The DOI matches its Crossref record.
Electron transfer complexes I and IV of platelets are abnormal in Parkinson's disease but normal in Parkinson-plus syndromes
Abstract
Using a technique which requires only 100 ml blood we investigated the electron transfer complexes (ETC) I, III and IV in platelet mitochondria of 44 control subjects, 27 patients with idiopathic Parkinson's disease and eight patients with Parkinson-plus syndromes due to multiple system atrophy. In both control subjects and patients, ETC measurements were repeated at intervals of several months. The activities varied considerably among normal subjects, but intra-individual variation of ETC activities were low at repetitive measurements. In normal subjects there was no correlation between enzyme activities and age or training state. There was no difference in enzyme activities between smokers and non-smokers in the control group. Complex I activity was lower in Parkinson's disease patients than in controls (14 versus 29 nmol/min/mg platelet protein; P < 0.001). Furthermore, the group difference in complex IV activity also reached statistical significance (83 versus 58 nmol/min/mg platelet protein; P < 0.001). Additionally, in some Parkinson's disease patients, activities of complex III were low and lay outside the control range, but the group difference did not reach significance. There was no correlation between complex I activity and disease duration or severity as well as the daily L-dopa dose in Parkinson's disease patients. Repeated measurements in five Parkinson's disease patients in the earliest stages of their illness demonstrated that the decrease in complex I and IV activities can develop rapidly within 1 year. In Parkinson-plus patients suffering from multiple system atrophy the ETC activities were normal.
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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 [13]
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Items 201–220 of 220
Mitochondrial Mutations in Parkinson's Disease and Dystonias
Simon, D. K. (2003) · Elsevier eBooks · doi:10.1016/b978-012566652-7/50043-5
Gautam, A. H. (2010) · Rutgers University Community Repository (Rutgers University) · doi:10.7282/t30c4vjx
Weiss, H. (1996) · VS Verlag für Sozialwissenschaften eBooks · doi:10.1007/978-3-322-98956-7_1
Self-citationThe cutting edge: apoptosis and therapeutic opportunity
Griffin, C., Gueorguieva, D., McLachlan-Burgess, A., Somayajulu‐Nitu, M., & Pandey, S. (2007) · Elsevier eBooks · doi:10.1533/9781845693077.2.117
Szalárdy, L. (2016) · SZTE Repository of Dissertations (University of Szeged) · doi:10.14232/phd.3120 · Cited by 1
“cortex [41], platelets [42, 43], and skeletal muscle [44, 45] of sporadic PD patients, suggesting a systemic impairment of mitochondrial functions in this disease.”
Background(1995) · Elsevier eBooks · doi:10.1016/b978-012165250-0/50023-4
Nutrition in Brain Aging: Its Relevance to Age-Associated Neurodegeneration
Maruyama, W., Shamoto‐Nagai, M., & Naoi, M. (2022) · Springer eBooks · doi:10.1007/978-3-319-56015-1_20-1
Nutrition in Brain Aging: Its Relevance to Age-Associated Neurodegeneration
Maruyama, W., Nagai, M. S., & Naoi, M. (2022) · Springer eBooks · doi:10.1007/978-3-030-62059-2_20 · Cited by 1
The Mechanistic Approach Involved in the Progression of Neurodegenerative Disorders
Rather, M. A., Khan, A., Alsharani, S., Jahan, S., Siddiqui, A. J., Mehan, S., & Alexiou, A. T. (2023) · Springer eBooks · doi:10.1007/978-981-99-3848-3_2
Habiba, B., & Pushkar, K. (2023) · International Journal of Zoological Investigations · doi:10.33745/ijzi.2023.v09i02.073
“Resveratrol's anti-inflammatory, antioxidant, estrogenic, and hypolipemic qualities have been linked to its neuroprotective abilities against ischemia, seizures, and Parkinson's disease (Benecke et al ., 1993; Tredici et al ., 1999; Robb and Stuart, 2010; Price et al ., 2011).”
BackgroundWill the antioxidant supplements impact the mitigation of oxidative stress in Parkinson's disease?
Kumar, D. A., Balasubramanian, B., Kathirvel, B., Pushparaj, K., Pappuswamy, M., Meyyazhagan, A., Sangeetha, T., Kaviya, M., & Anand, A. V. (2024) · Natural Resources for Human Health · doi:10.53365/nrfhh/192939
“In postmortem examinations of the substantia nigra and platelets from PD patients, there is decreased complex I activity (Benecke et al., 1993).”
BackgroundSuccinate Dehydrogenase in Mitochondrial Disorders
Tripathi, S., Sharma, Y., & Kumar, D. (2025) · Springer eBooks · doi:10.1007/978-981-96-6831-1_5
Ghosh, A. (2012) · Iowa State University Digital Repository (Iowa State University) · doi:10.31274/etd-180810-1769
“Additionally, impairment of complex-I activity has been reported in substantia nigra, platelets and skeletal muscles of PD patients (Benecke et al., 1993; Haas, 2007).”
BackgroundPlatelets in Neurodegenerative Diseases
Canobbio, I., Torti, M., & Guidetti, G. F. (2025) · Springer eBooks · doi:10.1007/978-3-031-96352-0_25 · Cited by 1
Neumane, S. (2011) · theses.fr (ABES) · doi:10.70675/4cb9b747z6b13z46eazb3cbzb58a8bffabf2
Profiling peripheral immune cells in Parkinson's disease: A scoping review
Recinto, S. J., Jernigan, J. E., Lefter, N., Vitic, Z., Overgaard, M. O., Liu, L., Howden, A. J. M., Eyer, K., Romero‐Ramos, M., Tansey, M. G., et al. (2026) · Journal of Parkinson s Disease · doi:10.1177/1877718x261479505 · Cited by 2
Common pesticides and the development of Parkinson's disease
Nisar, R. (2011) · OpenGrey (Institut de l'Information Scientifique et Technique)
Perspectives on Mitochondria in Carcinogenesis
Bandy, B., & Davison, A. J. (1998) · Springer eBooks · doi:10.1007/978-3-662-12509-0_15
Louis (1999) · doi:10.1002/1531-8257(199905)14:3
Metadata
- Authors
- Benecke, R., Strumper, P., & Weiss, H.
- Affiliations
- Heinrich Heine University Düsseldorf (DE)
- Corresponding author
- Benecke, R.
- ORCID
- Benecke, R.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 1993-12-01
- Volume
- 116
- Issue
- 6
- Pages
- 1451-1463
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2005045122
- Cited by
- 220
- References
- 0
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 5 · 2023: 6 · 2022: 6 · 2021: 1 · 2020: 7 · 2019: 5 · 2018: 9 · 2017: 6 · 2016: 4 · 2015: 6 · 2014: 4 · 2013: 5 · 2012: 6
- FWCI
- 4.83
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- 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, atypical parkinsonism, multiple system atrophy, electron transfer complex, complex I, cytochrome bc1 complex, cytochrome c oxidase, platelet mitochondria, mitochondrial enzyme activity, disease duration
- MeSH terms
- Aged, Aged, 80 and over, Blood Platelets, Electron Transport Complex IV, Electron Transport, Humans, Middle Aged, Mitochondria, Parkinson Disease, Parkinson Disease, Secondary, Syndrome, Electron Transport Complex III, NAD(P)H Dehydrogenase (Quinone)
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