![]() This hypothesis is largely derived from preclinical studies demonstrating that OPs trigger neuroinflammatory responses, and from clinical and preclinical data implicating neuroinflammation in the pathogenesis of neurological diseases with phenotypic outcomes similar to those associated with neurotoxic OP exposures. ![]() It is widely posited that neuroinflammation contributes, at least in part, to the neurotoxic effects of OPs. However, multiple lines of evidence suggest that mechanisms in addition to or other than AChE inhibition contribute to the long-term effects associated with acute OP intoxication and to neurobehavioral deficits linked to repeated, subclinical OP exposures. The canonical mechanism of OP neurotoxicity is inhibition of acetylcholinesterase (AChE). ![]() Organophosphates (OPs) are a group of synthetic compounds that are neurotoxic in humans and preclinical models. Lein, in Advances in Neurotoxicology, 2019 Abstract ![]()
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