Mitochondrial dysfunction in psychiatric and neurological diseases: Cause(s), consequence(s), and implications of antioxidant therapy

Authors

  • Deepak M. Kasote,

    Corresponding author
    • MACS-Agharkar Research Institute, Pune, MS, India
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  • Mahabaleshwar V. Hegde,

    1. Centre for Innovation in Nutrition, Health, Disease, Interactive Research School for Health Affairs (IRSHA), Bharati Vidyapeeth University, Dhankwadi, Pune, MS, India
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  • Surendra S. Katyare

    1. Real World Nutrition Laboratory, Bharati Vidyapeeth University, Dhankawadi, Pune, MS, India
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    • Surendra S. Katyare is formerly a Professor of Biochemistry at the M.S. University of Baroda.


  • All authors are contributed equally to this work.

Address for correspondence to: Deepak M. Kasote, Ph.D., MACS-Agharkar Research Institute, G.G. Agarkar Road, Pune 411004, MS, India. Tel.: +91 2025 654 357; Fax: +91 2025 651 542; E-mail: deepak_kasote@yahoo.com

Abstract

Mitochondrial dysfunction is at the base of development and progression of several psychiatric and neurologic diseases with different etiologies. MtDNA/nDNA mutational damage, failure of endogenous antioxidant defenses, hormonal malfunction, altered membrane permeability, metabolic dysregulation, disruption of calcium buffering capacity and ageing have been found to be the root causes of mitochondrial dysfunction in psychatric and neurodegenerative diseases. However, the overall consequences of mitochondrial dysfunction are only limited to increase in oxidative/nitrosative stress and cellular energy crises. Thus far, extensive efforts have been made to improve mitochondrial function through specific cause-dependent antioxidant therapy. However, owing to complex genetic and interlinked causes of mitochondrial dysfunction, it has not been possible to achieve any common, unique supportive antioxidant therapeutic strategy for the treatment of psychiatric and neurologic diseases. Hence, we propose an antioxidant therapeutic strategy for management of consequences of mitochondrial dysfunction in psychiatric and neurologic diseases. It is expected that this will not only reduces oxidative stress, but also promote anaerobic energy production. © 2013 BioFactors, 39(4):393–407, 2013

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