ArticleToxicology research2018
Role of GSK3β/α-synuclein axis in methamphetamine-induced neurotoxicity in PC12 cells.
Article in Toxicology research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Molecular mechanisms of programmed cell death in methamphetamine-induced neuronal damage.Frontiers in pharmacology · 2022Pooled it
- Bioinformatics-driven untargeted metabolomic profiling for clinical screening of methamphetamine abuse.Forensic toxicology · 2025Article
- The dual role of glycogen synthase kinase-3 beta (GSK3β) in neurodegenerative pathologies: interplay between autophagy and disease progression.Frontiers in pharmacology · 2025Review
- Distinct Hippocampal Expression Profiles of lncRNAs in Obese Type 2 Diabetes Mice Exhibiting Cognitive Impairment.Neuromolecular medicine · 2024Article
- Corydaline alleviates Parkinson's disease by regulating autophagy and GSK-3β phosphorylation.Psychopharmacology · 2024Article
- Key roles of autophagosome/endosome maturation mediated by Syntaxin17 in methamphetamine-induced neuronal damage in mice.Molecular medicine (Cambridge, Mass.) · 2024Article
- The Common Denominators of Parkinson's Disease Pathogenesis and Methamphetamine Abuse.Current neuropharmacology · 2024Review
- Nanowired Delivery of Mesenchymal Stem Cells with Antioxidant Compound H-290/51 Reduces Exacerbation of Methamphetamine Neurotoxicity in Hot Environment.Advances in neurobiology · 2023Article
- Autophagy and Its Association with Genetic Mutations in Parkinson Disease.Medical science monitor : international medical journal of experimental and clinical research · 2022Review
- Dopamine D1 receptors mediate methamphetamine-induced dopaminergic damage: involvement of autophagy regulation via the AMPK/FOXO3A pathway.Psychopharmacology · 2022Article
- Neurotoxicity of methamphetamine: Main effects and mechanisms.Experimental neurology · 2021Review
- The Role of α-Synuclein in Methamphetamine-Induced Neurotoxicity.Neurotoxicity research · 2021Review
- Methamphetamine leads to the alterations of microRNA profiles in the nucleus accumbens of rats.Pharmaceutical biology · 2020Article
- 25C-NBOMe, a Novel Designer Psychedelic, Induces Neurotoxicity 50 Times More Potent Than Methamphetamine In Vitro.Neurotoxicity research · 2019Article
- Tea Polyphenols Attenuate Methamphetamine-Induced Neuronal Damage in PC12 Cells by Alleviating Oxidative Stress and Promoting DNA Repair.Frontiers in physiology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methamphetamine (METH) is well-known as a potent psychostimulant of abuse worldwide. METH administration can cause neurotoxicity and neurodegenerative injury, which are similar to the two prevalent neurodegenerative disorders Alzheimer's disease (AD) and Parkinson's disease (PD). Recent results suggested that METH exposure increased the level of α-synuclein (α-syn) that could be a possible cause of neurotoxicity. However, the mechanism of METH-induced neurodegeneration remains unclear. This study was aimed at examining the effects of glycogen synthase kinase3β (GSK3β), α-syn, and tau on METH-induced neurotoxicity. Our results indicated that P-GSK3β (Tyr216), P-Tau (Ser396), α-syn, and P-α-syn (Ser129) levels were increased after METH administration in dose- and time-dependent manners. Upon inhibiting the GSK3β activity with LiCl or GSK3β-siRNA, these protein expressions were significantly decreased. We observed that LiCl protected the cells from METH-caused cytotoxicity by weakening the cell morphological damage and preventing cell apoptosis and death. We also found that P-GSK3β colocalized with P-Tau and α-syn by the immunofluorescence method. Further, METH disrupted the cellular autophagy by upregulation of LC3-II and P62 proteins, and the cellular autophagy was restored by LiCl and GSK3β-siRNA. The expressions of the α-syn-specific degradative enzyme glucocerebrosidase (GCase) with its regulator lysosomal integral membrane protein type-2 (LIMP-2) decreased inversely with the doses of METH treatment. The GCase inhibitor conduritol-β-epoxide (CβE) increased the α-syn levels, and LiCl restored GCase and LIMP-2 expressions disrupted by the METH treatment. In summary, we conclude that GSK3β plays key roles in METH-induced neurotoxicity and neurodegenerative injury by promoting abnormal protein phosphorylation and α-syn accumulation, blocking the autophagy-lysosomal degradation pathway, and finally leading to cell apoptosis and death. GSK3β may be a potential target to prevent METH-induced neurodegeneration.
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Registered trials
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