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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.
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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 [14]
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Oxidative Stress and Parkinson's Diseasea
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High frequency of mitochondrial complex I mutations in Parkinson’s disease and aging
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“In skeletal muscle of PD patients, reduced complex I activity was observed by some groups (Bindoff et al. 1989), but denied by others (Mann et al. 1992).”
BackgroundM itochondrial DNA and primary mitochondrial dysfunction in P arkinson's disease
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Pesticide Exposure Exacerbates α-Synucleinopathy in an A53T Transgenic Mouse Model
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Mechanistic Approaches to Parkinson's Disease Pathogenesis
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“Later on, reports indicated that the complex I defect is systemic in PD, affecting tissues outside the brain such as platelets, lymphocytes and muscle (8, 10, 15, 62, 69, 71, 84).”
BackgroundTargeting urate to reduce oxidative stress in Parkinson disease
Crotty, G. F., Ascherio, A., & Schwarzschild, M. A. (2017) · Experimental Neurology · doi:10.1016/j.expneurol.2017.06.017 · Cited by 134
“Subsequent studies also found complex I deficiency in the platelets, lymphocytes and skeletal muscle tissues of patients with PD, although this was not consistently seen in skeletal muscle (28,57).”
BackgroundResultCytochrome c Oxidase Deficiency Associated with the First Stop-Codon Point Mutation in Human mtDNA
Hanna, M. G., Nelson, I. P., Rahman, S., et al. (1998) · The American Journal of Human Genetics · doi:10.1086/301910 · Cited by 130
“Polarographic determination of mitochondrial function, spectrophotometric analysis of respiratorychain–enzyme activities, and low-temperature analysis of cytochrome content were performed as described elsewhere (Morgan-Hughes et al. 1977; Mann et al. 1992). mtDNA analysis.”
MethodSelf-citationAhmadi, F. A., Linseman, D. A., Grammatopoulos, T. N., Jones, S. M., Bouchard, R. J., Freed, C. R., Heidenreich, K. A., & Zawada, W. M. (2003) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2003.02068.x · Cited by 127
Apoptotic neuronal death in Parkinson's disease: Involvement of nitric oxide
Singh, S., & Dikshit, M. (2007) · Brain Research Reviews · doi:10.1016/j.brainresrev.2007.02.001 · Cited by 131
Brain mitochondrial dysfunction and oxidative damage in Parkinson’s disease
Navarro, A., & Boveris, A. (2009) · Journal of Bioenergetics and Biomembranes · doi:10.1007/s10863-009-9250-6 · Cited by 126
“Moreover, similar mitochondrial complex I dysfunctions were reported in skeletal muscle and platelets of PD patients (Mann et al. 1992).”
BackgroundFlønes, I. H., Fernández‐Vizarra, E., Lykouri, M., Brakedal, B., SKEIE, G. O., Miletić, H., Lilleng, P. K., Alves, G. W., Tysnes, O., Haugarvoll, K., et al. (2017) · Acta Neuropathologica · doi:10.1007/s00401-017-1794-7 · Cited by 122
“While this phenomenon has been consistently reproduced by multiple studies [17, 18, 23, 24, 34] its significance remains undetermined.”
Członkowska, A., Kurkowska‐Jastrzębska, I., Członkowski, A., Peter, D., & Stefano, G. B. (2002) · PubMed · Cited by 123
Baracca, A., Barogi, S., Carelli, V., Lenaz, G., & Solaini, G. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.6.4177 · Cited by 112
Parkin- and PINK1-Dependent Mitophagy in Neurons: Will the Real Pathway Please Stand Up?
Grenier, K., McLelland, G., & Fon, E. A. (2013) · Frontiers in Neurology · doi:10.3389/fneur.2013.00100 · Cited by 124
“Mitochondrial dysfunction has been a longstanding theme in PD following observations that mitochondrial toxins such as MPTP and rotenone could induce acute parkinsonism (3, 4) and that mitochondrial respiration was defective in the substantia nigra pars compacta (SNpc) of post-mortem PD patients (5).”
BackgroundInfluentialSomatic mitochondrial DNA mutations in cortex and substantia nigra in aging and Parkinson’s disease
Simon, D. K., Lin, M. T., Zheng, L., Liu, G.-J., Ahn, C. H., Kim, L. M., Mauck, W. M., Twu, F., Beal, M. F., & Johns, D. R. (2004) · Neurobiology of Aging · doi:10.1016/s0197-4580(03)00037-x · Cited by 118
“This decline occurs to a greater extent in PD compared to age-matched controls [27,40,52–54].”
ResultKawamata, J., & Shimohama, S. (2011) · Journal of Alzheimer's Disease · doi:10.3233/jad-2011-110173 · Cited by 111
de Sousa, S. C., Maciel, E. N., Vercesi, A. E., & Castilho, R. F. (2003) · FEBS Letters · doi:10.1016/s0014-5793(03)00421-6 · Cited by 109
Omega-3 fatty acids in neurodegenerative diseases: Focus on mitochondria
Eckert, G. P., Lipka, U., & Muller, W. E. (2012) · Prostaglandins Leukotrienes and Essential Fatty Acids · doi:10.1016/j.plefa.2012.05.006 · Cited by 111
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
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