Cybrids in Alzheimer's disease: a cellular model of the disease?
Abstract
The mitochondrial electron transport chain enzyme cytochrome c oxidase (COX) is defective in patients with sporadic Alzheimer's disease (AD). This defect arises from the mutation of mitochondrial DNA (mtDNA). To develop a tissue culture system that would express this genetically derived bioenergetic lesion and permit characterization of its functional consequences, we depleted Ntera2/D1 (NT2) teratocarcinoma cells of endogenous mtDNA and repopulated them with platelet mtDNA from AD patients. Cytochrome c oxidase activity was depressed in the resulting AD cytoplasmic hybrids (cybrids) compared with cybrids prepared with mtDNA from non-AD controls. Reactive oxygen species (ROS) production and free radical scavenging enzyme activities were significantly elevated in AD cybrids. A COX defect in NT2 AD cybrid lines indicates that AD patients possess mtDNA COX gene mutations that are sufficient for determining this biochemical lesion. Expression of unique functional characteristics (increased ROS production and free radical scavenging enzyme activities) relevant to neurodegeneration demonstrates the utility of these cells in defining AD pathophysiology at a cellular level. This in vitro tissue culture model of AD may prove useful in drug screening.
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Mean COX activity was lower in cybrid lines containing AD subject mtDNA than in cybrid lines containing control subject mtDNA.
“Mean COX activity was lower in cybrid lines containing AD subject mtDNA than it was in cybrid lines containing control subject mtDNA [90, 91].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [91]
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Self-citationCunha‐Oliveira, T., Rego, A. C., Cardoso, S. M., Borges, F., Swerdlow, R. H., Macedo, T., & Oliveira, C. R. (2006) · Brain Research · doi:10.1016/j.brainres.2006.03.061 · Cited by 126 · see citing works
Self-citationMitochondrial dysfunction and Alzheimer's disease
Maruszak, A., & Żekanowski, C. (2010) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2010.07.004 · Cited by 123 · see citing works
Transient receptor potential channels in Alzheimer's disease
Yamamoto, S., Wajima, T., Hara, Y., Nishida, M., & Mori, Y. (2007) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2007.03.006 · Cited by 124 · see citing works
Cassarino, D. S., Halvorsen, E. M., Swerdlow, R. H., Abramova, N. N., Parker, W. D., Sturgill, T. W., & Bennett, J. P. (2000) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2000.0741384.x · Cited by 121 · see citing works
Self-citationRedox signaling at the crossroads of human health and disease
Zuo, J., Zhang, Z., Luo, M., Zhou, L., Nice, E. C., Zhang, W., Wang, C., & Huang, C. (2022) · MedComm · doi:10.1002/mco2.127 · Cited by 120 · see citing works
Mitochondrial failures in Alzheimer's disease
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Human Mitochondrial Diseases: Answering Questions and Questioning Answers
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Esteves, A. R., Domingues, A. F., Ferreira, I. L., Januário, C., Swerdlow, R. H., Oliveira, C. R., & Cardoso, S. M. (2008) · Mitochondrion · doi:10.1016/j.mito.2008.03.004 · Cited by 110 · see citing works
Self-citationThe Impact of Mitochondrial Fusion and Fission Modulation in Sporadic Parkinson’s Disease
Santos, D., Esteves, A. R., Silva, D. F., Januário, C., & Cardoso, S. M. (2014) · Molecular Neurobiology · doi:10.1007/s12035-014-8893-4 · Cited by 111 · see citing works
Mitochondria, Cybrids, Aging, and Alzheimer's Disease
Swerdlow, R. H., Koppel, S., Weidling, I., Hayley, C., Ji, Y., & Wilkins, H. M. (2017) · Progress in Molecular Biology and Translational Science · doi:10.1016/bs.pmbts.2016.12.017 · Cited by 106 · see citing works
Self-citationMitochondrial ND5 mutations in idiopathic Parkinson’s disease
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Self-citationThe rescue of microtubule-dependent traffic recovers mitochondrial function in Parkinson's disease
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Reduced gray matter volume in normal adults with a maternal family history of Alzheimer disease
Honea, R. A., Swerdlow, R. H., Vidoni, E. D., Goodwin, J., & Burns, J. M. (2010) · Neurology · doi:10.1212/wnl.0b013e3181c918cb · Cited by 106 · see citing works
Self-citationCardiorespiratory fitness is associated with atrophy in Alzheimer's and aging over 2 years
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Self-citationTherapeutic potential of N-acetylcysteine in age-related mitochondrial neurodegenerative diseases
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Induction of cytochrome c-mediated apoptosis by amyloid β 25-35 requires functional mitochondria
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Self-citationMitochondrial function and abnormalities implicated in the pathogenesis of ASD
Castora, F. J. (2018) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2018.12.015 · Cited by 104 · see citing works
The Role of Mitochondria in the Pathogenesis of Neurodegenerative Diseases
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Mitochondria in Alzheimer's disease and their potential role in Alzheimer's proteostasis
Weidling, I. W., & Swerdlow, R. H. (2020) · Experimental Neurology · doi:10.1016/j.expneurol.2020.113321 · Cited by 100 · see citing works
Self-citationCybrids in Alzheimer's disease: A cellular model of the disease?
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Does the mitochondrial genome play a role in the etiology of Alzheimer’s disease?
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Cassarino, D. S., Swerdlow, R. H., Parks, J. K., Parker, W. D., & Bennett, J. P. (1998) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1998.8866 · Cited by 98 · see citing works
Self-citation
- Authors
- Swerdlow, R. H., Parks, J. K., Cassarino, D. S., Maguire, D. J., Maguire, R. S., Bennett, J. P., Davis, R. E., & Parker, W. D.
- Affiliations
- Griffith University (AU)
- Venue
- Neurology
- Published
- 1997-10
- Volume
- 49
- Issue
- 4
- Pages
- 918-925
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W4320578147
- Cited by
- 272
- References
- 18
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 4 · 2023: 11 · 2022: 8 · 2021: 7 · 2020: 7 · 2019: 9 · 2018: 4 · 2017: 5 · 2016: 6 · 2015: 4 · 2014: 4 · 2013: 12 · 2012: 11
- FWCI
- 4.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5t32ns007199-15)
- National Institute of Neurological Disorders and Stroke (NS-07199, NS34325)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Keywords
- Alzheimer's disease, cybrids, cytochrome c oxidase, mitochondrial DNA mutations, mitochondrial electron transport chain, reactive oxygen species, free radical scavenging enzymes, neurodegeneration, drug screening
- MeSH terms
- Alzheimer Disease, Brain, Electron Transport Complex IV, Cytoplasm, DNA, Mitochondrial, Genetic Techniques, Humans, Hybridization, Genetic, Mutation, Reference Values, Tumor Cells, Cultured, Reactive Oxygen Species, Gene Transfer Techniques, Teratocarcinoma
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