Overcoming challenges of clinical cell therapies for Parkinson's disease with photobiomodulation

Abstract

Photobiomodulation (PBM) has emerged as a rapidly growing and innovative therapeutic method for various illnesses in recent years. Due to the irreversible nature of Parkinson's disease (PD), it has proven challenging to impede or postpone the progression of the disease. Despite research on pharmacological approaches to halt neuronal degeneration, the viability of these techniques has been called into doubt due to apprehensions over potential side effects and the ethical implications associated with the utilization of embryonic cell transplantation. Hence, developing an innovative therapeutic approach to halting neuronal degeneration and safeguarding neurons from this neurodegenerative disorder is imperative. This review examines the pathogenesis, challenges, and limitations of conventional PD therapies, allowing a closer examination of PBM's distinctive approach within this medical context. Delving into PBM's therapeutic mechanisms in the cells, the effects of different wavelengths on cell therapies in PD patients, and considerations for patient care administration to overcome traditional challenges, this study offers insights into its potential as a promising avenue for PD management.

Keywords: dopaminergic neurons; light therapy; neurodegenerative disease; photobiology.

FIGURE 1

Schematic diagram on the role of innate (the activation of blood-born myeloid cells and microglia) and adaptive (the recruitment of T cells and antibody production) immune behaviors in neuroinflammation.

FIGURE 2

Schematic presence of the molecular mechanism of PBM therapy, illustrated from mitochondria functions. (A) Dr. Hossein Chamkouri, under the supervision of Professor Lei Chen, tested broadband luminescence with wavelengths ranging from 600–1100 nm with adjustable power density; (B) biological structure of the cell with mitochondria as a prominent part of light or PBM therapy; (C and D) resting metabolic activity and stimulated metabolic activity in the mitochondria; (E) the effect of light therapy in the mitochondrial and electron transport chain. The picture was created by biorender.com.

FIGURE 3

Results of animal research experiment at the Johnson & Johnson company, denoted with the experimental chronology, technique, and NIR light application. (A) The rats in a clear plexiglas cylinder and circles delineating the head surface from the eyes and ears, (B) long-term use of PBM reducing the loss of dopaminergic neurons produced by α-syn, (C) no significant variation been observed in the expression levels or pattern of human α-synuclein in nigral TH + dopaminergic neurons between experimental conditions after 3 and 6 weeks of abstinence, (D) long-term use of PBM reducing motor impairments caused by α-synuclein (D), long-term exposure to PBM minimizing the loss of dopaminergic nerve fibers in the striatum caused by α-synuclein (E). Reproduced under terms of the CC-BY license. Copyright 2015, The Authors, published by PLOS.

FIGURE 4

The CerebroLite and “Neuro” helmet PBM devices. (A) Image of PBM helmet for therapy, (B) the Montages showing the mobility of mitochondria tagged with MTRed during CNT68, CNT68-90 min post-LLLT, PD63 min, and PD63-88 min post-LLLT. (C) the PBM “Neuro” helmet gadget, viewed from the side and back, (D) the comparison of treatment outcomes in sham-to-active and active-to-no-treatment groups over 24 weeks, (E) schematic representation of enhanced cerebral blood flow after light therapy. Reproduced under terms of the CC-BY license. Copyright 2009, The Authors, published by Springer Nature. Reproduced under terms of the CC-BY license. Copyright 2023, The Authors, published by Elsevier.