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Current Neuropharmacology

Editor-in-Chief

ISSN (Print): 1570-159X
ISSN (Online): 1875-6190

Mitochondrial Dysfunction in Depression

Author(s): Yashika Bansal and Anurag Kuhad

Volume 14, Issue 6, 2016

Page: [610 - 618] Pages: 9

DOI: 10.2174/1570159X14666160229114755

Price: $65

Abstract

Background: Depression is the most debilitating neuropsychiatric disorder with significant impact on socio-occupational and well being of individual. The exact pathophysiology of depression is still enigmatic though various theories have been put forwarded. There are evidences showing that mitochondrial dysfunction in various brain regions is associated with depression. Recent findings have sparked renewed appreciation for the role of mitochondria in many intracellular processes coupled to synaptic plasticity and cellular resilience. New insights in depression pathophysiology are revolving around the impairment of neuroplasticity. Mitochondria have potential role in ATP production, intracellular Ca2+ signalling to establish membrane stability, reactive oxygen species (ROS) balance and to execute the complex processes of neurotransmission and plasticity. So understanding the various concepts of mitochondrial dysfunction in pathogenesis of depression indubitably helps to generate novel and more targeted therapeutic approaches for depression treatment.

Objective: The review was aimed to give a comprehensive insight on role of mitochondrial dysfunction in depression.

Result: Targeting mitochondrial dysfunction and enhancing the mitochondrial functions might act as potential target for the treatment of depression.

Conclusion: Literature cited in this review highly supports the role of mitochondrial dysfunction in depression. As impairment in the mitochondrial functions lead to the generation of various insults that exaggerate the pathogenesis of depression. So, it is useful to study mitochondrial dysfunction in relation to mood disorders, synaptic plasticity, neurogenesis and enhancing the functions of mitochondria might show promiscuous effects in the treatment of depressed patients.

Keywords: Depression, Mitochondrial dysfunction, Reactive oxygen species, neurotransmitter, Mitochondria, electron transport chain.

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