There is compelling evidence from a multitude of studies of various design indicating that foodborne excitotoxin additives can elevate blood and brain glutamate to levels known to cause neurodegeneration and in the developing brain, abnormal connectivity. Excitotoxins are also secreted by microglial activation when they are in an activated state. Recent studies, discussed in part 1 of this article, indicate that chronic microglial activation is common in the autistic brain. The interaction between excitotoxins, free radicals, lipid peroxidation products, inflammatory cytokines, and disruption of neuronal calcium homeostasis can result in brain changes suggestive of the pathological findings in cases of autism spectrum disorders. In addition, a number of environmental neurotoxins, such as fluoride, lead, cadmium, and aluminum, can result in these pathological and biochemical changes.
"negative gram bacteria infection and endogen peptide as well as toxic pollutant because lipopolisacharida from negative gram bacteria and toxic substance are able to activate glial cells(Block and Hong, 2007). Thus astrocyt and glial cells can be either target or mediator of neuron damage cased by neurotoxic(Blaylock, 2009). The most sensitif neuron to glial reactivity is dopaminergik neuron (neuron DA). "
[Show abstract][Hide abstract] ABSTRACT: Mercury exposure remain a problem since it is ubiquitous and human exposure is inevitable. Its potent neurotoxic effect is associated with permanent disability and death. Microtubulin and microglia are vulnerable to neurotoxict substance .The alteration of their number in respond to toxic agent will be destructif and deadly to central nervous system.Therefore the present study investigates the dose relationship between mercury exposure and their count in brain. Male rats (Rattus Novergicus) were used to determine the neurotoxic effect of methylmercurychloride on their brain using microglia and microtubulin as parameter. Varying dose of MeHgCl3 from 0,2 mg/BW to 0,8 mg/BW had been administered via nasogastric tube for 21 days, then the brains were removed and microglia & microtubulin count were scored. Microtubulin count were 54.3; 48.1; 39.25; 25.85; 15.65 (CI 95%) respectively. Microglia count were 9,75; 23.95; 32.5;44.4;58.35 (CI 95%) respectively. It could be conclude that methylmercury chloride exposure will decrease microtubulin count in an inverse dose relationship whereas microglia count will increase in dose dependent manner.
"The persistent alterations of brain opioid systems ensuing from early life exposure to THIM is just one element of a plethora of neurodevelopmental pathologies induced by this mercurial in animals and humans [6–9, 11]. Its harmful effects are likely to be augmented by other vaccine adjuvants, such as aluminum, formaldehyde or antibiotics, and by various environmental toxins [31, 43, 44]. Particularly aluminum compounds, added to vaccines to augment their immunogenicity, have been shown to synergistically potentiate THIM’s neurotoxicity . "
[Show abstract][Hide abstract] ABSTRACT: Thimerosal added to some pediatric vaccines is suspected in pathogenesis of several neurodevelopmental disorders. Our previous study showed that thimerosal administered to suckling rats causes persistent, endogenous opioid-mediated hypoalgesia. Here we examined, using immunohistochemical staining technique, the density of μ-opioid receptors (MORs) in the brains of rats, which in the second postnatal week received four i.m. injections of thimerosal at doses 12, 240, 1,440 or 3,000 μg Hg/kg. The periaqueductal gray, caudate putamen and hippocampus were examined. Thimerosal administration caused dose-dependent statistically significant increase in MOR densities in the periaqueductal gray and caudate putamen, but decrease in the dentate gyrus, where it was accompanied by the presence of degenerating neurons and loss of synaptic vesicle marker (synaptophysin). These data document that exposure to thimerosal during early postnatal life produces lasting alterations in the densities of brain opioid receptors along with other neuropathological changes, which may disturb brain development.
Neurochemical Research 11/2010; 35(11):1840-7. DOI:10.1007/s11064-010-0250-z · 2.59 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The autism spectrum disorders are a group of conditions with neurobehavioral impairment affecting approximately 0.6% of children. The clinical presentation is complex and the etiology is largely unknown, although a major role of genetic factors is widely accepted. A number of genetic studies led to the identification of genes and/or copy number variants whose alterations are associated with autism, but no specific factor has been found so far to be responsible for a substantial proportion of cases. Epigenetic modifications may also play a role, as demonstrated by the occurrence of autism in genetic conditions caused by mutations in imprinted genes or regions.
The article by Gregory et al. published this month in BMC Medicine, reports on genomic and epigenetic alterations of OXTR, the gene encoding the receptor for oxytocin. The involvement of this gene was suggested by its deletion in an autistic patient. The subsequent analysis of a group of unrelated autistic subjects did not show an OXTR deletion, but rather hypermethylation of the gene promoter, with a reduced mRNA expression.
These findings address two major points of the current debate on the etiology and pathogenesis of autism: the role of oxytocin, known to be involved in modeling human behavior, and the possible involvement of epigenetic mechanisms. The nature of this epigenetic dysregulation is unknown but, if proved to be true, might explain the failure to identify sequence alterations in a host of candidate genes. Practical implications of these findings may be forthcoming, however not before extension and validation on a larger scale have confirmed their value.
See the associated research paper by Gregory et al:
BMC Medicine 10/2009; 7(1):63. DOI:10.1186/1741-7015-7-63 · 7.25 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.