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
Items 201–300 of 345
Huang, J., Qin, X., Cai, X., & Huang, Y. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.00917 · Cited by 34
“of PD patients, which further corroborated the important role of reactive oxygen species in the pathogenesis of PD (13).”
BackgroundBrain Mitochondrial Complex I Inactivation by Oxidative Modification
Bautista, J., Corpas, R., Ramos, R., Cremades, O., Gutierrez-Gil, J. F., & Alegre, S. (2000) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.2000.3388 · Cited by 34
Ali, M. Z., & Dholaniya, P. S. (2022) · Neurochemistry International · doi:10.1016/j.neuint.2022.105344 · Cited by 33
Enzymes Involved in Processing Glutathione Conjugates
Cooper, A. J. L., & Hanigan, M. H. (2010) · Elsevier eBooks · doi:10.1016/b978-0-08-046884-6.00417-6 · Cited by 33
“V activities are relatively spared (Mann et al. 1992; Mizuno et al. 1989; Schapira et al. 1990).”
Shen, X.-M., Li, H., & Dryhurst, G. (2000) · Journal of Neural Transmission · doi:10.1007/s007020070045 · Cited by 33
“Such results raise the possibility that oxidative metabolites of 5-S-CySDA such as DHBT-1 may be endotoxins that contribute to the complex I deficiency in PD (Mizuno et al., 1989; Schapira et al., 1990; Mann et al., 1992) and evoked by MPTP/MPP1 (Sriram et al., 1997).”
BackgroundMetal attenuating therapies in neurodegenerative disease
Mot, A. I., Wedd, A. G., Sinclair, L., Brown, D. R., Collins, S. J., & Brazier, M. W. (2011) · Expert Review of Neurotherapeutics · doi:10.1586/ern.11.170 · Cited by 32
Pechstein, A. E., Gollie, J. M., & Guccione, A. A. (2020) · Journal of Functional Morphology and Kinesiology · doi:10.3390/jfmk5040078 · Cited by 33
Meurers, B. H., Zhu, C., Fernagut, P., Richter, F., Hsia, Y.-C., Fleming, S. M., Oh, M., Elashoff, D. A., DiCarlo, C. D., Seaman, R. L., et al. (2008) · Neurobiology of Disease · doi:10.1016/j.nbd.2008.10.001 · Cited by 32
“Deletions of mitochondrial DNA (Bender et al., 2006) and a decreased activity of complex I of the respiratory chain (Schapira et al., 1989; Schapira et al., 1990; Mann et al., 1992; Swerdlow et al., 1996) have implicated mitochondrial dysfunction in the degenerative process occurring in sporadic PD.”
BackgroundMolina, J. A., de Bustos, F., Jiménez‐Jiménez, F. J., Benito‐León, J., Gasalla, T., Pareja, M. O., Vela, L., Bermejo, F., Martín, M. A., Campos, Y., et al. (1997) · Neurology · doi:10.1212/wnl.48.3.636 · Cited by 32
Pathogenesis of Parkinson’s Disease
Xiao, B., Zhou, Z., Chao, Y., & Tan, E.-K. (2025) · Neurologic Clinics · doi:10.1016/j.ncl.2024.12.003 · Cited by 36
Nuclear and mitochondrial genetics in Parkinson's disease.
Schapira, A. H. V. (1995) · Journal of Medical Genetics · doi:10.1136/jmg.32.6.411 · Cited by 31
Self-citationBlood-Based Protein Biomarkers for Diagnosis and Classification of Neurodegenerative Diseases
Noelker, C., Hampel, H. J., & Dodel, R. C. (2011) · Molecular Diagnosis & Therapy · doi:10.1007/bf03256398 · Cited by 29
“3 Apolipoprotein E and Apolipoprotein E Genotype TheAPOE e4 allele is of special interest in AD research since the presence of this allele is associated with a two- to fourfold increased risk for late-onset AD, increased risk of sporadic and familial late-onset AD, earlier age of AD onset, increased amyloid plaque loa…”
Shimohama, S., & Kawamata, J. (2018) · Springer eBooks · doi:10.1007/978-981-10-8488-1_8 · Cited by 33
“Epidemiological studies suggest that the use of pesticides increases the risk of PD, possibly via reduced activity of complex I in the mitochondrial respiratory chain in the substantia nigra (Parker et al. 1989; Mann et al. 1992; Mizuno et al. 1998).”
BackgroundParkin interacts with Klokin1 for mitochondrial import and maintenance of membrane potential
Kuroda, Y., Sako, W., Goto, S., Sawada, T., Uchida, D., Izumi, Y., Takahashi, T., Kagawa, N., Matsumoto, M., Matsumoto, M., et al. (2011) · Human Molecular Genetics · doi:10.1093/hmg/ddr530 · Cited by 28
Ciregia, F., Kollipara, L., Giusti, L., Zahedi, R. P., Giacomelli, C., Mazzoni, M. R., Giannaccini, G., Scarpellini, P., Urbani, A., Sickmann, A., et al. (2016) · Translational Psychiatry · doi:10.1038/tp.2016.184 · Cited by 27
Ehrhart, J., & Zeevalk, G. D. (2001) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2001.00355.x · Cited by 27
Ling, X. (2011) · International Journal of Oncology · doi:10.3892/ijo.2011.1181 · Cited by 26
Varghese, M., Pandey, M., Samanta, A., Gangopadhyay, P. K., & Mohanakumar, K. P. (2009) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2008.12.021 · Cited by 26
“[13], using platelet homogenates, reported the lack of any difference between complex I activities of control andPD samples.”
Backgroundde Sousa, S. C., & Castilho, R. F. (2005) · Antioxidants and Redox Signaling · doi:10.1089/ars.2005.7.1110 · Cited by 26
“Also, Parkinson’s disease patients typically present partial inhibition (20–40%) of respiratory chain complex I activity (26, 36), further supporting the idea that chronic treatment of rodents with rotenone provides an interesting and relevant experimental model to study neuropathological events in this disorder.”
Wang, J., Aung, L. H. H., Prabhakar, B. S., & Li, P. (2016) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.12914 · Cited by 26
Yap, Y. W., Chen, M. J., Peng, Z. F., Manikandan, J., Ng, J. M. J., Llanos, R. M., Fontaine, S. L., Beart, P. M., & Cheung, N. S. (2012) · Neurochemistry International · doi:10.1016/j.neuint.2012.11.011 · Cited by 26
Mouse models of Parkinson's disease associated with mitochondrial dysfunction
Pickrell, A. M., Pinto, M., & Moraes, C. T. (2012) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2012.08.002 · Cited by 27
“Complex I alone probably is not the sole causal factor in the pathophysiology of PD and could be a secondary side effect as this deficiency is even present in platelets and other tissues unaffected in PD patients (Gu et al., 1997; Mann et al., 1992).”
BackgroundCardoso, F., & Jankovic, J. J. (1993) · Neurologic Clinics · doi:10.1016/s0733-8619(18)30143-9 · Cited by 26
Transgenic Zebrafish Expressing mCherry in the Mitochondria of Dopaminergic Neurons
Noble, S., Godoy, R. S., Affaticati, P., et al. (2015) · Zebrafish · doi:10.1089/zeb.2015.1085 · Cited by 24
Mitochondrial uncoupling agents antagonize rotenone actions in rat substantia nigra dopamine neurons
Wu, Y.-N., Munhall, A. C., & Johnson, S. W. (2011) · Brain Research · doi:10.1016/j.brainres.2011.04.032 · Cited by 24
Application of serial analysis of gene expression to the study of human genetic disease
Horan, M. P. (2009) · Human Genetics · doi:10.1007/s00439-009-0719-5 · Cited by 23
“ND3 is a component of mitochondrial complex I, and biochemical defects of this respiratory chain complex are found in the substantia nigra of Parkinsonian brains (Schapira et al. 1990; Mann et al. 1992).”
BackgroundMonoamine oxidase inhibitors, cognitive functions and neurodegenerative diseases
Delumeau, J.-C., Bentué‐Ferrer, D., Gandon, J. M., Amrein, R., Belliard, S., & Allain, H. (1994) · Springer eBooks · doi:10.1007/978-3-7091-9324-2_34 · Cited by 24
Sulfonylurea-sensitive potassium current evoked by sodium-loading in rat midbrain dopamine neurons
Seutin, V., Shen, K., NORTH, R. A., et al. (1996) · Neuroscience · doi:10.1016/0306-4522(95)00489-0 · Cited by 24
Ketotherapeutics for neurodegenerative diseases
Norwitz, N. G., Gilbert‐Jaramillo, J., Clarke, K., & Soto-Mota, A. (2020) · International review of neurobiology · doi:10.1016/bs.irn.2020.02.003 · Cited by 24
Ben‐Shachar, D. (2019) · Journal of Neural Transmission · doi:10.1007/s00702-019-02120-x · Cited by 23
“Mitochondrial dysfunction is also widely recognized in both disorders with the following potential primary causative factors, deficits in the first complex (NADH:ubiquinone oxidoreductase—CoI) and less so in CoIV (cytochrome c oxidase) of the electron transfer chain (Mizuno et al. 1990; Mann et al. 1992; Schapira 1993…”
BackgroundBiomarkers in Parkinson’s disease
Dorsey, E. R., Holloway, R. G., & Ravina, B. M. (2006) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.6.6.823 · Cited by 23
Platelet morphology in Parkinson's disease: An electron microscopic study
Factor, S. A., Ortof, E., Dentinger, M. P., et al. (1994) · Journal of the Neurological Sciences · doi:10.1016/0022-510x(94)90056-6 · Cited by 22
Targeting Mitochondria as a Therapeutic Approach for Parkinson’s Disease
Abrishamdar, M., Jalali, M. S., & Farbood, Y. (2022) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-022-01265-w · Cited by 22
“There have also been several reports of a selective loss in the respiratory chain complex I in the SN of Parkinson's disease patients after measuring enzyme activity (Schapira et al. 1990; Mann et al. 1992; Janetzky et al. 1994).”
BackgroundEnhancement of nicotinic receptors alleviates cytotoxicity in neurological disease models
Kawamata, J., Suzuki, S., & Shimohama, S. (2011) · Therapeutic Advances in Chronic Disease · doi:10.1177/2040622310397691 · Cited by 17
“Epidemiological studies suggest that the use of pesticides increases the risk of PD, possibly via reduced activity of complex I in the mitochondrial respiratory chain in the substantia nigra [Mizuno et al. 1998; Mann et al. 1992; Parker et al. 1989].”
BackgroundMitochondrial DNA polymorphism in substantia nigra
Kapsa, R. M. I., Jean-François, M. J. B., Lertrit, P., Weng, S., Siregar, N. C., Ojaimi, J., Donnan, G. A., Masters, C. L., & Byrne, E. (1996) · Journal of the Neurological Sciences · doi:10.1016/s0022-510x(96)00247-x · Cited by 21
Ghrelin mediated hippocampal neurogenesis
Davies, J. S. (2022) · Vitamins and hormones · doi:10.1016/bs.vh.2021.12.003 · Cited by 23
Zheng, R., Yan, Y., Pu, J., & Zhang, B. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23169088 · Cited by 19
“Mitochondrial complex I plays a central role in PD, and deficits in its subunits and activities have been consistently detected in the SN of PD patients [66].”
BackgroundOXPHOS toxicogenomics and Parkinson's disease
López‐Gallardo, E., Iceta, R., Iglesias, E., Montoya, J., & Ruiz‐Pesini, E. (2011) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2011.06.004 · Cited by 19
Mitochondrial dysfunction in the striatum of aged chronic mouse model of Parkinson’s disease
Patki, G. (2009) · Frontiers in Aging Neuroscience · doi:10.3389/neuro.24.003.2009 · Cited by 20
“The concept of neuronal oxidative stress and mitochondrial complex-1 inhibition has also been verifi ed in the substantia nigra pars compacta from human PD (Parker Jr. et al., 1989; Schapira et al., 1990; Mann et al., 1992; Floor and Wetzel, 1998).”
Less is more: Caloric regulation of neurogenesis and adult brain function
Morgan, A. H., Andrews, Z. B., & Davies, J. S. (2017) · Journal of Neuroendocrinology · doi:10.1111/jne.12512 · Cited by 22
Parkinson's disease: animal models
Betarbet, R. S., & Greenamyre, J. T. (2007) · Handbook of clinical neurology · doi:10.1016/s0072-9752(07)83011-9 · Cited by 18
“…reductions in mitochondrial complex I function in a variety of tissues from PD patients, including brain, platelets, muscle and fibroblasts (Bindoff et al., 1989; Parker et al., 1989; Schapira et al., 1989; Shoffner et al., 1991; Mann et al., 1992; Cardellach et al., 1993; Blin et al., 1994).”
BackgroundMitochondrial Dysfunction in Parkinson’s Disease
Swerdlow, R. H., Parks, J. K., Miller, S. W., Davis, J. N., Trimmer, P. A., Tuttle, J. B., Bennett, J. P., Wooten, G. F., Davis, R. E., & Parker, W. D. (1998) · Advances in behavioral biology · doi:10.1007/978-1-4615-5337-3_11 · Cited by 19
Bal‐Price, A., Leist, M., Schildknecht, S., Monnet‐Tschudi, F., Paini, A., & Terron, A. (2018) · OECD series on adverse outcome pathways · doi:10.1787/b46c3c00-en · Cited by 22
Platelet mitochondrial activity and pesticide exposure in early Parkinson's disease
Bronstein, J. M., Paul, K. C., Yang, L., Haas, R., Shults, C. W., Le, T. P., & Ritz, B. R. (2015) · Movement Disorders · doi:10.1002/mds.26164 · Cited by 18
Systems Biology of Parkinson's Disease
Wellstead, P. E., & Cloutier, M. (2012) · Springer eBooks · doi:10.1007/978-1-4614-3411-5 · Cited by 17
“These DA neurons have a strong influence on the following: (1) emotion, motivation, and cognitive processes, mainly by the projection from the VTA to limbic forebrain areas, and (2) motor control, chiefly by the projection from the SNc and RRF to the neostriatum [3, 31].”
BackgroundInfluentialToxin-induced mitochondrial dysfunction
Browne, S. E., & Beal, M. F. (2002) · International review of neurobiology · doi:10.1016/s0074-7742(02)53010-5 · Cited by 17
Li, C., & Beal, M. F. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0508350102 · Cited by 17
Ricketts, M., Hamer, R. M., Manowitz, P., Feng, F., Sage, J. I., Paola, R. D., & Menza, M. A. (1998) · Clinical Genetics · doi:10.1111/j.1399-0004.1998.tb03690.x · Cited by 18
Fish Models for Exploring Mitochondrial Dysfunction Affecting Neurodegenerative Disorders
Otsuka, T., & Matsui, H. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24087079 · Cited by 17
“Similarly, mitochondrial complex I dysfunction has been reported in the skeletal muscle and platelets of PD patients [52].”
BackgroundBrill, L. B., & Bennett, J. P. (2003) · Experimental Neurology · doi:10.1016/s0014-4886(02)00045-6 · Cited by 16
Kuter, K. Z., Olech, Ł., & Dencher, N. A. (2018) · Mitochondrion · doi:10.1016/j.mito.2018.12.002 · Cited by 16
Kuter, K. Z., Kratochwil, M., Marx, S.-H., Hartwig, S., Lehr, S., Sugawa, M. D., & Dencher, N. A. (2016) · Archives of Physiology and Biochemistry · doi:10.1080/13813455.2016.1197948 · Cited by 15
“There have been previous reports that overall Cx I activity in PD patients brains was decreased (Janetzky et al., 1994; Mann et al., 1992; Schapira et al., 1990a, 1990b).”
BackgroundMichalak, S., Florczak‐Wyspianska, J., Rybacka-Mossakowska, J., Ambrosius, W., Osztynowicz, K., Baszczuk, A., Kozubski, W. P., & Wysocka, E. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/9703574 · Cited by 15
Mitochondrial dysfunction in neurodegenerative disorders and aging
Schapira, A. H. V. (1994) · Elsevier eBooks · doi:10.1016/b978-0-7506-0585-4.50017-4 · Cited by 18
Self-citationPlatelet mitochondrial membrane potential in Parkinson's disease
Antony, P. M. A., Boyd, O., Trefois, C., et al. (2014) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.151 · Cited by 14
“Finally, the reported levels of complex I deficiency in substantia nigra outreach the reported levels of complex I deficiency in platelets.(16,18,25) The study has several limitations.”
BackgroundResultThe genetics of Parkinson's disease and parkinsonian syndromes
Bajaj, N. P. S., Shaw, C. E., Warner, T. T., & Chaudhuri, К. R. (1998) · Journal of Neurology · doi:10.1007/s004150050258 · Cited by 13
The neuroprotectant properties of glutamate antagonists and antiglutamatergic drugs
Pedersen, V., & Schmidt, W. (2000) · Neurotoxicity Research · doi:10.1007/bf03033793 · Cited by 14
Burbaeva, G. S., Бокша, И. С., Turishcheva, M. S., Savushkina, O. K., Beniashvili, A. G., Rupchev, G., & Ma, M. (2011) · Health · doi:10.4236/health.2011.31003 · Cited by 11
Pienaar, I. S., & Chinnery, P. F. (2012) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2012.08.010 · Cited by 11
“In addition, evidence revealed a 30–40% decreased activity of mitochondrial complex I activity in the post-mortem SN of PD patients (Schapira et al., 1989; Mann et al., 1992; Finsterer, 2011).”
BackgroundPlatelets in Neurological Disorders
Canobbio, I., Guidetti, G. F., & Torti, M. (2017) · Springer eBooks · doi:10.1007/978-3-319-47462-5_35 · Cited by 13
Stokes, A. H., Bernard, L. P., Nicklas, W. J., et al. (2001) · Journal of Neuroscience Research · doi:10.1002/jnr.1052 · Cited by 11
“These results suggested that GABA transport inhibitors could have therapeutic value in patho- logical situations such as hypoxia/ischemia or in neurodegenerative diseases which involve mitochondrial dysfunction (Lewitt et al, 1989; Mizuno et al., 1989; Schapira et al., 1990; Mann et al., 1992).”
BackgroundOxidative Stress in Parkinson`s Disease
Friedlich, A. L., Smith, M. A., Zhu, X., Takeda, A., Nunomura, A., Moreira, P. I., & Perry, G. L. (2009) · The Open Pathology Journal · doi:10.2174/1874375700903010038 · Cited by 10
“Similar deficits in respiratory transport chain complex I have also been reported in peripheral cells, such as myocytes and platelets [24, 25].”
Vos, M. H., Verstreken, P., & Klein, C. (2015) · Biochemical Society Transactions · doi:10.1042/bst20140325 · Cited by 10
Munhall, A. C., Wu, Y.-N., Belknap, J. K., Meshul, C. K., & Johnson, S. W. (2012) · NeuroToxicology · doi:10.1016/j.neuro.2012.04.006 · Cited by 10
Spatiotemporal Oscillations in Biological Molecules:Hydrogen Peroxide and Parkinson’s Disease
Krishnan, C. V., Garnett, M., & Chu, B. (2008) · International Journal of Electrochemical Science · doi:10.1016/s1452-3981(23)15530-1 · Cited by 10
Mitochondria in neurodegeneration
Beal, M. F. (2002) · Springer eBooks · doi:10.1007/978-2-8178-0929-8_3 · Cited by 10
Mitochondrial disorders in degenerative ataxias
Schöls, L. J., Reichmann, H., Amoiridis, G., Seibel, P., Wagener, S., Seufert, S., & Przuntek, H. (1996) · European Journal of Neurology · doi:10.1111/j.1468-1331.1996.tb00190.x · Cited by 9
Biochemical and molecular features of deficiencies of Complexes I, II and III
Schapira, A. H. V., & Cooper, J. A. D. (1994) · Elsevier eBooks · doi:10.1016/b978-0-7506-0585-4.50009-5 · Cited by 9
Self-citationMitochondria and Parkinson's Disease
Simon, D. K., Chu, C. T., & Swerdlow, R. H. (2011) · Parkinson s Disease · doi:10.4061/2011/261791 · Cited by 8
Finch, C. C., Ho, S. L., Williams, A. C., et al. (1995) · Progress in brain research · doi:10.1016/s0079-6123(08)61205-4 · Cited by 8
Korlipara, L. V. P., & Schapira, A. H. V. (2002) · International review of neurobiology · doi:10.1016/s0074-7742(02)53011-7 · Cited by 8
Self-citationJin, X., Wei, J., Min, X., Fan, Y., Yuan, Z., Du, Z., Su, Z., Xun, T., Du, Q., Liang, T., et al. (2025) · iScience · doi:10.1016/j.isci.2025.114185 · Cited by 15
“171”
Biochemical evaluations in skeletal muscles of primates with MPTP parkinson-like syndrome
Pastoris, O. (1995) · Pharmacological Research · doi:10.1016/1043-6618(95)80090-5 · Cited by 7
Increased energy expenditure during posture maintenance and exercise in early Parkinson disease
Kalifa, T. M., Ziv, N., Bergman, H., et al. (2017) · Health Science Reports · doi:10.1002/hsr2.14 · Cited by 7
Turski, G. N., & Ikonomidou, C. (2014) · Springer eBooks · doi:10.1007/978-1-4614-5836-4_84 · Cited by 7
What's wrong with mitochondria in Parkinson's disease?
Greenamyre, J. T. (2018) · Movement Disorders · doi:10.1002/mds.98 · Cited by 7
Baracca, A., Bucchi, L., Ghelli, A. M., et al. (1997) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1997.6807 · Cited by 7
Bioenergetics and excitotoxicity
Greene, J. G., & Greenamyre, J. T. (1996) · Elsevier eBooks · doi:10.1016/b978-012525445-8/50010-2 · Cited by 7
Brain microvascular endothelial cell metabolism and its ties to barrier function
Weber, C. M., Moiz, B., & Clyne, A. M. (2024) · Vitamins and hormones · doi:10.1016/bs.vh.2024.05.002 · Cited by 6
Turski, G. N., & Ikonomidou, C. (2022) · Springer eBooks · doi:10.1007/978-3-031-15080-7_84 · Cited by 5
Drion, G., Seutin, V., & Sepulchre, R. J. (2012) · Springer eBooks · doi:10.1007/978-1-4614-3411-5_4 · Cited by 5
“Mitochondrial dysfunction and metabolic issues are known to have a strong implication in the pathogenesis of PD [1–10].”
BackgroundManneschi, L., Dotti, M. T., Battisti, C., et al. (1994) · Archives of Gerontology and Geriatrics · doi:10.1016/s0167-4943(05)80060-3 · Cited by 5
Aspectos moleculares y prospectos de terapias en la enfermedad de Parkinson
Hernández-Montiel, H. L. (2006) · Redalyc (Universidad Autónoma del Estado de México) · Cited by 5
Impact of the 25th chromosome on mitochondrial dysfunction in human disease
Walker, U. A., Jean-Francois, B., & Byrne, E. (1995) · Journal of Clinical Neuroscience · doi:10.1016/0967-5868(95)90001-2 · Cited by 5
van Diemen, M. P. J., Hart, E. P., Hameeteman, P. W., Coppen, E. M., Winder, J. Y., den Heijer, J. M., Moerland, M., Kan, H. E., van der Grond, J., WEBB, A. G., et al. (2020) · Journal of Huntington s Disease · doi:10.3233/jhd-200413 · Cited by 3
“In a study comparing mitochondrial function in brain, skeletal muscle and platelet homogenates from idiopathic PD patients [39], mitochondrial dysfunction was found to be part of the pathophysiology of PD (complex 1 deficiency), but limited to the substantia nigra, with normal mitochondrial function…”
Clinical Trial Highlights: Modulators of Mitochondrial Function
Capriglia, F., Burgess, T., Bandmann, O., & Mortiboys, H. (2023) · Journal of Parkinson s Disease · doi:10.3233/jpd-239003 · Cited by 5
The Energy Crisis in Parkinson’s Disease: A Therapeutic Target
Abou-Hamdan, M., Cornille, E., Khrestchatisky, M., de, M. B. A. B., & Gharib, B. (2011) · InTech eBooks · doi:10.5772/17369 · Cited by 5
“Several studies showed impaired complex I, II+III, and IV activities in PD muscle (Bindoff et al., 1991; Blin et al., 1994; Cardellach et al., 1993); whereas no differences were observed in other studies (DiDonato et al., 1993; Mann et al., 1992; Reichmann et al., 1994).”
ResultLin, W., & Kang, U. J. (2005) · Journal of Clinical Neurology · doi:10.3988/jcn.2005.1.2.107 · Cited by 4
Kielian, T., & Drew, P. D. (2005) · Humana Press eBooks · doi:10.1385/1-59259-905-2:041 · Cited by 4
Ercan, A., Kulaksiz-Erkmen, G., Dalmızrak, Ö., Müftüoğlu, M., Öğüş, İ. H., Cavdar, L. Y., İnan, L. E., & Özer, N. K. (2009) · Turkish Journal of Biochemistry · Cited by 4
Studies on the pathogenesis of Parkinson's disease in Japan
Mizuno, Y., Ikebe, S., Hattori, N., Mochizuki, H., Nakagawa-Hattori, Y., & Kondo, T. (1994) · Archives of Gerontology and Geriatrics · doi:10.1016/0167-4943(94)90033-7 · Cited by 4
Neuroprotection by Physical Activity
Mitchell, A. (2010) · Cited by 4
Mitochondria at the Base of Neuronal Innate Immunity in Alzheimer’s and Parkinson’s Diseases
Esteves, A. R., Silva, D. F., Santos, D., Candeias, E., Filipe, F., & Cardoso, S. M. (2018) · InTech eBooks · doi:10.5772/intechopen.72612 · Cited by 4
“[156] Mann VM, Cooper JM, Krige D, Daniel SE, Schapira AH, Marsden CD.”
BackgroundMitochondrial Dysfunction and Oxidative Stress in Bipolar Disorder
Tang, V. M., & Wang, J.-F. (2014) · Springer eBooks · doi:10.1007/978-3-642-30018-9_83 · Cited by 4
Brain Mitochondrial Dysfunction and Complex I Syndrome in Parkinson s Disease
Laura, B., Manuel, J., Navarro, A., & Boveris, A. (2011) · InTech eBooks · doi:10.5772/34847 · Cited by 3
“Moreover, similar mitochondrial complex I dysfunctions were reported in skeletal muscle and platelets of PD patients (Mann et al., 1992).”
BackgroundMitochondrial dysfunction in neurodegeneration
Schapira, A. H. V. (1996) · Elsevier eBooks · doi:10.1016/b978-012525445-8/50009-6 · Cited by 3
Self-citationSegura‐Aguilar, J. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-822120-4.00001-0 · Cited by 4
Parkinson’s Disease: From Metabolism to Genetics—A Comprehensive Review
Duarte, C. P., de Souza, E. B., Dias-Pinto, J. R., & Araldi, R. P. (2026) · Current Issues in Molecular Biology · doi:10.3390/cimb48030254 · Cited by 3
Complex I Assay in Mitochondrial Preparations from CNS
Diwakar, L., Ray, A., & Ravindranath, V. (2008) · Current Protocols in Toxicology · doi:10.1002/0471140856.tx1710s38 · Cited by 2
Bywood, P. T., & Johnson, S. M. (2001) · Neurotoxicity Research · doi:10.1007/bf03033207 · Cited by 2
“deficiency (Mann et al., 1992; Parker et al., 1989)”
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