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Autophagy of Mitochondria: A Promising Therapeutic Target for Neurodegenerative Disease

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Abstract

The autophagic process is the only known mechanism for mitochondrial turnover and it has been speculated that dysfunction of autophagy may result in mitochondrial error and cellular stress. Emerging investigations have provided new understanding of how autophagy of mitochondria (also known as mitophagy) is associated with cellular oxidative stress and its impact on neurodegeneration. This impaired autophagic function may be considered as a possible mechanism in the pathogenesis of several neurodegenerative disorders including Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis, and Huntington disease. It can be suggested that autophagy dysfunction along with oxidative stress is considered main events in neurodegenerative disorders. New therapeutic approaches have now begun to target mitochondria as a potential drug target. This review discusses evidence supporting the notion that oxidative stress and autophagy are intimately associated with neurodegenerative disease pathogenesis. This review also explores new approaches that can prevent mitochondrial dysfunction, improve neurodegenerative etiology, and also offer possible cures to the aforementioned neurodegenerative diseases.

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Abbreviations

AD:

Alzhiemers disease

PD:

Parkinson disease

ALS:

Amyotrophic lateral sclerosis

HD:

Huntington’s disease

ROS:

Reactive oxygen species

MS:

Multiple sclerosis

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Acknowledgments

This work was supported by the National Institutes of Health grants HL107640-NT.

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Authors and Affiliations

  1. Department of Physiology and Biophysics, School of Medicine, Health Sciences Center, University of Louisville, A-1201, Louisville, KY, 40202, USA

    Pradip K. Kamat, Anuradha Kalani, Philip Kyles, Suresh C. Tyagi & Neetu Tyagi

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  1. Pradip K. Kamat
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  2. Anuradha Kalani
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  3. Philip Kyles
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Correspondence to Neetu Tyagi.

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Kamat, P.K., Kalani, A., Kyles, P. et al. Autophagy of Mitochondria: A Promising Therapeutic Target for Neurodegenerative Disease. Cell Biochem Biophys 70, 707–719 (2014). https://doi.org/10.1007/s12013-014-0006-5

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