The DOI matches its Crossref record.
BRAIN, SKELETAL MUSCLE AND PLATELET HOMOGENATE MITOCHONDRIAL FUNCTION IN PARKINSON'S DISEASE
Abstract
The recent discovery of mitochondrial complex I deficiency in the substantia nigra of patients with idiopathic Parkinson's disease has provided new understanding into the possible mechanisms that may underlie this neurodegenerative disorder. The biochemical defect is identical to that induced in humans, primates and mice exposed to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. We have studied mitochondrial respiratory chain function in various brain regions, in skeletal muscle and in blood platelets from patients with idiopathic Parkinson's disease and from matched controls. We provide evidence suggesting that the complex I deficiency in Parkinson's disease is limited to the brain and that this defect is specific for the substantia nigra. The tissue specificity of the complex I deficiency in Parkinson's disease and its localization to the substantia nigra support the proposition that complex I deficiency may be directly involved in the cause of dopaminergic cell death in Parkinson's disease. An understanding of the molecular basis of this biochemical defect will provide valuable insight into the cause of Parkinson's disease. Our findings of normal mitochondrial function in platelet homogenates suggests that this tissue cannot be used to develop a 'diagnostic test' for Parkinson's disease.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“An impairment of mitochondrial complex-I activity has been observed in the substantia nigra (SN), platelets, and skeletal muscle of PD patients 1, 9-13, in some but not in all studies14, 15.”
From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [14]
Citations
Cited by
Sorted by citations
Chronic systemic pesticide exposure reproduces features of Parkinson's disease
Betarbet, R. S., Sherer, T., MacKenzie, G. M., Garcia‐Osuna, M., Panov, A. V., & Greenamyre, J. T. (2000) · Nature Neuroscience · doi:10.1038/81834 · Cited by 3,770
Lang, A. E., & Lozano, A. M. (1998) · New England Journal of Medicine · doi:10.1056/nejm199810083391506 · Cited by 2,072
Mitochondria in the aetiology and pathogenesis of Parkinson's disease
Schapira, A. H. (2008) · The Lancet Neurology · doi:10.1016/s1474-4422(07)70327-7 · Cited by 883
Self-citationMcLelland, G., Soubannier, V., Chen, C. X., McBride, H. M., & Fon, E. A. (2014) · The EMBO Journal · doi:10.1002/embj.201385902 · Cited by 743
“In the time-course experiment, cells were treated with DMSO, 25 lM antimycin A, 25 lM antimycin A and 10 lM oligomycin, 25 lM antimycin A and 50 lM EUK134, and 20 lM CCCP for the indicated time prior to fixation.”
MethodResultThe Role of Excitotoxicity in Neurodegenerative Disease
Doble, A. (1999) · Pharmacology & Therapeutics · doi:10.1016/s0163-7258(98)00042-4 · Cited by 723
Metadata
- Authors
- MANN, V. M., COOPER, J. M., KRIGE, D., DANIEL, S. E., SCHAPIRA, A. H. V., & MARSDEN, C. D.
- Affiliations
- The Royal Free Hospital (GB)
- Parkinson's UK (GB)
- UCL Queen Square Institute of Neurology (GB)
- Corresponding author
- MANN, V. M.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 1992
- Volume
- 115
- Issue
- 2
- Pages
- 333-342
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2016905315
- Cited by
- 346
- References
- 0
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 2 · 2023: 4 · 2022: 7 · 2021: 6 · 2020: 9 · 2019: 4 · 2018: 11 · 2017: 11 · 2016: 8 · 2015: 10 · 2014: 6 · 2013: 9 · 2012: 14
- FWCI
- 14.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Eisai
- Medical Research Council
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Keywords
- Parkinson's disease, mitochondrial complex I deficiency, substantia nigra, mitochondrial respiratory chain, MPTP, dopaminergic neuron loss, skeletal muscle mitochondria, platelet mitochondria, tissue specificity, diagnostic testing
- MeSH terms
- Aged, Blood Platelets, Brain, Histocytochemistry, Humans, Middle Aged, Mitochondria, Mitochondria, Muscle, Parkinson Disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
