ReviewNeural regeneration research2017
On the role of endogenous neurotoxins and neuroprotection in Parkinson's disease.
Review in Neural regeneration research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- A tardive dyskinesia drug target VMAT-2 participates in neuronal process elongation.Scientific reports · 2025Article
- Negative Association of Cognitive Performance With Blood Serum Neurotoxicity and Its Modulation by Human Herpes Virus 5 (HHV5) Seropositivity in Healthy Women.Neuroscience insights · 2024Article
- Protective Effects of Flavonoid Rutin Against Aminochrome Neurotoxicity.Neurotoxicity research · 2023Article
- Aminochrome Induces Neuroinflammation and Dopaminergic Neuronal Loss: A New Preclinical Model to Find Anti-inflammatory and Neuroprotective Drugs for Parkinson's Disease.Cellular and molecular neurobiology · 2023Article
- Role of Microgliosis and NLRP3 Inflammasome in Parkinson's Disease Pathogenesis and Therapy.Cellular and molecular neurobiology · 2022Review
- Empagliflozin attenuates neurodegeneration through antioxidant, anti-inflammatory, and modulation of α-synuclein and Parkin levels in rotenone-induced Parkinson's disease in rats.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022Article
- Dopaminergic Axons: Key Recitalists in Parkinson's Disease.Neurochemical research · 2022Review
- Neuroprotection against Aminochrome Neurotoxicity: Glutathione Transferase M2-2 and DT-Diaphorase.Antioxidants (Basel, Switzerland) · 2022Review
- Neurotoxicity and Underlying Mechanisms of Endogenous Neurotoxins.International journal of molecular sciences · 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
- Cellular Trafficking of Glutathione Transferase M2-2 Between U373MG and SHSY-S7 Cells is Mediated by Exosomes.Neurotoxicity research · 2021Article
- The "Sick-but-not-Dead" Phenomenon Applied to Catecholamine Deficiency in Neurodegenerative Diseases.Seminars in neurology · 2020Review
- 3,4-Dihydroxyphenylacetaldehyde Is More Efficient than Dopamine in Oligomerizing and QuinonizingThe Journal of pharmacology and experimental therapeutics · 2020Article
- The catecholaldehyde hypothesis: where MAO fits in.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Implications of alpha-synuclein nitration at tyrosine 39 in methamphetamine-induced neurotoxicityNeural regeneration research · 2019Article
- Novel Alpha-Synuclein Oligomers Formed with the Aminochrome-Glutathione Conjugate Are Not Neurotoxic.Neurotoxicity research · 2019Article
- Protective Effects of Crude Plant Extracts against Aminochrome-induced toxicity in Human Astrocytoma Cells: Implications for Parkinson's Disease.Clinical pharmacology and translational medicine · 2019Article
- On the Role of Aminochrome in Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Parkinson's Disease.Frontiers in neuroscience · 2019Article
- Overexpression of Vesicular Monoamine Transporter-2 may Block Neurotoxic Metabolites from Cytosolic Dopamine: a Potential Neuroprotective Therapy for Parkinson's Disease.Clinical pharmacology and translational medicine · 2019Article
- Neurotoxins as Preclinical Models for Parkinson's Disease.Neurotoxicity research · 2018Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For 50 years ago was introduced L-3,4-dihydroxyphenylalanine (L-dopa) in Parkinson's disease treatment and during this significant advances has been done but what trigger the degeneration of the nigrostriatal system remain unknown. There is a general agreement in the scientific community that mitochondrial dysfunction, protein degradation dysfunction, alpha-synuclein aggregation to neurotoxic oligomers, neuroinflammation, oxidative and endoplasmic reticulum stress are involved in the loss of dopaminergic neurons containing neuromelanin in Parkinson's disease. The question is what triggers these mechanisms. The age of normal onset in idiopathic Parkinson's disease suggests that environmental factors such as metals, pollutants or genetic mutations cannot be involved because these factors are related to early onset of Parkinsonism. Therefore, we have to search for endogenous neurotoxins and neuroprotection in order to understand what trigger the loss of dopaminergic neurons. One important feature of Parkinson's disease is the rate of the degenerative process before the motor symptoms are evident and during the disease progression. The extremely slow rate of Parkinson's disease suggests that the neurotoxins and the neuroprotection have to be related to dopamine metabolism. Possible candidates for endogenous neurotoxins are alpha-synuclein neurotoxic oligomers, 4-dihydroxyphenylacetaldehyde and ortho-quinones formed during dopamine oxidation to neuromelanin. Vesicular monoamine transporter-2, DT-diaphorase and glutathione transferase M2-2 seems to be the most important neuroprotective mechanism to prevent neurotoxic mechanism during dopamine oxidation.
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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.