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Review

Mitochondrial Quality Control in Alzheimer’s Disease: Insights from Caenorhabditis elegans Models

1
Department of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center (URMC), Rochester, NY 14642, USA
2
Department of Pathology, University of Rochester Medical Center (URMC), Rochester, NY 14642, USA
3
Department of Medicine, Nephrology Division, University of Rochester Medical Center (URMC), Rochester, NY 14642, USA
*
Author to whom correspondence should be addressed.
Antioxidants 2024, 13(11), 1343; https://doi.org/10.3390/antiox13111343
Submission received: 12 September 2024 / Revised: 16 October 2024 / Accepted: 24 October 2024 / Published: 1 November 2024
(This article belongs to the Special Issue Oxidative Stress and Alzheimer’s Disease)

Abstract

Alzheimer’s disease (AD) is a complex neurodegenerative disorder that is classically defined by the extracellular deposition of senile plaques rich in amyloid-beta (Aβ) protein and the intracellular accumulation of neurofibrillary tangles (NFTs) that are rich in aberrantly modified tau protein. In addition to aggregative and proteostatic abnormalities, neurons affected by AD also frequently possess dysfunctional mitochondria and disrupted mitochondrial maintenance, such as the inability to eliminate damaged mitochondria via mitophagy. Decades have been spent interrogating the etiopathogenesis of AD, and contributions from model organism research have aided in developing a more fundamental understanding of molecular dysfunction caused by Aβ and toxic tau aggregates. The soil nematode C. elegans is a genetic model organism that has been widely used for interrogating neurodegenerative mechanisms including AD. In this review, we discuss the advantages and limitations of the many C. elegans AD models, with a special focus and discussion on how mitochondrial quality control pathways (namely mitophagy) may contribute to AD development. We also summarize evidence on how targeting mitophagy has been therapeutically beneficial in AD. Lastly, we delineate possible mechanisms that can work alone or in concert to ultimately lead to mitophagy impairment in neurons and may contribute to AD etiopathology.
Keywords: Alzheimer’s disease; mitochondria; Caenorhabditis elegans; model organism; mitochondria quality control; mitophagy; aging; neurodegeneration Alzheimer’s disease; mitochondria; Caenorhabditis elegans; model organism; mitochondria quality control; mitophagy; aging; neurodegeneration

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MDPI and ACS Style

Ganguly, U.; Carroll, T.; Nehrke, K.; Johnson, G.V.W. Mitochondrial Quality Control in Alzheimer’s Disease: Insights from Caenorhabditis elegans Models. Antioxidants 2024, 13, 1343. https://doi.org/10.3390/antiox13111343

AMA Style

Ganguly U, Carroll T, Nehrke K, Johnson GVW. Mitochondrial Quality Control in Alzheimer’s Disease: Insights from Caenorhabditis elegans Models. Antioxidants. 2024; 13(11):1343. https://doi.org/10.3390/antiox13111343

Chicago/Turabian Style

Ganguly, Upasana, Trae Carroll, Keith Nehrke, and Gail V. W. Johnson. 2024. "Mitochondrial Quality Control in Alzheimer’s Disease: Insights from Caenorhabditis elegans Models" Antioxidants 13, no. 11: 1343. https://doi.org/10.3390/antiox13111343

APA Style

Ganguly, U., Carroll, T., Nehrke, K., & Johnson, G. V. W. (2024). Mitochondrial Quality Control in Alzheimer’s Disease: Insights from Caenorhabditis elegans Models. Antioxidants, 13(11), 1343. https://doi.org/10.3390/antiox13111343

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