The DOI matches its Crossref record; 76 of the 76 references it cites were found in a registry or an index.
Amyloid beta, mitochondrial structural and functional dynamics in Alzheimer's disease
Open accessAbstract
Mitochondria are the major source of energy for the normal functioning of brain cells. Increasing evidence suggests that the amyloid precursor protein (APP) and amyloid beta (Aβ) accumulate in mitochondrial membranes, cause mitochondrial structural and functional damage, and prevent neurons from functioning normally. Oligomeric Ab is reported to induce intracellular Ca2+ levels and to promote the excess accumulation of intracellular Ca2+ into mitochondria, to induce the mitochondrial permeability transition pore to open, and to damage mitochondrial structure. Based on recent gene expression studies of APP transgenic mice and AD postmortem brains, and APP/Aβ and mitochondrial structural studies, we propose that the overexpression of APP and the increased production of Aβ may cause structural changes of mitochondria, including a increase in the production of defective mitochondria, a decrease in mitochondrial trafficking, and the alteration of mitochondrial dynamics in neurons affected by AD. This article discusses some critical issues of APP/Aβ associated with mitochondria, mitochondrial structural and functional damage, and abnormal intracellular calcium regulation in neurons from AD patients. This article also discusses the link between Aβ and impaired mitochondrial dynamics in AD.
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Cites
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ABAD Directly Links Aß to Mitochondrial Toxicity in Alzheimer's Disease
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Self-citationCalcium dyshomeostasis and intracellular signalling in alzheimer's disease
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Self-citationNeuronal calcium mishandling and the pathogenesis of Alzheimer's disease
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Cited by
Zhang, J., Zhang, Y., Wang, J., Xia, Y., Zhang, J., & Chen, L. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01911-3 · Cited by 1,138
The effects of aging in the hippocampus and cognitive decline
Bettio, L. E. B., Rajendran, L., & Gil-Mohapel, J. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.04.030 · Cited by 649
Calkins, M. J., Manczak, M., Mao, P., Shirendeb, U., & Reddy, P. H. (2011) · Human Molecular Genetics · doi:10.1093/hmg/ddr381 · Cited by 646
Self-citationAmyloid Beta and Phosphorylated Tau-Induced Defective Autophagy and Mitophagy in Alzheimer’s Disease
Reddy, P. H., & Oliver, D. M. (2019) · Cells · doi:10.3390/cells8050488 · Cited by 496
Self-citationMitochondria-targeted antioxidants protect against amyloid-β toxicity in Alzheimer's disease neurons
Manczak, M., Mao, P., Calkins, M. J., Cornea, A., Reddy, A. P., Murphy, M. P., Szeto, H. H., Park, B., & Reddy, P. H. (2010) · Journal of Alzheimer's Disease · doi:10.3233/jad-2010-100564 · Cited by 469
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Metadata
- Authors
- Reddy, P. H.
- Venue
- Experimental Neurology
- Publisher
- Elsevier BV
- Published
- 2009-08
- Volume
- 218
- Issue
- 2
- Pages
- 286-292
- ISSN
- 0014-4886 (ISSN-L)
- OpenAlex
- W2139206850
- Cited by
- 264
- References
- 76
- FWCI
- 16.93
- Type
- journal article
- Language
- en
- Open access
- green
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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.
