ReviewAmerican journal of human genetics1998
Mitochondrial dysfunction in idiopathic Parkinson disease.
Review in American journal of human genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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Who cites it
37 citing papers in PubMed.
- Microbial Metabolism of Levodopa as an Adjunct Therapeutic Target in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- Mitophagy Upregulation Occurs Early in the Neurodegenerative Process Mediated by α-Synuclein.Molecular neurobiology · 2024Article
- Restricting α-synuclein transport into mitochondria by inhibition of α-synuclein-VDAC complexation as a potential therapeutic target for Parkinson's disease treatment.Cellular and molecular life sciences : CMLS · 2022Article
- Contributions and Limitations of Mitochondria-Targeted and Non-Targeted Antioxidants in the Treatment of Parkinsonism: an Updated Review.Neurotoxicity research · 2022Review
- Deletion of DJ-1 in rats affects protein abundance and mitochondrial function at the synapse.Scientific reports · 2020Article
- Misfolded α-synuclein causes hyperactive respiration without functional deficit in live neuroblastoma cells.Disease models & mechanisms · 2020Article
- Oxidative Stress in Neurodegenerative Diseases: From a Mitochondrial Point of View.Oxidative medicine and cellular longevity · 2019Review
- Mitochondrial function and autophagy: integrating proteotoxic, redox, and metabolic stress in Parkinson's disease.Journal of neurochemistry · 2018Review
- Adverse outcome pathways: Application to enhance mechanistic understanding of neurotoxicity.Pharmacology & therapeutics · 2017Review
- Gene expression profiling of midbrain dopamine neurons upon gestational nicotine exposure.Medical & biological engineering & computing · 2017Article
- Immortalized Parkinson's disease lymphocytes have enhanced mitochondrial respiratory activity.Disease models & mechanisms · 2016Article
- Systems biology analysis of the proteomic alterations induced by MPP(+), a Parkinson's disease-related mitochondrial toxin.Frontiers in cellular neuroscience · 2015Article
- Mitochondria-targeted antioxidants for treatment of Parkinson's disease: preclinical and clinical outcomes.Biochimica et biophysica acta · 2014Review
- Bioenergetic medicine.British journal of pharmacology · 2014Review
- Ret rescues mitochondrial morphology and muscle degeneration of Drosophila Pink1 mutants.The EMBO journal · 2014Article
- Cytoplasmic hybrid (cybrid) cell lines as a practical model for mitochondriopathies.Redox biology · 2014Review
- Identification of licopyranocoumarin and glycyrurol from herbal medicines as neuroprotective compounds for Parkinson's disease.PloS one · 2014Article
- Signaling with homeoprotein transcription factors in development and throughout adulthood.Current genomics · 2013Article
- TRAP1 rescues PINK1 loss-of-function phenotypes.Human molecular genetics · 2013Article
- Neuroprotective and anti-inflammatory properties of a coffee component in the MPTP model of Parkinson's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disordered mitochondrial metabolism may play an important role in a number of idiopathic neurodegenerative disorders. The question of mitochondrial dysfunction is particularly attractive in the case of idiopathic Parkinson disease (PD), since Vyas et al. recognized in the 1980s that the parkinsonism-inducing compound N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine is a mitochondrial toxin. The unique genetic properties of mitochondria also make them worthy of consideration for a pathogenic role in PD, as well as in other late-onset, sporadic neurodegenerative disorders. Although affected persons occasionally do provide family histories that suggest Mendelian inheritance, the vast majority of the time these diseases appear sporadically. Because of unique features such as heteroplasmy, replicative segregation, and threshold effects, mitochondrial inheritance can allow for the apparent sporadic nature of these diseases.
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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.