebellum; (19) increased pro-inflammatory cytokine levels in the brain (TNF-alppha, IFN-gamma, IL-1beta, IL-8); and (20) aberrant nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB). This review also discusses the ability of mercury to potentiate and work synergistically with other toxins and pathogens in a way that may contribute to the brain pathology in ASD. The evidence suggests that mercury may be either causal or contributory in the brain pathology in ASD, possibly working synergistically with other toxic compounds or pathogens to produce the brain pathology observed in those diagnosed with an ASD.