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Cited by 435Parkinson's Disease Mechanisms and TreatmentsMitochondrial Function and PathologyCoenzyme Q10 studies and effects

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

Haas, Richard H., Nasirian, Fatemeh, Nakano, Kazutoshi, Ward, David, Pay, Mary, Hill, Robert, Shults, Clifford W.·1995·Annals of Neurology
DOI 10.1002/ana.410370604
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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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  1. Lang AET, 1989, Quantification of neurological deficit, 289

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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)
ORCID
Venue
Annals of Neurology
Publisher
Wiley
Published
1995-06
Volume
37
Issue
6
Pages
714-722
ISSN
  • 0364-5134 (ISSN-L)
  • 1531-8249
DOI
10.1002/ana.410370604
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
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 3417 d)
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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