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Mitochondrial Dysfunction: a Potential Therapeutic Target to Treat Alzheimer’s Disease

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Abstract

Mitochondrial dysfunction plays a very vital role in the pathogenesis of Alzheimer’s disease (AD). Several shreds of evidence have indicated that the mitochondrial function is severely compromised under AD pathogenesis. Most of the recent therapeutic strategies have been conversed to treat AD by pinpointing the pathways involved in the pathophysiology of AD. In AD, mitochondria progressively lose their proper functions that are ultimately responsible for their accumulation and removal via the autophagic process, which is called mitophagy that further worsens the progression of this incapacitating disease. Preclinical and clinical studies have suggested that mitochondrial dysfunction along with mitophagy significantly contributes to the accumulation of amyloid-beta (Aβ) fibrils and hyperphosphorylated tau protein tangles which lead to synaptic dysfunctions and cognitive impairments such as memory loss through reactive oxygen species (ROS)–mediated pathway. The present review is intended to discuss the recent advancements in the frontiers of mitochondrial dysfunction and consequent therapeutic strategies that have been employed to treat AD.

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Acknowledgments

Authors would like to acknowledge UGC Dr. D.S. Kothari Postdoctoral scheme for awarding the fellowship to S.N.R (Ref. No-F.4-2/2006 (BSR)/BL/19-20/0032). The authors also would like to acknowledge Bio-render (www.biorender.com) for providing an efficient platform to create all the figures.

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Authors and Affiliations

  1. Centre of Biotechnology, University of Allahabad, Prayagraj, 211002, India

    Sachchida Nand Rai & M. P. Singh

  2. Department of Pharmaceutics ISF College of Pharmacy, Moga, Affiliated to IK Gujral Punjab Technical University, Jalandhar, Punjab, 142001, India

    Charan Singh

  3. Department of Pharmacology, ISF College of Pharmacy, Moga, Affiliated to IK Gujral Punjab Technical University, Jalandhar, Punjab, India

    Arti Singh

  4. Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY, USA

    Brijesh Kumar Singh

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  1. Sachchida Nand Rai
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S.N.R. and B.K.S. designed the study and wrote the manuscript along with creating all the figures. C.S., A.S., and M.P.S. edited the final manuscript.

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Correspondence to Brijesh Kumar Singh.

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Rai, S.N., Singh, C., Singh, A. et al. Mitochondrial Dysfunction: a Potential Therapeutic Target to Treat Alzheimer’s Disease. Mol Neurobiol 57, 3075–3088 (2020). https://doi.org/10.1007/s12035-020-01945-y

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