Evidence of parallels between mercury intoxication and the brain pathology in autism

Institute of Chronic Illnesses, Inc., Silver Spring, MD, USA.
Acta neurobiologiae experimentalis (Impact Factor: 1.29). 07/2012; 72(2):113-53.
Source: PubMed


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.

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Available from: Mark R Geier,
    • "The use of mercury-based amalgam for material fillings in dentistry has declined over recent years due its potential negative health effects. These may vary from autoimmunity (Nielsen and Hultman, 2002; Pigatto and Guzzi, 2010; Rowley and Monestier, 2005) to neurological problems (Kern et al., 2012; Mutter, 2011). Yet, negative reports are still scarce or disputed, and certainly in developing countries amalgam fillings are still widely being used nowadays. "
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    ABSTRACT: Gold, nickel, copper and mercury, i.e. four metals frequently used in dental applications, were explored for their capacity to induce innate immune activation in keratinocytes (KC). Due to their anatomical location the latter epithelial cells are key in primary local irritative responses of skin and mucosa. Fresh foreskin-derived keratinocytes and skin and gingiva KC cell lines were studied for IL-8 release as a most sensitive parameter for NF-kB activation. First, we verified that viral-defense mediating TLR3 is a key innate immune receptor in both skin- and mucosa derived keratinocytes. Second, we found that, in line with our earlier finding that ionized gold can mimic viral dsRNA in triggering TLR3, gold is very effective in KC activation. It would appear that epithelial TLR3 can play a key role in both skin- and mucosa localized irritation reactivities to gold. Subsequently we found that not only gold, but also nickel, copper and mercury salts can activate innate immune reactivity in keratinocytes, although the pathways involved remain unclear. Although current alloys have been optimized for minimal leakage of metal ions, secondary factors such as mechanical friction and acidity may still facilitate such leakage. Subsequently, these metal ions may create local irritation, itching and swelling by triggering innate immune reactions, potentially also facilitating the development of metal specific adaptive immunity.
    Toxicology in Vitro 10/2015; DOI:10.1016/j.tiv.2015.10.003 · 2.90 Impact Factor
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    • "Mercury poisoning and autism show very similar symptoms, both mental disturbances and physical disorders (Bernard et al. 2001; Geier et al. 2008). In addition, many parallels between the effects of Hg intoxication on the brain and the brain pathology found in individuals with ASD include dendritic overgrowth, neuroinflammation, brain immune response , oxidative stress and lipid peroxidation, mitochondrial dysfunction, neuronal necrosis, axonal demyelination, and gliosis (Geier et al. 2010; Kern et al. 2012) (Table 1). Collectively, much evidence suggests the biological plausibility of mercury as an etiological agent in autism. "
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    ABSTRACT: An increasing evidence supports the role of industrial chemicals as contributors to the development of neurobehavioral disorders, including autism spectrum disorders, whose prevalence has progressively increased in recent years. Heavy metals, in particular, are recognized as neurodevelopmental toxins since they can be responsible of fetal damages which lead to neurological defects, developmental delays, learning disabilities and behavioral abnormalities. Most of the reviewed studies reported a relationship between exposure to metals during perinatal and early childhood periods and increased risk for autism. Moreover, the effects resulting from co-exposure to multiple metals should not be underestimated, especially in the assessment of children who live in developing countries or near heavily contaminated sites.
    06/2014; 1(4). DOI:10.1007/s40489-014-0028-3
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    • "with our findings, Fido and Al-Saad [16] detected higher hair lead, mercury and uranium levels in autistic children compared to healthy controls. In contrast, Kern and colleagues [18] measured hair arsenic, cadmium, lead and mercury levels of autistic children 1-6 years old and found reduced levels of these heavy metals. Lead is a toxic heavy metal with a long half-time in the body. "
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    ABSTRACT: Dilek Kaya Akyuzlu, Zeliha Kayaalti, Esma Soylemez and Tulin Soylemezoglu
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