Evidence of parallels between mercury intoxication and the brain pathology in autism.
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-α, IFN-γ, IL-1β, 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.
Institute of Chronic Illnesses, Inc., Silver Spring, MD, USA. jkern@dfwair.net.
Janet K
JK
Kern
David A
DA
Geier
Tapan
T
Audhya
Paul G
PG
King
Lisa K
LK
Sykes
Mark R
MR
Geier
D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D000818:Animals; D001321:Autistic Disorder / Q000276:immunology / Q000473:pathology* / Q000523:psychology; D001921:Brain / Q000276:immunology / Q000473:pathology*; D002118:Calcium / Q000378:metabolism; D002531:Cerebellum / Q000473:pathology; D016207:Cytokines / Q000378:metabolism / Q000502:physiology; D004660:Encephalitis / Q000473:pathology; D004730:Endothelium, Vascular / Q000473:pathology; D018698:Glutamic Acid / Q000502:physiology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D015227:Lipid Peroxidation / Q000187:drug effects; D020262:Mercury Poisoning, Nervous System / Q000276:immunology / Q000473:pathology* / Q000523:psychology; D017628:Microglia / Q000187:drug effects / Q000473:pathology; D008870:Microtubules / Q000473:pathology; D028361:Mitochondrial Diseases / Q000139:chemically induced / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism / Q000502:physiology; D016501:Neurites / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D016564:Amyloid beta-Protein Precursor; D016207:Cytokines; D016328:NF-kappa B; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D007334:Insulin-Like Growth Factor I; D002118:Calcium