CommentaryGlutamate, excitotoxicity, and programmed cell death in parkinson disease
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2020, Environmental PollutionCitation Excerpt :Therefore, we conclude that EVs are the primary instigator in facilitating GLS1 release and neurotoxicity in PM2.5-activated microglia. Excessive glutamate generation by glutaminase causes neurotoxicity and has been linked to many neurological diseases, including AD (Hynd et al., 2004), PD (Caudle and Zhang, 2009), and HIV-1-associated neurocognitive disorders (Zhao et al., 2004). Indeed, patients with PD, AD, or other neuronal diseases presented the elevated glutamate levels produced by microglia or macrophages (Wu et al., 2015).
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2017, Pharmacological ResearchCitation Excerpt :Another similarity between Alzheimer’s and Parkinson’s disease is the demonstrated increased brain AT1 receptor activity in animal models of aging with their associated dopamine vulnerability and Parkinson’s disease. In these models, excessive AT1 activation was associated with dopaminergic cell injury, a hallmark of Parkinson’s disease [102–123]. Consequently, ARB administration ameliorated dopaminergic cell death, reduced motor deficiencies, protected rodents from neurotoxin induced Parkinson’s disease, and ameliorated the pathological manifestations characteristic of aging, cerebral hypoperfusion and menopause, major risk factors in Parkinson’s disease.