The Molecular Mechanisms of Action of Photobiomodulation Against Neurodegenerative Diseases: A Systematic Review
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REVIEW PAPER
The Molecular Mechanisms of Action of Photobiomodulation Against Neurodegenerative Diseases: A Systematic Review Mayukha Bathini1,2 · Chandavalli Ramappa Raghushaker2 · Krishna Kishore Mahato2 Received: 1 August 2020 / Accepted: 18 November 2020 © The Author(s) 2020
Abstract Neurodegenerative diseases might be slow but relentless, as we continue to fail in treating or delaying their progression. Given the complexity in the pathogenesis of these diseases, a broad-acting approach like photobiomodulation can prove promising. Photobiomodulation (PBM) uses red and infrared light for therapeutic benefits, working by stimulating growth and proliferation. The implications of photobiomodulation have been studied in several neurodegenerative disease models. It has been shown to improve cell survival, decrease apoptosis, alleviate oxidative stress, suppress inflammation, and rescue mitochondrial function. In in vivo models, it has reportedly preserved motor and cognitive skills. Beyond mitochondrial stimulation, the molecular mechanisms by which photobiomodulation protects against neurodegeneration have not been very well studied. This review has systematically been undertaken to study the effects of photobiomodulation at a molecular level and identify the different biochemical pathways and molecular changes in the process. The data showed the involvement of pathways like extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MAPK), and protein kinase B (Akt). In addition, the expression of several genes and proteins playing different roles in the disease mechanisms was found to be influenced by PBM, such as neurotrophic factors and secretases. Studying the literature indicated that PBM can be translated to a potential therapeutic tool, acting through a spectrum of mechanisms that work together to decelerate disease progression in the organism, which is difficult to achieve through pharmacological interventions. Keywords Neurodegenerative diseases · Photobiomodulation · Molecular pathway · Neuroprotection Abbreviations ABCB1 ATP-binding cassette subfamily B member 1 p-Akt (phosphorylated) protein kinase B APPswe Swedish mutation of APP ATP Adenosine triphosphate Bcl2 B cell lymphoma 2 Bcl-xL B cell lymphoma-extra large CD45 Leukocyte common antigen (p-)cPLA2 (phosphorylated) Cytoplasmic phospholipase 2 CREB cAMP response element-binding protein DAG Diacylglycerol GSK3β Glycogen synthase kinase 3 beta * Krishna Kishore Mahato [email protected] 1
Manipal School of Life Sciences, Manipal Academy of Higher Education, Manipal, Karnataka 576104, India
Department of Biophysics, Manipal School of Life Sciences, Manipal Academy of Higher Education, Manipal, Karnataka 576104, India
2
IP3 Inositol triphosphate IP3R Inositol triphosphate receptor JAK Janus kinase JNK c-Jun N-terminal kinase mTOR Mammalian target of rapamycin NADPH Nicotinamide adenine dinucleotide phosphate NRF2 Nuclear factor erythroid 2-related factor PGC-1α Peroxisome proliferator-activated rec
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