ReviewNeurochemical research2004
Initiation of neuronal damage by complex I deficiency and oxidative stress in Parkinson's disease.
Review in Neurochemical research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 198 citations in OpenAlex.
- Parkinson's Disease: From Metabolism to Genetics-A Comprehensive Review.Current issues in molecular biology · 2026Review
- Regulatory role of the circHIPK3/miR-125a-5p/NDUFA5 axis in diabetic retinopathy: combined analysis of single-cell and bulk transcriptomes.American journal of translational research · 2026Article
- From Obesity to Mitochondrial Dysfunction in Peripheral Tissues and in the Central Nervous System.Biomolecules · 2025Review
- Article
- The Role of Magnesium in Parkinson's Disease: Status Quo and Implications for Future Research.International journal of molecular sciences · 2024Review
- Contrasting consequences of podocyte insulin-like growth factor 1 receptor inhibition.iScience · 2024Article
- GUCY2C signaling limits dopaminergic neuron vulnerability to toxic insults.NPJ Parkinson's disease · 2024Article
- Review
- Mitochondrial Dysfunction and Parkinson's Disease: Pathogenesis and Therapeutic Strategies.Neurochemical research · 2023Review
- Monoterpenoid Epoxidiol Ameliorates the Pathological Phenotypes of the Rotenone-Induced Parkinson's Disease Model by Alleviating Mitochondrial Dysfunction.International journal of molecular sciences · 2023Article
- Metabolic Features of Brain Function with Relevance to Clinical Features of Alzheimer and Parkinson Diseases.Molecules (Basel, Switzerland) · 2022Review
- Exosome Release Is Modulated by the Mitochondrial-Lysosomal Crosstalk in Parkinson's Disease Stress Conditions.Molecular neurobiology · 2021Article
- Polymerized Whey Protein Concentrate-Based Glutathione Delivery System: Physicochemical Characterization, Bioavailability and Sub-Chronic Toxicity Evaluation.Molecules (Basel, Switzerland) · 2021Article
- Control of Reactive Oxygen Species for the Prevention of Parkinson's Disease: The Possible Application of Flavonoids.Antioxidants (Basel, Switzerland) · 2020Review
- Cannabinoids: A New Perspective on Epileptogenesis and Seizure Treatment in Early Life in Basic and Clinical Studies.Frontiers in behavioral neuroscience · 2020Article
- Purinergic Signalling in Parkinson's Disease: A Multi-target System to Combat Neurodegeneration.Neurochemical research · 2019Review
- Transcriptome profiles of hypothalamus and adrenal gland linked to haplotype related to coping behavior in pigs.Scientific reports · 2019Article
- Enzymatic synthesis of selenium-containing amphiphilic aliphatic polycarbonate as an oxidation-responsive drug delivery vehicle.RSC advances · 2019Article
- Salidroside Protects Dopaminergic Neurons by Preserving Complex I Activity via DJ-1/Nrf2-Mediated Antioxidant Pathway.Parkinson's disease · 2019Article
- Pinocembrin Suppresses HMolecular neurobiology · 2018Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress and partial deficiencies of mitochondrial complex I appear to be key factors in the pathogenesis of Parkinson's disease. They are interconnected; complex I inhibition results in an enhanced production of reactive oxygen species (ROS), which in turn will inhibit complex I. Partial inhibition of complex I in nerve terminals is sufficient for in situ mitochondria to generate more ROS. H2O2 plays a major role in inhibiting complex I as well as a key metabolic enzyme, alpha-ketoglutarate dehydrogenase. The vicious cycle resulting from partial inhibition of complex I and/or an inherently higher ROS production in dopaminergic neurons leads over time to excessive oxidative stress and ATP deficit that eventually will result in cell death in the nigro-striatal pathway.
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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.