ArticleNeurotoxicity research2009
Molecular and neurochemical mechanisms in PD pathogenesis.
Article in Neurotoxicity research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Combined enrichment of neuromelanin granules and synaptosomes from human substantia nigra pars compacta tissue for proteomic analysis.Journal of proteomics · 2013Trial
- The Catecholaldehyde Hypothesis for the Pathogenesis of Catecholaminergic Neurodegeneration: What We Know and What We Do Not Know.International journal of molecular sciences · 2021Review
- The "Sick-but-not-Dead" Phenomenon Applied to Catecholamine Deficiency in Neurodegenerative Diseases.Seminars in neurology · 2020Review
- Review
- The catecholaldehyde hypothesis: where MAO fits in.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- 3,4-Dihydroxyphenylacetaldehyde Is More Efficient than Dopamine in Oligomerizing and QuinonizingThe Journal of pharmacology and experimental therapeutics · 2020Article
- Epigenetic Regulatory Mechanisms Induced by Resveratrol.Nutrients · 2017Review
- Lack of additive role of ageing in nigrostriatal neurodegeneration triggered by α-synuclein overexpression.Acta neuropathologica communications · 2015Article
- DT-Diaphorase Prevents Aminochrome-Induced Alpha-Synuclein Oligomer Formation and Neurotoxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- One-electron reduction of 6-hydroxydopamine quinone is essential in 6-hydroxydopamine neurotoxicity.Neurotoxicity research · 2013Article
- Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.Movement disorders : official journal of the Movement Disorder Society · 2013Review
- Autophagy protects against aminochrome-induced cell death in substantia nigra-derived cell line.Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
- Lipid-mediated oxidative stress and inflammation in the pathogenesis of Parkinson's disease.Parkinson's disease · 2011Article
- Aminochrome induces disruption of actin, alpha-, and beta-tubulin cytoskeleton networks in substantia-nigra-derived cell line.Neurotoxicity research · 2010Article
Corrections and comments
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Oxidation of dopamine to aminochrome seems to be a normal process leading to aminochrome polymerization to form neuromelanin, since normal individuals have this pigment in their dopaminergic neurons in the substantia nigra. The neurons lost in individuals with Parkinson's disease are dopaminergic neurons containing neuromelanin. This raises two questions. First, why are those cells containing neuromelanin lost in this disease? Second, what is the identity of the neurotoxin that induces this cell death? We propose that aminochrome is the agent responsible for the death of dopaminergic neurons containing neuromelanin in individuals with Parkinson's disease. The normal oxidative pathway of dopamine, in which aminochrome polymerizes to form neuromelanin, can be neurotoxic if DT-diaphorase is inhibited under certain conditions. Inhibition of DT-diaphorase allows two neurotoxic reactions to proceed: (i) the formation of aminochrome adducts with alpha-synuclein, which induce and stabilize the formation of neurotoxic protofibrils; and (ii) the one electron reduction of aminochrome to the neurotoxic leukoaminochrome o-semiquinone radical. Therefore, we propose that DT-diaphorase is an important neuroprotective enzyme in dopaminergic neurons containing neuromelanin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.