The DOI matches its Crossref record.
Cytochrome oxidase deficiency in Alzheimer’s disease
Abstract
We assayed cytochrome oxidase and other electron transport chain activities in platelet mitochondria isolated from patients with Alzheimer's disease (AD). Five of 6 patients had striking reductions of platelet cytochrome oxidase activity (patient mean, 83.72 +/- 82.99 nmol/min/mg; control mean, 167.14 +/- 36.21 nmol/min/mg; n = 8). Other electron transport chain catalytic activities were not significantly different than control values. AD may be a systemic illness, a primary defect in cytochrome oxidase may be pathogenically important in its production, and the mitochondrial genes encoding cytochrome oxidase subunits may be important in producing the defect.
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
“however, in mitochondria isolated from AD platelets, the activity of complex IV, or cytochrome c oxidase, is significantly decreased [109,110,111]”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [109]
In the citing paper
“In addition to the brain, reduced COX activity is also seen in AD subject platelets and fibroblasts [127, 128].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [127]
Citations
Cited by
Sorted by citations
Items 201–300 of 597
Mosconi, L., de Leon, M., Murray, J., E, L., Lu, J., Javier, E., McHugh, P., & Swerdlow, R. H. (2011) · Journal of Alzheimer s Disease · doi:10.3233/jad-2011-110866 · Cited by 97
“Upon receipt, platelets were isolated by centrifugation and enriched mitochondrial fractions were prepared using previously described methods [13, 14].”
Mitochondrial Dysfunction in Idiopathic Parkinson Disease
Parker, W. D., & Swerdlow, R. H. (1998) · The American Journal of Human Genetics · doi:10.1086/301812 · Cited by 97
Self-citationNo evidence for systemic oxidant stress in Parkinson's or Alzheimer's disease
Ahlskog, J. E., Uitti, R. J., Low, P. A., Tyce, G. M., Nickander, K. K., Petersen, R. C., & Kokmen, E. (1995) · Movement Disorders · doi:10.1002/mds.870100507 · Cited by 90
Jadiya, P., Garbincius, J. F., & Elrod, J. W. (2021) · Acta Neuropathologica Communications · doi:10.1186/s40478-021-01224-4 · Cited by 94
Selective inactivation of redox-sensitive mitochondrial enzymes during cardiac reperfusion
Sadek, H. A., Humphries, K. M., Szweda, P. A., & Szweda, L. I. (2002) · Archives of Biochemistry and Biophysics · doi:10.1016/s0003-9861(02)00446-0 · Cited by 91
Ghosh, S. S., Swerdlow, R. H., Miller, S. W., Sheeman, B., Parker, W. D., & DAVIS, R. E. (1999) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1999.tb07825.x · Cited by 91
Self-citationEntorhinal cortex of the human, monkey, and rat: Metabolic map as revealed by cytochrome oxidase
Hevner, R. F., & Wong‐Riley, M. T. T. (1992) · The Journal of Comparative Neurology · doi:10.1002/cne.903260310 · Cited by 91
Tannenberg, R. K., Scott, H. L., Tannenberg, A. E. G., & Dodd, P. R. (2006) · Neurochemistry International · doi:10.1016/j.neuint.2006.05.004 · Cited by 89
Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease
Butterfield, D. A., & Boyd-Kimball, D. (2020) · Antioxidants · doi:10.3390/antiox9090818 · Cited by 85
Austad, S. N., Ballinger, S. W., Buford, T. W., Carter, C. S., Smith, D. L., Darley-Usmar, V. M., & Zhang, J. (2021) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2021.06.014 · Cited by 94
Platelets, a reliable source for peripheral Alzheimer’s disease biomarkers?
Veitinger, M., Varga, B., Guterres, S. B., & Zellner, M. (2014) · Acta Neuropathologica Communications · doi:10.1186/2051-5960-2-65 · Cited by 88
Effect of energy shortage and oxidative stress on amyloid precursor protein metabolism in COS cells
Gasparini, L., Racchi, M., Benussi, L., Curti, D., Binetti, G., Bianchetti, A., Trabucchi, M., & Govoni, S. (1997) · Neuroscience Letters · doi:10.1016/s0304-3940(97)00536-3 · Cited by 89
Turski, L., & Turski, W. A. (1993) · Cellular and Molecular Life Sciences · doi:10.1007/bf01929915 · Cited by 88
Cell death mechanisms: Cross-talk and role in disease
Zhivotovsky, B., & Orrenius, S. (2010) · Experimental Cell Research · doi:10.1016/j.yexcr.2010.02.037 · Cited by 90
Park, S.-S., Park, H.-S., Kim, C., Kang, H., Kim, D., Baek, S., & Kim, T.-W. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-00631-4 · Cited by 94
Ammonia and Alzheimer’s disease
Seiler, N. (2002) · Neurochemistry International · doi:10.1016/s0197-0186(02)00041-4 · Cited by 88
Is the mitochondrial outermembrane protein VDAC1 therapeutic target for Alzheimer's disease?
Reddy, P. H. (2012) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2012.09.003 · Cited by 88
Insulin signalling in Alzheimer′s disease and diabetes: from epidemiology to molecular links
Ribé, E. M., & Lovestone, S. (2016) · Journal of Internal Medicine · doi:10.1111/joim.12534 · Cited by 88
Nicotine protects rat brain mitochondria against experimental injuries
Cormier, A., Morin, C., Zini, R., Tillement, J. P., & Lagrue, G. (2003) · Neuropharmacology · doi:10.1016/s0028-3908(03)00041-8 · Cited by 86
Mitochondrial Abnormalities in Alzheimer’s Disease
Silva, D. F., Selfridge, J. E., Lu, J., E, L., Cardoso, S. M., & Swerdlow, R. H. (2012) · Advances in Pharmacology · doi:10.1016/b978-0-12-394816-8.00003-9 · Cited by 86
Free radical theory of aging: Alzheimer’s disease pathogenesis
Harman, D. (1995) · AGE · doi:10.1007/bf02436085 · Cited by 87
Dimebon (Latrepirdine) Enhances Mitochondrial Function and Protects Neuronal Cells from Death
Zhang, S., Hedskog, L., Petersen, C. H., Winblad, B. G., & Ankarcrona, M. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-100174 · Cited by 85
Cognitive decline: A vitamin B perspective
Mikkelsen, K., Stojanovska, L., Tangalakis, K., Bosevski, M., & Apostolopoulos, V. (2016) · Maturitas · doi:10.1016/j.maturitas.2016.08.001 · Cited by 86
“It has been postulated that an increase in life expectancy in western cultures has coincided with an increase in the prevalence of cognitive impairments (dementia, AD etc), and perhaps this is less about disease process and more about the natural process of ageing [4].”
Maternal transmission of Alzheimer's disease: prodromal metabolic phenotype and the search for genes
Mosconi, L., Berti, V., Swerdlow, R. H., Pupi, A., Duara, R., & de Leon, M. (2010) · Human Genomics · doi:10.1186/1479-7364-4-3-170 · Cited by 85
Nehls, U., Friedrich, T., Schmiede, A., Ohnishi, T., & Weiss, H. (1992) · Journal of Molecular Biology · doi:10.1016/0022-2836(92)90519-p · Cited by 84
Swerdlow, R. H. (2020) · International review of neurobiology · doi:10.1016/bs.irn.2020.01.008 · Cited by 88
The multifaceted role of platelets in mediating brain function
Burnouf, T., & Walker, T. L. (2022) · Blood · doi:10.1182/blood.2022015970 · Cited by 86
Protective Effect of Isorhynchophylline Against β-Amyloid-Induced Neurotoxicity in PC12 Cells
Xian, Y., Lin, Z., Mao, Q., Ip, S., Su, Z., & Lai, X. (2011) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-011-9763-5 · Cited by 84
Szabados, T., Dul, C., Majtényi, K., Hargitai, J., Pénzes, Z., & Urbanics, R. (2004) · Behavioural Brain Research · doi:10.1016/j.bbr.2004.01.016 · Cited by 84
Kish, S. J. (1997) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1997.tb48473.x · Cited by 83
Lott, I. T. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.12.010 · Cited by 86
Kish, S. J., Mastrogiacomo, F., Guttman, M., Furukawa, Y., Taanman, J., Dozic, S., Pandolfo, M., Lamarche, J. B., DiStefano, L. M., & Chang, L. (1999) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1999.0720700.x · Cited by 85
The protective role of plant biophenols in mechanisms of Alzheimer's disease
Omar, S. H., Scott, C., Hamlin, A. S., & Obied, H. K. (2017) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2017.02.016 · Cited by 84
Treating neurodegeneration by modifying mitochondria: potential solutions to a “complex” problem
Swerdlow, R. H. (2007) · Antioxidants & Redox Signaling · doi:10.1089/ars.2007.1676 · Cited by 81
Studzinski, C. M., MacKay, W. A., Beckett, T. L., Henderson, S. T., Murphy, M. P., Sullivan, P. G., & Burnham, W. M. (2008) · Brain Research · doi:10.1016/j.brainres.2008.06.005 · Cited by 82
Alzheimer's Disease and Amyloid: Culprit or Coincidence?
Skaper, S. D. (2012) · International review of neurobiology · doi:10.1016/b978-0-12-386986-9.00011-9 · Cited by 82
“Ab inhibits a-ketoglutarate dehydrogenase activity in isolated mitochondria (Casley et al., 2002), and deficiency of a-ketoglutarate dehydrogenase (Gibson et al., 1988) and cytochrome oxidase activities (Parker et al., 1990) has been found in the brain and other tissues in AD.”
BackgroundBrenner-Lavie, H., Klein, E., Zuk, R., Gazawi, H., Ljubuncić, P., & Ben‐Shachar, D. (2007) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2007.10.006 · Cited by 79
Cytochrome Oxidase Deficiency in Alzheimer's Diseasea
Parker, W. D. (1991) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1991.tb00191.x · Cited by 79
Self-citationThe Alzheimer’s Disease Mitochondrial Cascade Hypothesis: A Current Overview
Swerdlow, R. H. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-221286 · Cited by 88
Maternal family history is associated with Alzheimer's disease biomarkers
Honea, R. A., Initiative, F. T. A. D. N., Vidoni, E. D., Swerdlow, R. H., & Burns, J. M. (2012) · Journal of Alzheimer s Disease · doi:10.3233/jad-2012-120676 · Cited by 79
“Mitochondrial DNA is exclusively maternally inherited in humans, and may differ between persons with and without AD [34].”
Cell cycle and cell death in disease: past, present and future
Zhivotovsky, B., & Orrenius, S. (2010) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2010.02282.x · Cited by 81
Cytochrome Oxidase Inhibition: A Novel Animal Model of Alzheimer's Disease
Bennett, M. C., Diamond, D. M., Stryker, S. L., Parks, J. K., & Parker, W. D. (1992) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/002383099200500206 · Cited by 77
Self-citationElectron transfer complex I defect in idiopathic dystonia
Benecke, R., Strümper, P., & Weiss, H. (1992) · Annals of Neurology · doi:10.1002/ana.410320512 · Cited by 77
Influence of mutation type and X chromosome inactivation on Rett syndrome phenotypes
Amir, R. E., den Veyver, I. B. V., Schultz, R., Malicki, D. M., Tran, C. Q., Dahle, E. J., Philippi, A., Tímár, L., Percy, A. K., Motil, K. J., et al. (2000) · Annals of Neurology · doi:10.1002/1531-8249(200005)47:5 · Cited by 351
ET-GRU: using multi-layer gated recurrent units to identify electron transport proteins
Le, N. Q. K., Yapp, E. K. Y., & Yeh, H. (2019) · BMC Bioinformatics · doi:10.1186/s12859-019-2972-5 · Cited by 75
Wang, Z., Ye, J., Zhang, K., Li, D., Granzier-Nakajima, T., Ranasinghe, J. C., Xue, Y., Sharma, S., Biase, I., Terrones, M., et al. (2022) · ACS Nano · doi:10.1021/acsnano.2c00538 · Cited by 77
Perkins, M., Wolf, A. B., Chavira, B., Shonebarger, D., Meckel, J. P., Leung, L., Ballina, L. E., Ly, S., Saini, A., Jones, T. B., et al. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-151205 · Cited by 79
“Here, mitochondrial oxidative metabolism is altered in young adult APOE4 carriers in a manner that is opposite to what is seen in the disease state.”
ResultNeuroprotective activity of acetyl‐L‐carnitine: Studies in vitro
Forloni, G., Angeretti, N., & Smiroldo, S. (1994) · Journal of Neuroscience Research · doi:10.1002/jnr.490370112 · Cited by 73
Leuner, K., Pantel, J., Frey, C., Schindowski, K., Schulz, K. L., Wegat, T., Maurer, K., Eckert, A., & Müller, W. E. G. (2007) · Springer eBooks · doi:10.1007/978-3-211-73574-9_27 · Cited by 74
Mancuso, M., Filosto, M., Bosetti, F., Ceravolo, R., Rocchi, A., Tognoni, G., Manca, M. L., Solaini, G., Siciliano, G., & Murri, L. (2003) · Experimental Neurology · doi:10.1016/s0014-4886(03)00092-x · Cited by 73
Reduced VDAC1 Protects Against Alzheimer's Disease, Mitochondria, and Synaptic Deficiencies
Mańczak, M., Sheiko, T. V., Craigen, W. J., & Reddy, P. H. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-130761 · Cited by 73
Genetic risk factors in Alzheimer's disease.
Tilley, L. A., Morgan, K., & Kalsheker, N. A. (1998) · Molecular Pathology · doi:10.1136/mp.51.6.293 · Cited by 72
Hroudová, J., Singh, N., Fišar, Z., & Ghosh, K. K. (2016) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2016.03.084 · Cited by 71
Cytochrome c Oxidase and Its Role in Neurodegeneration and Neuroprotection
Arnold, S. (2012) · Advances in experimental medicine and biology · doi:10.1007/978-1-4614-3573-0_13 · Cited by 77
Is Parkinson's disease a mitochondrial disorder?
Nakagawa-Hattori, Y., Yoshino, H., Kondo, T., Mizuno, Y., & Horai, S. (1992) · Journal of the Neurological Sciences · doi:10.1016/0022-510x(92)90205-y · Cited by 71
Verma, S., Shakya, V. P. S., & Idnurm, A. (2018) · Virulence · doi:10.1080/21505594.2017.1414133 · Cited by 67
Ben‐Shachar, D., Bonne, O. B., Chisin, R., Klein, E., Lester, H., Aharon‐Peretz, J., Yona, I., & Freedman, N. (2007) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2006.12.025 · Cited by 72
Lim, S. C., Tajika, M., Shimura, M., et al. (2018) · Scientific Reports · doi:10.1038/s41598-017-18530-4 · Cited by 70
Role of platelets in neurodegenerative diseases: a universal pathophysiology
Behari, M., & Shrivastava, M. (2013) · International Journal of Neuroscience · doi:10.3109/00207454.2012.751534 · Cited by 68
Alzheimer's Disease: From Mitochondrial Perturbations to Mitochondrial Medicine
Cardoso, S., Carvalho, C., Correia, S. C., Seiça, R. M. F., & Moreira, P. I. (2016) · Brain Pathology · doi:10.1111/bpa.12402 · Cited by 69
Alzheimer’s Disease Pathologic Cascades: Who Comes First, What Drives What
Swerdlow, R. H. (2011) · Neurotoxicity Research · doi:10.1007/s12640-011-9272-9 · Cited by 69
Mitochondrial abnormalities in muscle and other aging cells: Classification, causes, and effects
DiMauro, S., Tanji, K., Bonilla, E., Pallotti, F., & Schon, E. A. (2002) · Muscle & Nerve · doi:10.1002/mus.10194 · Cited by 64
Luft, R., & Landau, B. R. (1995) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.1995.tb01218.x · Cited by 66
Swerdlow, N., & Wilkins, H. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21249661 · Cited by 66
“enzyme, COX (or complex IV), has reduced Vmax in AD brain, fibroblasts, and blood samples [128,131-142].”
BackgroundFarber, S. A., Slack, B. E., & Blusztajn, J. K. (2000) · The FASEB Journal · doi:10.1096/fj.99-0853 · Cited by 63
Mitochondrial Metabolism in Major Neurological Diseases
Zhou, Z., Austin, G. L., Young, L. E. A., Johnson, L. A., & Sun, R. C. (2018) · Cells · doi:10.3390/cells7120229 · Cited by 67
“This included reductions in cytochrome oxidase (COX) activity in AD patients [88], and decreases in mitochondrial enzymes such as PDH, and other enzymes in the early part of the TCA cycle, such as isocitrate dehydrogenase and”
BackgroundHarman, D. (1993) · AGE · doi:10.1007/bf02436127 · Cited by 63
“For example, the mutation(s) responsible for the depressed cytochrome oxidase of platelet mitochondria found in five out of a group of six Alzheimer's patients (13) and the point mutations in cedon 331 of mitochondrial NADH dehydrogenase subunit 2 (ND 2) detected in 10 of 19 Alzheimer's brains (106).”
BackgroundImpact of Tau on Neurovascular Pathology in Alzheimer's Disease
Canepa, E., & Fossati, S. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2020.573324 · Cited by 67
Fišar, Z., Hansíková, H., Křížová, J., Jirák, R., Kitzlerová, E., Zvěřová, M., Hroudová, J., Wenchich, L., Zeman, J., & Raboch, J. (2019) · Mitochondrion · doi:10.1016/j.mito.2019.07.013 · Cited by 64
Mitochondrial Microheteroplasmy and a Theory of Aging and Age-Related Disease
Smigrodzki, R. M., & Khan, S. M. (2005) · Rejuvenation Research · doi:10.1089/rej.2005.8.172 · Cited by 62
de Lustig, E. S., Serra, J. A., Kohan, S., et al. (1993) · Journal of the Neurological Sciences · doi:10.1016/0022-510x(93)90062-4 · Cited by 63
Korábečný, J., Nepovimová, E., Cikánková, T., Špilovská, K., Vašková, L., Mezeiová, E., Kuča, K., & Hroudová, J. (2018) · Neuroscience · doi:10.1016/j.neuroscience.2017.06.034 · Cited by 64
Functional Foods: An Approach to Modulate Molecular Mechanisms of Alzheimer’s Disease
Atlante, A., Amadoro, G., Bobba, A., & Latina, V. (2020) · Cells · doi:10.3390/cells9112347 · Cited by 67
Wilkins, H., Koppel, S. J., Bothwell, R. J., Mahnken, J. D., Burns, J. M., & Swerdlow, R. H. (2017) · Redox Biology · doi:10.1016/j.redox.2017.04.010 · Cited by 61
“The AD COX deficit manifests across several tissues, including platelets [24].”
BackgroundRegional hypometabolism in the 3xTg mouse model of Alzheimer's disease
Adlimoghaddam, A., Snow, W. M., Stortz, G., Perez, C., Djordjevic, J., Goertzen, A. L., Ko, J. H., & Albensi, B. C. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.03.008 · Cited by 61
Wang, Y., Mishra, A., & Brinton, R. D. (2020) · F1000Research · doi:10.12688/f1000research.21599.1 · Cited by 65
Shi, C., Wu, F., & Xu, J. (2012) · Journal of Bioenergetics and Biomembranes · doi:10.1007/s10863-012-9495-3 · Cited by 60
Mitochondrial Dysfunction and Stress Responses in Alzheimer’s Disease
Weidling, I. W., & Swerdlow, R. H. (2019) · Biology · doi:10.3390/biology8020039 · Cited by 59
“showed altered COX activity in AD platelets, later extending their findings to AD brain tissue [4,27].”
BackgroundRethinking Alzheimer's Disease Therapy: Are Mitochondria the Key?
Ankarcrona, M., Mangialasche, F., & Winblad, B. G. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-100327 · Cited by 60
“vulnerable neurons [32], brain glucose metabolism is decreased [33], and the activities of both tricarboxylic acid cycle enzymes [34] and cytochrome c oxidase are reduced [35–38].”
BackgroundThe Frequency of Point Mutations in Mitochondrial DNA Is Elevated in the Alzheimer's Brain
Chang, S.-W., Zhang, D., Chung, H. D., & Zassenhaus, H. P. (2000) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.2000.2885 · Cited by 58
Mitochondrial function in neurodegeneration and ageing
Schapira, A. H. V., & Cooper, J. A. D. (1992) · Mutation Research/DNAging · doi:10.1016/0921-8734(92)90018-k · Cited by 59
Cada, A. M., Gonzalez-Lima, F., Rose, G. M., & Bennett, M. C. (1995) · Metabolic Brain Disease · doi:10.1007/bf02109361 · Cited by 58
“Cytochrome oxidase has been shown to be more vulnerable to insult in Alzheimer's disease than are other enzymes of the respiratory chain (Parker et al., 1990; 1994a,b; Kish et al., 1992, Beal et al., 1993, Mecocci et al ., 1994, Mutisya et al., 1994).”
BackgroundLe, N. Q. K., Ho, Q., Yapp, E. K. Y., et al. (2019) · Neurocomputing · doi:10.1016/j.neucom.2019.09.070 · Cited by 58
Mitochondria, Cognitive Impairment, and Alzheimer's Disease
Mancuso, M., Calsolaro, V., Orsucci, D., Carlesi, C., Choub, A., Piazza, S., & Siciliano, G. (2009) · International Journal of Alzheimer s Disease · doi:10.4061/2009/951548 · Cited by 58
“…of mitochondrial dementia requires neuropsychological testing, cerebrospinal fluid investigations, visually-evoked potentials, EEG, brain CT and MRI scans, phosphorus or protonmagnetic resonance spectroscopy, SPECT, or positron emission tomography with fluorine 18-labeled deoxyglucose…”
Nuclear and mitochondrial DNA oxidation in Alzheimer's disease
Santos, R. X., Correia, S. C., Zhu, X., Lee, H.-G., Petersen, R. B., Nunomura, A., Smith, M. A., Perry, G., & Moreira, P. I. (2012) · Free Radical Research · doi:10.3109/10715762.2011.648188 · Cited by 57
Theurey, P., Connolly, N. M. C., Fortunati, I., Basso, E., Lauwen, S., Ferrante, C., Pinho, C. M., Joselin, A. P., Gioran, A., Bano, D., et al. (2019) · Aging Cell · doi:10.1111/acel.12924 · Cited by 57
Oxidative stress, antioxidants, aging and disease
Packer, L. (1995) · Birkhäuser Basel eBooks · doi:10.1007/978-3-0348-7337-6_1 · Cited by 56
Mitochondrial Cascade Hypothesis of Alzheimer's Disease: Myth or Reality?
Mancuso, M., Coppedè, F., Murri, L., & Siciliano, G. (2007) · Antioxidants and Redox Signaling · doi:10.1089/ars.2007.1761 · Cited by 56
“Deficient COX activity has been reported by several authors in different brain regions (7, 71, 93, 116), as well as in platelets (83) and fibroblasts (99) of sAD patients.”
Mitochondrial Dysfunction in Neurodegenerative Disorders and Ageing
Turner, C., & Schapira, A. H. V. (2001) · Advances in experimental medicine and biology · doi:10.1007/978-1-4615-1249-3_19 · Cited by 56
Mitochondria, Amyloid β, and Alzheimer′s Disease
Readnower, R. D., Sauerbeck, A. D., & Sullivan, P. G. (2011) · International Journal of Alzheimer s Disease · doi:10.4061/2011/104545 · Cited by 58
“The most documented reduction of mitochondrial enzyme activity in AD is the activity of complex IV [5, 21–23].”
BackgroundFunctional analyses of major cancer-related signaling pathways in Alzheimer's disease etiology
Guo, J., Cheng, J., North, B. J., & Wei, W. (2017) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2017.07.001 · Cited by 55
Mitochondrial enzyme deficiencies in Down's syndrome
Prince, J. A., Jia, S., Båve, U., et al. (1994) · Journal of Neural Transmission - Parkinsons Disease and Dementia Section · doi:10.1007/bf02260938 · Cited by 54
Is a point mutation in the mitochondrial ND2 gene associated with alzheimer's disease?
Petruzzella, V., Chen, X., & Schon, E. A. (1992) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(05)80834-4 · Cited by 53
Mitochondrial links between brain aging and Alzheimer’s disease
Wilkins, H., & Swerdlow, R. H. (2021) · Translational Neurodegeneration · doi:10.1186/s40035-021-00261-2 · Cited by 53
Quantitative Histochemistry of Cytochrome Oxidase Activity
Gonzalez-Lima, F., & Cada, A. M. (1998) · Springer eBooks · doi:10.1007/978-1-4757-9936-1_2 · Cited by 53
Hamblet, N. S., Ragland, B. D., Ali, M. A., Conyers, B., & Castora, F. J. (2005) · Electrophoresis · doi:10.1002/elps.200500420 · Cited by 53
Bennett, M. C., Mlady, G. W., Fleshner, M., & Rose, G. M. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.3.1330 · Cited by 53
- Self-citation
Mitochondrial function and Aβ in Alzheimer's disease postmortem brain
Troutwine, B. R., Strope, T. A., Franczak, E., Lysaker, C. R., Hamid, L., Mansel, C., Stopperan, J. A., Gouvion, C. M., Haeri, M., Swerdlow, R. H., et al. (2022) · Neurobiology of Disease · doi:10.1016/j.nbd.2022.105781 · Cited by 51
“Mitochondrial-localized APP and γ-secretase lead to generation of Aβ within mitochondria (Del Prete et al., 2017; Devi and Anandatheerthavarada, 2010; Hansson Petersen et al., 2008; Pavlov et al., 2011).”
BackgroundTriad of Risk for Late Onset Alzheimer’s: Mitochondrial Haplotype, APOE Genotype and Chromosomal Sex
Wang, Y., & Brinton, R. D. (2016) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2016.00232 · Cited by 52
“In the early 1990’s, reduced cytochrome c oxidase (complex IV) activity was observed in both platelets and postmortem AD brain Frontiers in Aging Neuroscience | www.frontiersin.org 3 October 2016 | Volume 8 | Article 232 (Parker et al., 1990, 1994).”
Background
Metadata
- Authors
- Parker, W. D., Filley, C. M., & Parks, J. K.
- Affiliations
- University of Colorado Denver (US)
- Venue
- Neurology
- Published
- 1990-08
- Volume
- 40
- Issue
- 8
- Pages
- 1302-1302
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W1988731658
- Cited by
- 598
- References
- 0
- Citations by year
- 2026: 19 · 2025: 10 · 2024: 12 · 2023: 20 · 2022: 9 · 2021: 22 · 2020: 25 · 2019: 19 · 2018: 18 · 2017: 18 · 2016: 28 · 2015: 10 · 2014: 10 · 2013: 21 · 2012: 15
- FWCI
- 7.27
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (7r01ns025382-06)
- National Institute of Neurological Disorders and Stroke (NS25382)
- National Center for Research Resources (RR-69)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- cytochrome oxidase deficiency, Alzheimer's disease, platelet mitochondria, electron transport chain, mitochondrial dysfunction, systemic disease
- MeSH terms
- Aged, Alzheimer Disease, Blood Platelets, Electron Transport Complex IV, Electron Transport, Female, Humans, Kinetics, Male, Mitochondria, Reference Values, Cytochrome-c Oxidase Deficiency
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