Neurotoxins, parkinsonism and Parkinson's disease
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Cited by (66)
PINK1 and Parkin: The odd couple
2020, Neuroscience ResearchMethamphetamine use and future risk for Parkinson's disease: Evidence and clinical implications
2018, Drug and Alcohol DependenceCitation Excerpt :Thus, smoking nicotine may attenuate MA-induced neurotoxic effects and reduce the likelihood of later development of parkinsonism. Potential individual-level modulators include male gender, Hispanic ethnicity, exposure to neurotoxins, comorbid physical illness such as HIV (associated with parkinsonism-like symptoms) or psychiatric illnesses and their treatments (Langston et al., 1987; Tse et al., 2004; Van Den Eeden et al., 2003). Several case reports of drug-induced PD/parkinsonism have been reported in men aged below 45 years treated on antipsychotic treatment who were also taking prescribed or illicit amphetamines (Matthew and Gedzior, 2015; Tcheremissine and Englert, 2013).
Environmental Exposures and Risks for Parkinson's Disease
2015, Environmental Factors in Neurodevelopmental and Neurodegenerative DisordersAntiparkinson's and free radical scavenging study of ethyl acetate fraction of ethanolic extract of Leucas lanata
2013, Drug Invention TodayCitation Excerpt :There will be formation and deposition of intracellular eosinophilic insoluble cytoplasmic inclusion designated as lewy bodies, as well as dystrophic thread like insoluble neuritis called as lewy neuritis.2 Several pathogenic mechanisms were proposed for PD and major include, oxidative stress and free radical formation,3 mitochondrial dysfunction,4 neurotoxin,5 and neuronal excitotoxicity.6 Among all, oxidative stress and excessive free radical formation produced as a result of mitochondrial dysfunction considered as primary contributor in the pathogenesis of PD.
Solvents and Parkinson disease: A systematic review of toxicological and epidemiological evidence
2013, Toxicology and Applied PharmacologyCitation Excerpt :To date, there is no animal model that can faithfully recapitulate all aspects of human PD. The most widely used models, are MPTP (Langston et al., 1987) and 6-hydroxydopamine (6-OHDA) (Blandini et al., 2008), which reproducibly yield nigral neuronal loss. Because rodents do not have pigments in nigral neurons, neuronal loss is typically assessed after tyrosine hydroxylase immunoreactivity (TH+).
Apparent opposite effects of tetrabenazine and reserpine on the toxic effects of 1-methyl-4-phenylpyridinium or 6-hydroxydopamine on nigro-striatal dopaminergic neurons
2003, Brain ResearchCitation Excerpt :6-OHDA, as a hydroxylated analogue of dopamine shares common structural features, which may explain its uptake in catecholaminergic neurons by plasma membrane catecholamine transporters [2]. The main toxicity of 6-OHDA originates from its ability to produce radical oxygen species (superoxide, hydroxyl radicals) and hydrogen peroxide (H2O2), which are toxic for neurons [37,21,18]. MPTP is a powerful toxin which produces a syndrome with striking similarities to PD [41].