Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics.

Authors

Jasbir Bisht, Priyanka Rawat, Andrew C Shin, Vijay Hegde

Published in

Cells. Volume 15. Issue 11. May 28, 2026. Epub May 28, 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 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.

PMID:
42274583
Bibliographic data and abstract were imported from PubMed on 12 Sep 2026.

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