ArticleBrain and behavior2020
Effect of Parkin on methamphetamine-induced α-synuclein degradation dysfunction in vitro and in vivo.
Article in Brain and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Increase of α-Synuclein in the Peripheral Blood of Subjects with Methamphetamine Use Disorder.Psychiatry investigation · 2025Article
- Brain dysfunctions and neurotoxicity induced by psychostimulants in experimental models and humans: an overview of recent findings.Neural regeneration research · 2024Article
- Application of clinical blood metabogram for diagnosis of early-stage Parkinson's disease: a pilot study.Frontiers in molecular biosciences · 2024Article
- An update: epigenetic mechanisms underlying methamphetamine addiction.Frontiers in cell and developmental biology · 2024Review
- Linking Heat Shock Protein 70 and Parkin in Parkinson's Disease.Molecular neurobiology · 2023Review
- Protein clearance strategies for disease intervention.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Icariside II Attenuates Methamphetamine-Induced Neurotoxicity and Behavioral Impairments via Activating the Keap1-Nrf2 Pathway.Oxidative medicine and cellular longevity · 2022Article
- Polo-Like Kinase 2: From Principle to Practice.Frontiers in oncology · 2022Review
- Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling.Oxidative medicine and cellular longevity · 2022Review
- Methamphetamine-induced dopaminergic neurotoxicity as a model of Parkinson's disease.Archives of pharmacal research · 2021Review
- Effect of Parkin on methamphetamine-induced α-synuclein degradation dysfunction in vitro and in vivo.Brain and behavior · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
introductionMethamphetamine (METH) is a psychostimulant drug with complicated neurotoxicity, and abuse of METH is very common. Studies have shown that METH exposure causes alpha-synuclein (α-syn) accumulation. However, the mechanism of α-syn accumulation has not been determined.
methodsIn this study, we established cell and animal models of METH intoxication to evaluate how METH affects α-syn expression. In addition, to explore METH-induced neurotoxicity, we measured the level of Parkin and the phosphorylation levels of α-syn, Polo-like kinase 2 (PLK2), the proteasome activity marker CD3δ, and the apoptosis-related proteins Caspase-3 and PARP. Parkin is a key enzyme in the ubiquitin-proteasome system. In addition, the effect of Parkin on METH-induced neurotoxicity was investigated by overexpressing it in vitro and in vivo.
resultsMETH exposure increased polyubiquitin and α-syn expression, as did MG132. Furthermore, the level of Parkin and the interaction between Parkin and α-syn decreased after METH exposure. Importantly, the increases in α-syn expression and neurotoxicity were relieved by Parkin overexpression.
conclusionsBy establishing stable cell lines and animal models that overexpress Parkin, we confirmed Parkin as an important factor in METH-induced α-syn degradation dysfunction in vitro and in vivo. Parkin may be a promising target for the treatment of METH-induced neurotoxicity.
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