Med Lasers 2024; 13(3): 109-118  https://doi.org/10.25289/ML.24.023
Restoring mitochondrial dynamics in neuronal health through photobiomodulation
Ken Woo
Department of Ecology and Evolutionary Biology, University of California, Los Angeles, California, LA, USA
Correspondence to: Ken Woo
E-mail: starlord0214@gmail.com
ORCID: https://orcid.org/0000-0001-8560-1865
Received: August 2, 2024; Accepted: August 13, 2024; Published online: August 28, 2024.
© Korean Society for Laser Medicine and Surgery. All rights reserved.

This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Mitochondrial dysfunction is a critical factor in the pathogenesis of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and amyotrophic lateral sclerosis. Disruptions in mitochondrial fusion and fission lead to the accumulation of damaged mitochondria and elevated oxidative stress, contributing to neuronal cell death. Photobiomodulation (PBM) therapy, utilizing low-level laser light or light-emitting diodes, has shown promise in restoring mitochondrial dynamics by stimulating cytochrome c oxidase in the mitochondrial respiratory chain. This enhances adenosine triphosphate production, promotes mitochondrial fusion, and reduces fission. Additionally, PBM attenuates neuroinflammation by reducing pro-inflammatory cytokine and reactive oxygen species production, creating a favorable environment for neuronal survival. This review explores the mechanisms through which PBM influences mitochondrial dynamics and its therapeutic potential in neurodegenerative diseases. By restoring mitochondrial balance and reducing neuroinflammation, PBM offers a unique approach to mitigating mitochondrial dysfunction and enhancing neuronal function.
Keywords: Photobiomodulation; Mitochondrial dysfunction; Mitochondrial dynamics; Neuroinflammation; Neurodegenerative diseases

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