ArticleExperimental neurology2015
Neuroprotective effects of aldehyde dehydrogenase 2 activation in rotenone-induced cellular and animal models of parkinsonism.
Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 87 citations in OpenAlex.
- Metabolic trajectories in developing human neocortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Putamen dopamine synthesis, vesicular storage, and metabolism in Parkinson disease.medRxiv : the preprint server for health sciences · 2026Article
- Amyloid-β and Tau in Alzheimer's disease: pathogenesis, mechanisms, and interplay.Cell death & disease · 2026Review
- ALDH2 protects against dopaminergic neuronal cell ferroptosis by enhancing the enzyme activity of PRDX6 in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Oenological tannins mitigate rotenone-induced mitochondrial impairments and oxidative stress, with concomitant detection of urolithin A in the brain.Biochemistry and biophysics reports · 2025Article
- Lessons learned from aldehyde dehydrogenases as non-P450 aldehyde-oxidizing enzymes: implications for the 'exposome' and human health.Expert opinion on drug metabolism & toxicology · 2025Review
- Review
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- Molecular and Cellular Interactions in Pathogenesis of Sporadic Parkinson Disease.International journal of molecular sciences · 2022Review
- The epigenetic mechanisms involved in mitochondrial dysfunction: Implication for Parkinson's disease.Brain pathology (Zurich, Switzerland) · 2022Review
- TheBiology of sport · 2022Article
- The rat rotenone model reproduces the abnormal pattern of central catecholamine metabolism found in Parkinson's disease.Disease models & mechanisms · 2022Article
- Integrated Brain Metabolomics and Network Pharmacology Analysis to Reveal the Improvement Effect of Bai Chan Ting on Parkinson's Disease.BioMed research international · 2022Article
- The NRF2-Dependent Transcriptional Regulation of Antioxidant Defense Pathways: Relevance for Cell Type-Specific Vulnerability to Neurodegeneration and Therapeutic Intervention.Antioxidants (Basel, Switzerland) · 2021Review
- Aldehyde dehydrogenase 2 protects against acute kidney injury by regulating autophagy via the Beclin-1 pathway.JCI insight · 2021Article
- Neurotoxin-Induced Rodent Models of Parkinson's Disease: Benefits and Drawbacks.Neurotoxicity research · 2021Review
- The Catecholaldehyde Hypothesis for the Pathogenesis of Catecholaminergic Neurodegeneration: What We Know and What We Do Not Know.International journal of molecular sciences · 2021Review
- Multifactoriality of Parkinson's Disease as Explored Through Human Neural Stem Cells and Their Transplantation in Middle-Aged Parkinsonian Mice.Frontiers in pharmacology · 2021Article
- "Sick-but-not-dead": multiple paths to catecholamine deficiency in Lewy body diseases.Stress (Amsterdam, Netherlands) · 2020Review
- Article
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12 authors at 3 institutions in 2 countries.
Funding
Abstract
Many studies have shown that mitochondrial aldehyde dehydrogenase 2 (ALDH2) functions as a cellular protector against oxidative stress by detoxification of cytotoxic aldehydes. Within dopaminergic neurons, dopamine is metabolized by monoamine oxidase to yield 3,4-dihydroxyphenylacetaldehyde (DOPAL) then converts to a less toxic acid product by ALDH. The highly toxic and reactive DOPAL has been hypothesized to contribute to the selective neurodegeneration in Parkinson's disease (PD). In this study, we investigated the neuroprotective mechanism and therapeutic effect of ALDH2 in rotenone models for parkinsonism. Overexpression of wild-type ALDH2 gene, but not the enzymatically deficient mutant ALDH2*2 (E504K), reduced rotenone-induced cell death. Application of a potent activator of ALDH2, Alda-1, was effective in protecting against rotenone-induced apoptotic cell death in both SH-SY5Y cells and primary cultured substantia nigra (SN) dopaminergic neurons. In addition, intraperitoneal administration of Alda-1 significantly reduced rotenone- or MPTP-induced death of SN tyrosine hydroxylase (TH)-positive dopaminergic neurons. The attenuation of rotenone-induced apoptosis by Alda-1 resulted from decreasing ROS accumulation, reversal of mitochondrial membrane potential depolarization, and inhibition of activation of proteins related to mitochondrial apoptotic pathway. The present study demonstrates that ALDH2 plays a crucial role in maintaining normal mitochondrial function to protect against neurotoxicity and that Alda-1 is effective in ameliorating mitochondrial dysfunction and inhibiting mitochondria-mediated apoptotic pathway. These results indicate that ALDH2 activation could be a neuroprotective therapy for PD.
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