The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Mitochondria dysfunction of Alzheimer's disease cybrids enhances Aβ toxicity
Open accessAbstract
Alzheimer's disease (AD) brain reveals high rates of oxygen consumption and oxidative stress, altered antioxidant defences, increased oxidized polyunsaturated fatty acids, and elevated transition metal ions. Mitochondrial dysfunction in AD is perhaps relevant to these observations, as such may contribute to neurodegenerative cell death through the formation of reactive oxygen species (ROS) and the release of molecules that initiate programmed cell death pathways. In this study, we analyzed the effects of beta‐amyloid peptide (Aβ) on human teratocarcinoma (NT2) cells expressing endogenous mitochondrial DNA (mtDNA), mtDNA from AD subjects (AD cybrids), and mtDNA from age‐matched control subjects (control cybrids). In addition to finding reduced cytochrome oxidase activity, elevated ROS, and reduced ATP levels in the AD cybrids, when these cell lines were exposed to Aβ 1–40 we observed excessive mitochondrial membrane potential depolarization, increased cytoplasmic cytochrome c, and elevated caspase‐3 activity. When exposed to Aβ, events associated with programmed cell death are activated in AD NT2 cybrids to a greater extent than they are in control cybrids or the native NT2 cell line, suggesting a role for mtDNA‐derived mitochondrial dysfunction in AD degeneration.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease.
Smith, C. D., Carney, J. M., Starke-Reed, P. E., Oliver, C. N., Stadtman, E. R., Floyd, R. A., & Markesbery, W. R. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.23.10540 · Cited by 1,296
Oxidative damage to mitochondrial DNA is increased in Alzheimer’s disease
Mecocci, P., MacGarvey, U., & Beal, M. F. (1994) · Annals of Neurology · doi:10.1002/ana.410360510 · Cited by 1,037
Gabuzda, D., Busciglio, J., Chen, L. B., Matsudaira, P., & Yankner, B. A. (1994) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)36875-8 · Cited by 373
Cytochrome c oxidase is decreased in Alzheimer’s disease platelets
Cardoso, S. M., Proença, M. T., Santos, S., Santana, I., & Oliveira, C. R. (2004) · Neurobiology of Aging · doi:10.1016/s0197-4580(03)00033-2 · Cited by 281
Self-citationCybrids in Alzheimer's disease: a cellular model of the disease?
Swerdlow, R. H., Parks, J. K., Cassarino, D. S., Maguire, D. J., Maguire, R. S., Bennett, J. P., Davis, R. E., & Parker, W. D. (1997) · Neurology · doi:10.1212/wnl.49.4.918 · Cited by 272
Self-citationFunctional mitochondria are required for amyloid β‐mediated neurotoxicity
Cardoso, S. M., Santos, S., Swerdlow, R. H., & Oliveira, C. R. (2001) · The FASEB Journal · doi:10.1096/fj.00-0561fje · Cited by 203
Self-citation
Cited by
Querfurth, H. W., & LaFerla, F. M. (2010) · New England Journal of Medicine · doi:10.1056/nejmra0909142 · Cited by 4,569
Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease
Tönnies, E., & Trushina, E. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161088 · Cited by 1,750
Manczak, M., Anekonda, T. S., Henson, E., Park, B. S., Quinn, J., & Reddy, P. H. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddl066 · Cited by 1,104
Yao, J., Irwin, R. W., Zhao, L., Nilsen, J., Hamilton, R. T., & Brinton, R. D. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0903563106 · Cited by 940
Du, H., Guo, L., Fang, F., Chen, D., A Sosunov, A., M McKhann, G., Yan, Y., Wang, C., Zhang, H., Molkentin, J. D., et al. (2008) · Nature Medicine · doi:10.1038/nm.1868 · Cited by 932
Metadata
- Authors
- Cardoso, S. M., Santana, I., Swerdlow, R. H., & Oliveira, C. R.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2004-04-20
- Volume
- 89
- Issue
- 6
- Pages
- 1417-1426
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2141594388
- Cited by
- 261
- References
- 6
- FWCI
- 8.55
- Type
- journal article
- Language
- en
- Open access
- green
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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Mitochondria dysfunction of Alzheimer's disease cybrids enhances Aβ toxicity. https://app.cochat.ai/papers/10.1111/j.1471-4159.2004.02438.x
- The paper
- Cardoso, S. M., Santana, I., Swerdlow, R. H., & Oliveira, C. R. (2004). Mitochondria dysfunction of Alzheimer's disease cybrids enhances Aβ toxicity. Journal of Neurochemistry. https://doi.org/10.1111/j.1471-4159.2004.02438.x
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.