A rapid thaw, 1607

Terry, F. C. Birkbeck

doi:10.1093/nq/s6-v.123.355h

Cited by 1 publication

(2 citation statements)

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“…Furthermore, AD has also been associated with all these pathological processes thus linking AD and OPPs exposure. [ 17,154 ]…”

Section: Effect Of Opps On Glial Cellsmentioning

confidence: 99%

“…Furthermore, it triggers toxicity signs like involuntary movements, respiratory depression (that could lead to death), muscle fasciculation, and autonomic dysfunction. [ 17 ] There are several other important mechanisms that are believed to be inhibited or interrupted by repeated OPPs exposure, which may be significant in contributing to AD pathology. Some of them are the 5‐ Hydroxytryptamine system (5‐HT system), which plays a role in mood disorder etiology, axonal transport deficit, neurotrophins, and so forth.…”

Section: Introductionmentioning

confidence: 99%

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Implications of organophosphate pesticides on brain cells and their contribution toward progression of Alzheimer's disease

Yadav,

Kaur,

Yadav

et al. 2024

J Biochem & Molecular Tox

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The most widespread neurodegenerative disorder, Alzheimer's disease (AD) is marked by severe behavioral abnormalities, cognitive and functional impairments. It is inextricably linked with the deposition of amyloid β (Aβ) plaques and tau protein in the brain. Loss of white matter, neurons, synapses, and reactive microgliosis are also frequently observed in patients of AD. Although the causative mechanisms behind the neuropathological alterations in AD are not fully understood, they are likely influenced by hereditary and environmental factors. The etiology and pathogenesis of AD are significantly influenced by the cells of the central nervous system, namely, glial cells and neurons, which are directly engaged in the transmission of electrical signals and the processing of information. Emerging evidence suggests that exposure to organophosphate pesticides (OPPs) can trigger inflammatory responses in glial cells, leading to various cascades of events that contribute to neuroinflammation, neuronal damage, and ultimately, AD pathogenesis. Furthermore, there are striking similarities between the biomarkers associated with AD and OPPs, including neuroinflammation, oxidative stress, dysregulation of microRNA, and accumulation of toxic protein aggregates, such as amyloid β. These shared markers suggest a potential mechanistic link between OPP exposure and AD pathology. In this review, we attempt to address the role of OPPs on altered cell physiology of the brain cells leading to neuroinflammation, mitochondrial dysfunction, and oxidative stress linked with AD pathogenesis.

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“…Furthermore, AD has also been associated with all these pathological processes thus linking AD and OPPs exposure. [ 17,154 ]…”

Section: Effect Of Opps On Glial Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%