The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
Low platelet mitochondrial complex I and complex II/III activity in early untreated parkinson's disease
Abstract
Following the discovery of inhibition of electron transport complex I by the neurotoxin 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP), which produces a parkinsonian syndrome in humans, monkeys, and mice, several laboratories have reported abnormalities of complex I and other electron transport complexes (ETCs) in various tissues from patients with Parkinson's disease (PD). Criticism of the significance of these findings in the etiology of PD has centered on whether drug treatments or the debilitation of the disease process itself produced the low ETC activities. We present results from a blinded study of platelet mitochondrial ETC activities in 18 early untreated PD patients and 18 age‐ and sex‐matched controls and in 13 spousal controls. Lower complex I activity in platelet mitochondria of PD patients was seen in early untreated disease and thus cannot be due to debilitation or drug therapy. Home environmental factors seem an unlikely explanation for the reduced complex I activity in PD patients but have not been excluded. Complex II/III activity was also reduced by 20% in PD compared with age‐/sex‐matched controls. The low complex I and II/III activities in platelet mitochondria appear to be related to the etiology of PD.
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“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 [9]
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Metadata
- Authors
- Haas, R. H., Nasirian, F., Nakano, K., Ward, D., Pay, M., Hill, R., & Shults, C. W.
- Affiliations
- University of California San Diego (US)
- Veterans Health Administration (US)
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 1995-06
- Volume
- 37
- Issue
- 6
- Pages
- 714-722
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2112777355
- Cited by
- 435
- References
- 47
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 6 · 2023: 9 · 2022: 14 · 2021: 14 · 2020: 19 · 2019: 23 · 2018: 13 · 2017: 18 · 2016: 8 · 2015: 22 · 2014: 9 · 2013: 15 · 2012: 11
- FWCI
- 7.62
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ns029504-03)
- National Institute of Neurological Disorders and Stroke (R01 NS29504)
- 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, platelet mitochondria, mitochondrial electron transport chain, complex I, MPTP, etiology, mitochondrial dysfunction
- MeSH terms
- Adult, Aged, Blood Platelets, Citrate (si)-Synthase, Female, Humans, Male, Middle Aged, Mitochondria, Multienzyme Complexes, Oxidoreductases, Parkinson Disease, Smoking, Succinate Dehydrogenase, Electron Transport Complex III, NAD(P)H Dehydrogenase (Quinone), Electron Transport Complex II
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