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Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics.
Bisht J, Rawat P, Shin AC, Hegde V.
Cells · 2026
Abstract
Alzheimer's disease (AD) is the most prevalent form of dementia and is characterized by progressive cognitive decline due to the loss of neurons. The accumulation of extracellular senile plaques (Aβ) and intracellular tau neurofibrillary tangles (NFTs) is a key pathological feature of AD. Mitochondrial dysfunction(definition) is implicated in all key AD pathologies, whether as a cause or a consequence of disease progression. Growing evidence indicates that mitochondrial impairment plays a central role in AD pathogenesis by disrupting cellular homeostasis, promoting oxidative stress, and contributing to progressive neuronal death. Therefore, targeting mitochondria may offer promising insights into the development of disease-modifying therapies. In this review, we summarize current evidence on the role of mitochondrial dysfunction in the pathophysiology of AD and on its therapeutic potential.
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Provenance
- Source
- Europe PMC
- DOI
- 10.3390/cells15110990
- Canonical
- link ↗
- Fetched
- 2026-07-01 MST
Cite this
APA
J, B., P, R., AC, S., & V., H. (2026). Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics. <em>Cells</em>. https://doi.org/10.3390/cells15110990
Vancouver
J B, P R, AC S, V. H. Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics. Cells. 2026. doi:10.3390/cells15110990.
BibTeX
@article{bisht2026Mitoch,
title = {Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics.},
author = {Bisht J and Rawat P and Shin AC and Hegde V.},
journal = {Cells},
year = {2026},
doi = {10.3390/cells15110990},
}
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