Med Lasers 2024; 13(2): 90-97  https://doi.org/10.25289/ML.24.015
Photobiomodulation therapy in neurodegenerative diseases: mechanisms, clinical applications, and future directions
Ken Woo
Department of Molecular, Cell, and Developmental 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: June 15, 2024; Accepted: June 24, 2024; Published online: June 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
Photobiomodulation (PBM) therapy, using red to near-infrared light (600-1,000 nm), is becoming a promising non-invasive treatment for neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. This review examines the mechanistic insights and the preclinical and clinical evidence supporting the efficacy of PBM in enhancing mitochondrial function, reducing oxidative stress, and modulating neuroinflammation. The impact of PBM therapy on cellular energy production, gene expression, and inflammatory responses provides a comprehensive therapeutic approach targeting multiple pathological pathways in neurodegenerative conditions. Preclinical studies demonstrated the potential of PBM therapy in improving neuronal health and cognitive function, while early clinical trials revealed significant benefits in motor performance and cognitive outcomes with minimal adverse effects. By highlighting the necessity for personalized PBM therapy and its integration with other therapeutic modalities, the literature aims to optimize the treatment efficacy and expand the clinical applications of PBM technology. Further large-scale randomized controlled trials are essential to validate these findings and establish standardized treatment protocols, as current promising results position PBM as a viable and innovative therapeutic option for managing and potentially altering the course of neurodegenerative diseases.
Keywords: Photobiomodulation; Neurodegenerative diseases; Laser; Brain; Nerve
INTRODUCTION

Low-level light therapy, also known as photobiomodulation (PBM), is a growing field within medical therapeutics that uses light wavelengths in the red to near-infrared spectrum (600-1,000 nm) to enhance cellular function and promote healing [1]. PBM is applied to tissues intending to stimulate biological processes such as enhancing cell viability, differentiation, proliferation, and migration [2]. PBM’s versatile applications in various medical fields while having little to no safety concerns in both application and effect on cells makes it a rising technology obtaining recognition concerned with regenerative medicine and biomedical science [3,4]. The technique has been used across various in vivo trials, including wound healing, tissue regeneration, and neurodegenerative diseases [5,6].

Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), make up some of the most challenging conditions in medicine today [7-9]. The gradual loss of neuronal function and structure in these conditions leads to severe cognitive and motor impairments, significantly impacting the lives of those affected [10]. However, contemporary therapeutic approaches primarily focus on managing symptoms rather than halting or reversing the disease progressions [11]. Therefore, new treatments that can address the underlying pathophysiological mechanisms of these diseases are needed.

Common neurodegenerative diseases are complex and involve a combination of genetic, environmental, and behavioral factors. Pathologic characteristics prevalent in these conditions include mitochondrial dysfunction, oxidative stress, protein misfolding, and chronic neuroinflammation, with these interdependent processes being responsible for the gradual decline in neuronal function [12-16]. As our understanding of these mechanisms grows, it becomes increasingly apparent that effective therapeutic approaches must encompass multiple aspects, aiming at multiple pathological pathways simultaneously, to yield meaningful therapeutic outcomes.

Recent advances in PBM research suggest that this therapy has the potential to perform those necessary therapeutic functions. PBM has the potential to provide neuroprotective benefits across a diverse range of neurodegenerative conditions by enhancing mitochondrial function, reducing oxidative stress, and regulating inflammatory responses. Preclinical studies have shown promising outcomes, showing improvements in neuronal function and overall health. Therefore, this review aims to highlight both an overview of these neurodegenerative diseases and the technological advancements and trials of PBM to call for further research in fully understanding its therapeutic potential.

MECHANISMS OF PHOTOBIOMODULATION

Mitochondrial function and cellular energy

While there are competing theories on how PBM exerts its therapeutic effects on individual cells and tissues, with the complete mechanism not fully elucidated yet [17,18], one primary theory has to do with the mitochondria. PBM has been reported to impact mitochondrial function by playing a critical role in energy production, especially through the stimulation of cytochrome c oxidase, a key enzyme in the electron transport chain [19], thereby increasing adenosine triphosphate production [20]. This enhancement in cellular energy has the potential to allow better functioning and survival of neurons, which are highly dependent on mitochondrial activity for sustaining their functions [21].

Improved mitochondrial function also helps reduce oxidative stress [22], which is a significant contributor to neuronal damage in neurodegenerative diseases [23]. Increasing the effectiveness of the electron transport chain, PBM decreases the production of reactive oxygen species (ROS) [24], which at high levels can cause oxidative harm to cellular components [25]. Furthermore, it has been demonstrated that PBM can upregulate antioxidant defenses, thereby enhancing the protection of neurons against oxidative stress [26]. Thus, PBM is shown to have the dual effect of increasing energy production and reducing oxidative damage, making it a potentially powerful tool for therapeutic purposes.

Beyond energy production and oxidative stress reduction, PBM influences the expression of genes related to cell survival and repair [27,28]. Furthermore, PBM has been shown to increase the expression of heat shock proteins, which play a key role in protein folding and protection against cellular stress [29]. This regulation of gene expression contributes to another layer of protection, supporting cellular viability and repair mechanisms in the face of neurodegenerative challenges. Fig. 1 [6] provides a brief summary of the reported effects PBM has on neurodegenerative diseases.

Figure 1. The effects of photobiomodulation (PBM) in neurodegenerative diseases. Reused from the article of Shen et al. (Int J Mol Sci 2024; 25:1625) [6].

Neuroinflammation modulation

Neuroinflammation is widely recognized as a type of inflammatory response occurring in the brain or spinal cord. It is a common feature of neurodegenerative diseases, including AD, PD, and ALS [30]. It has been demonstrated that PBM can regulate inflammatory responses within the brain. Studies have indicated that PBM can reduce the activation of microglia and astrocytes, the primary immune cells in the central nerve system (CNS) [31]. Here, by inhibiting the release of proinflammatory cytokines such as tumor necrosis factor-α and interleukin (IL)-1β, PBM has demonstrated its ability to contribute to a more protected neuronal environment [32].

Furthermore, PBM can enhance the production of anti-inflammatory cytokines like IL-10, which helps to mitigate proinflammatory processes [33]. It is particularly important to regulate the inflammatory milieu in the CNS, as chronic inflammation can exacerbate neuronal damage and contribute to the progression of neurodegenerative diseases [34]. Therefore, PBM’s anti-inflammatory effects represent a crucial mechanism through which it may exert neuroprotective benefits.

Other than influencing cytokines, PBM has been shown to influence other aspects of the immune response, such as reducing the permeability of the blood-brain barrier (BBB) [35]. Stabilizing the BBB prevents the infiltration of peripheral immune cells into the central nervous system, reducing irritation and neuronal damage. This stabilization is especially relevant in neurodegenerative diseases, BBB integrity is often compromised, leading to further neuroinflammation [36,37].

PHOTOBIOMODULATION IN ALZHEIMER’S DISEASE

Mechanistic insights and preclinical studies

AD is a neurodegenerative disease characterized by the accumulation of amyloid-beta plaques and neurofibrillary tangles, leading to neuronal death and decline in cognitive ability. PBM has shown promise in preclinical models of AD. For example, a study by Lu et al. [38] demonstrated that PBM could reduce amyloid-beta deposition and improve cognitive function in an AD rat model. This investigation suggested that PBM could enhance the elimination of amyloid-beta by stimulating phagocytic microglia, thereby reducing the toxic burden on neural cells.

PBM has also been shown to enhance synaptic function and plasticity in AD models. According to Johnstone et al. [39], PBM increased the expression of brain-derived neurotrophic factor (BDNF), a critical molecule for synaptic health and neuroplasticity. BDNF supports the survival of existing neurons and encourages the growth and differentiation of new neurons and synapses [40]. These new neurons and synapses are crucial for cognitive functions such as learning [41], allowing this study as a demonstration of PBM reducing pathological features of AD and supporting synaptic resilience and function.

Furthermore, PBM has been observed to improve mitochondrial function in various models of AD. Increasing mitochondrial activity can result in less oxidative stress and enhanced energy generation, which are vital for preserving brain health [42]. By focusing on these fundamental cellular functions, PBM presents a comprehensive strategy for combating the diverse mechanisms of AD.

Clinical studies and cognitive outcomes

Initial results from clinical studies on the effects of PBM in AD patients are promising. A pilot study by Berman et al. [43] examined the cognitive outcomes of transcranial PBM in individual mice models with mild to moderate AD. A series of PBM treatments resulted in significant improvements in cognitive performance, including recall, focus, and decision-making abilities. The effects were maintained for several weeks after treatment, suggesting that PBM may have lasting benefits. Furthermore, the administration of PBM proved to be well-tolerated, with no notable adverse effects reported.

Reports like this highlight the potential of PBM to bring improvements in cognitive function and quality of life in individuals with AD. Combined with the observed cognitive benefits, the safe operative mechanisms of PBM technology underscores the potential of it as a therapeutic option for AD patients. However, larger, placebo-controlled trials are necessary to confirm these findings and establish optimal treatment protocols. To maximize the therapeutic efficacy of PBM therapy for AD patients, ongoing research should aim to refine its parameters, such as wavelength, dosage, and duration [44]. Table 1 summarizes the results of preclinical and clinical studies of applying PBM on AD models.

Table 1 . Results of research on the effects of photobiomodulation on models of neurodegenerative diseases

Disease typeStudy typeEffects of photobiomodulation treatmentReference
Alzheimer’s disease (AD)PreclinicalReduces toxic burden on neural cells[38]
PreclinicalImproves synaptic health and neuroplasticity[39]
ClinicalImprovements in recall, focus, and decision-making abilities[43]
Parkinson’s disease (PD)PreclinicalProtect dopaminergic neurons and improve motor function[42]
PreclinicalReduce production of proinflammatory cytokines[45,46]
ClinicalImproved motor performance[49]
ClinicalReduce cognitive impairment and mood dysregulation[51]
Amyotrophic lateral sclerosis (ALS)PreclinicalImprove motor function[53]
PreclinicalImprove neuronal survival and motor performance[54]
PreclinicalSupport motor neuron health and function[55]

PHOTOBIOMODULATION IN PARKINSON’S DISEASE

Mechanistic insights and preclinical studies

PD is characterized by the loss of dopaminergic neurons in the substantia nigra, resulting in motor dysfunction and non-motor symptoms [44]. The pathological hallmark of PD includes the presence of Lewy bodies, abnormal aggregates of alginate, and PBM has shown potential in preclinical models of this disease. In a rat model of PD, Huang et al. [42] demonstrated that PBM could protect dopaminergic neurons and improve motor function. Neuroprotective effects were attributed to the enhancement of mitochondrial function and the reduction of oxidative stress in the affected neurons.

Furthermore, it has been demonstrated that PBM can regulate neuroinflammation responses in PD models. Bicknell et al. [45] and Alrouji et al. [46] reported that PBM reduced microglial activation and the production of proinflammatory cytokines in disease models. This reduction in neuroinflammation was associated with reduced neuronal damage and improved behavioral outcomes.

Another important finding was the impact of PBM on mitochondrial function in dopaminergic neurons [47]. The enhancement of mitochondrial activity facilitates neuronal maintenance and increases cell viability [48]. Considering that mitochondrial dysfunction is a critical factor in the pathogenesis of PD, these findings highlight the potential of PBM to address a core aspect of the disease.

Clinical studies and motor function improvement

Clinical evidence for PBM in PD is emerging, with several studies showing promising results. Liebert et al. [49] investigated the effects of PBM on motor function in PD patients, finding that PBM treatment improved motor performance, including tremor, rigidity, and bradykinesia. These improvements were observed after a relatively short treatment period, suggesting the potential for rapid therapeutic effects.

PBM has also been shown to be safe and tolerable in PD patients, with no significant adverse effects reported in clinical studies [50]. This favorable safety profile is important for PD patients, who often require long-term treatment strategies before significant recovery. The non-invasive nature of PBM makes it an attractive option for managing motor symptoms and possibly modifying disease progression.

Moreover, recent studies have examined the impact of PBM on non-motor symptoms of PD, including cognitive impairment and mood dysregulation. Initial findings proposed that PBM may have beneficial effects on these aspects, improving the overall quality of life for PD patients [51]. As research progresses, there is hope that PBM could become an integral part of comprehensive care for PD, addressing both motor and non-motor symptoms. Table 1 summarizes the results of preclinical and clinical studies of applying PBM on PD models.

PHOTOBIOMODULATION IN AMYOTROPHIC LATERAL SCLEROSIS

Mechanistic insights and preclinical studies

ALS is a progressive degeneration of motor neurons that leads to muscle weakness, atrophy, and eventually respiratory failure. The pathogenesis of ALS involves several complex mechanisms, including mitochondrial dysfunction, oxidative stress, glutamate excitotoxicity, and neuroinflammation [52]. With various methods being highlighted for tackling ALS mechanisms, one rising technology is PBM, which has shown promise in preclinical models of the disease. One study by Longo et al. [53] demonstrated that PBM treatment in an ALS mouse model reduced neuroinflammation and improved motor function, including mediation of microglial activity and proinflammatory cytokines.

Moreover, it has been demonstrated that PBM enhances mitochondrial function and reduces oxidative stress in ALS models. Research by Dubbioso et al. [54] found that PBM improved mitochondrial respiration and reduced the accumulation of ROS in motor neurons, with these effects also improving neuronal survival and motor performance. By targeting mitochondrial dysfunction and oxidative stress, PBM addresses two critical aspects of ALS pathology.

Additionally, PBM has been observed to affect the expression of genes related to neuronal survival and repair. For example, PBM may upregulate neuroprotective factors such as BDNF and glial cell line-derived neurotrophic factor, which support motor neuron health and function [55]. These findings imply that PBM not only mitigates neurodegenerative processes, but also enhances neuronal resilience and recovery.

Clinical studies and functional outcomes

Importantly, this preliminary evidence suggests that PBM may provide functional advantages to those with ALS. The efficacy of PBM and its lack of safety concerns are particularly favorable for ALS patients, who frequently encounter severe physical limitations and require treatment methods with a low-risk profile. The findings are encouraging, but larger, randomized controlled trials are needed to confirm these benefits and to determine optimal treatment protocols. With further studies, PBM may help to slow disease progression and alleviate some debilitating symptoms of ALS, becoming a valuable addition to the therapeutic arsenal for ALS and providing patients with new options for managing their condition. Table 1 summarizes the results of preclinical and clinical studies of applying PBM on ALS models.

CLINICAL APPLICATIONS AND FUTURE DIRECTIONS

Personalized PBM therapy

In neurodegenerative diseases, the future of PBM lies in personalized medicine, which tailors treatment protocols to individual patient needs and disease characteristics. PBM therapy involves the optimization of parameters such as wavelength, intensity, duration, and treatment frequency to achieve the best therapeutic outcomes for each patient [44]. This approach requires an in-depth understanding of the biological mechanisms of PBM and the factors that affect individual variability in these treatments.

Personalized PBM therapy also considers the specific features of each neurodegenerative disease. For example, targeting mitochondrial dysfunction may be particularly relevant for PD, while modulating neuroinflammation may be more relevant for neurodegenerative disease. By aligning PBM parameters with disease-specific mechanisms, personalized therapy could enhance the effectiveness and safety of PBM treatments.

Integration with other therapies

Another promising direction for PBM research is its integration with other therapeutic modalities. The integration of PBM with pharmacotherapy, physical therapy, and cognitive rehabilitation has the potential to enhance treatment outcomes and provide comprehensive care to patients with neurodegenerative diseases. For instance, integrating PBM with drugs that enhance mitochondrial function or reduce neuroinflammation could offer synergistic benefits [56]. Similarly, integrating PBM with physical therapy has the potential to enhance motor function and overall rehabilitation outcomes in conditions such as PD and ALS [6]. By establishing a collaborative environment for neuronal health and function, PBM has the potential to enhance the efficacy of the combined advanced treatments. Research efforts should focus on understanding how PBM interacts with other therapies and developing combination treatment protocols that use the unique strengths of each modality.

Technological advancements

Technological advances in PBM devices may play a critical role in expanding its clinical applications. Advanced PBM devices with improved precision and control will enable targeted treatment of specific brain regions and neural pathways. Research could also be directed towards examining the potential of PBM to enhance cognitive and motor functions in healthy individuals, which may have implications in fields such as sports medicine, military training, and cognitive enhancement. As PBM technology continues to evolve, its applications are expected to expand beyond traditional clinical settings, offering new opportunities for improving health and performance across a wide range of populations.

CONCLUSION

PBM is a promising therapeutic approach for neurodegenerative diseases, providing a non-invasive approach to enhance neuronal health and function. PBM has shown that it can slow down disease progression and improve functional outcomes in conditions like AD, PD, and ALS. Initial results are encouraging, and ongoing studies aim to optimize treatment parameters and prove PBM’s effectiveness in larger patient populations.

The future of PBM is promising, as technological advancements and a deeper understanding of its biological mechanisms are poised to enhance its therapeutic potential and broaden its applications in neurodegenerative diseases. The future of PBM is promising, as technological advances and a better understanding of its biological mechanisms are expected to improve its therapeutic potential and expand its applications in neurodegenerative diseases.

SUPPLEMENTARY MATERIALS

None.

ACKNOWLEDGMENTS

None.

AUTHOR CONTRIBUTIONS

All work was done by KW.

CONFLICT OF INTEREST

No potential conflict of interest relevant to this article was reported.

FUNDING

None.

DATA AVAILABILITY

None.

References
  1. Woo K, Abueva C. Photobiomodulation improves the therapeutic efficacy of mesenchymal stem cells in regenerative medicine. Med Lasers 2022;11:134-42.
    CrossRef
  2. Dompe C, Moncrieff L, Matys J, Grzech-Leśniak K, Kocherova I, Bryja A, et al. Photobiomodulation-underlying mechanism and clinical applications. J Clin Med 2020;9:1724.
    Pubmed KoreaMed CrossRef
  3. Ebrahimpour-Malekshah R, Amini A, Zare F, Mostafavinia A, Davoody S, Deravi N, et al. Combined therapy of photobiomodulation and adipose-derived stem cells synergistically improve healing in an ischemic, infected and delayed healing wound model in rats with type 1 diabetes mellitus. BMJ Open Diabetes Res Care 2020;8:e001033.
    Pubmed KoreaMed CrossRef
  4. Kim HB, Baik KY, Choung PH, Chung JH. Pulse frequency dependency of photobiomodulation on the bioenergetic functions of human dental pulp stem cells. Sci Rep 2017;7:15927.
    Pubmed KoreaMed CrossRef
  5. Szymczyszyn A, Doroszko A, Szahidewicz-Krupska E, Rola P, Gutherc R, Jasiczek J, et al. Effect of the transdermal low-level laser therapy on endothelial function. Lasers Med Sci 2016;31:1301-7.
    Pubmed KoreaMed CrossRef
  6. Shen Q, Guo H, Yan Y. Photobiomodulation for neurodegenerative diseases: a scoping review. Int J Mol Sci 2024;25:1625.
    Pubmed KoreaMed CrossRef
  7. Harding BN, Kariya S, Monani UR, Chung WK, Benton M, Yum SW, et al. Spectrum of neuropathophysiology in spinal muscular atrophy type I. J Neuropathol Exp Neurol 2015;74:15-24.
    Pubmed KoreaMed CrossRef
  8. Hague SM, Klaffke S, Bandmann O. Neurodegenerative disorders: Parkinson's disease and Huntington's disease. J Neurol Neurosurg Psychiatry 2005;76:1058-63.
    Pubmed KoreaMed CrossRef
  9. Martin JB. Molecular basis of the neurodegenerative disorders. N Engl J Med 1999;340:1970-80.
    Pubmed CrossRef
  10. Przedborski S, Vila M, Jackson-Lewis V. Neurodegeneration: what is it and where are we? J Clin Invest 2003;111:3-10.
    Pubmed KoreaMed CrossRef
  11. Lamptey RNL, Chaulagain B, Trivedi R, Gothwal A, Layek B, Singh J. A review of the common neurodegenerative disorders: current therapeutic approaches and the potential role of nanotherapeutics. Int J Mol Sci 2022;23:1851.
    Pubmed KoreaMed CrossRef
  12. Bhatt R, Singh D, Prakash A, Mishra N. Development, characterization and nasal delivery of rosmarinic acid-loaded solid lipid nanoparticles for the effective management of Huntington's disease. Drug Deliv 2015;22:931-9.
    Pubmed KoreaMed CrossRef
  13. Schulz-Schaeffer WJ. The synaptic pathology of alpha-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia. Acta Neuropathol 2010;120:131-43.
    Pubmed KoreaMed CrossRef
  14. Moore DJ, West AB, Dawson VL, Dawson TM. Molecular pathophysiology of Parkinson's disease. Annu Rev Neurosci 2005;28:57-87.
    Pubmed CrossRef
  15. Bartels AL, Leenders KL. Parkinson's disease: the syndrome, the pathogenesis and pathophysiology. Cortex 2009;45:915-21.
    Pubmed CrossRef
  16. Spires-Jones TL, Attems J, Thal DR. Interactions of pathological proteins in neurodegenerative diseases. Acta Neuropathol 2017;134:187-205.
    Pubmed KoreaMed CrossRef
  17. Poyton RO, Ball KA. Therapeutic photobiomodulation: nitric oxide and a novel function of mitochondrial cytochrome c oxidase. Discov Med 2011;11:154-9.
    Pubmed
  18. de Freitas LF, Hamblin MR. Proposed mechanisms of photobiomodulation or low-level light therapy. IEEE J Sel Top Quantum Electron 2016;22:7000417.
    Pubmed KoreaMed CrossRef
  19. Watson SA, McStay GP. Functions of cytochrome c oxidase assembly factors. Int J Mol Sci 2020;21:7254.
    Pubmed KoreaMed CrossRef
  20. Hamblin MR. Photobiomodulation or low-level laser therapy. J Biophotonics 2016;9:1122-4.
    Pubmed KoreaMed CrossRef
  21. Rangaraju V, Lewis TL Jr, Hirabayashi Y, Bergami M, Motori E, Cartoni R, et al. Pleiotropic mitochondria: the influence of mitochondria on neuronal development and disease. J Neurosci 2019;39:8200-8.
    Pubmed KoreaMed CrossRef
  22. Kowalczyk P, Sulejczak D, Kleczkowska P, Bukowska-Ośko I, Kucia M, Popiel M, et al. Mitochondrial oxidative stress-a causative factor and therapeutic target in many diseases. Int J Mol Sci 2021;22:13384.
    Pubmed KoreaMed CrossRef
  23. Oladele JO, Oladiji AT, Oladele OT, Oyeleke OM. Reactive oxygen species in neurodegenerative diseases: implications in pathogenesis and treatment strategies. In: Ahmad R, editor. Reactive oxygen species. IntechOpen; 2021.
    CrossRef
  24. Rupel K, Zupin L, Colliva A, Kamada A, Poropat A, Ottaviani G, et al. Photobiomodulation at multiple wavelengths differentially modulates oxidative stress in vitro and in vivo. Oxid Med Cell Longev 2018;2018:6510159.
    Pubmed KoreaMed CrossRef
  25. Shields HJ, Traa A, Van Raamsdonk JM. Beneficial and detrimental effects of reactive oxygen species on lifespan: a comprehensive review of comparative and experimental studies. Front Cell Dev Biol 2021;9:628157.
    Pubmed KoreaMed CrossRef
  26. Huang YY, Sharma SK, Carroll J, Hamblin MR. Biphasic dose response in low level light therapy - an update. Dose Response 2011;9:602-18.
    Pubmed KoreaMed CrossRef
  27. Oyebode OA, Houreld NN. Photobiomodulation at 830 nm stimulates migration, survival and proliferation of fibroblast cells. Diabetes Metab Syndr Obes 2022;15:2885-900.
    Pubmed KoreaMed CrossRef
  28. Jere SW, Houreld NN, Abrahamse H. Photobiomodulation and the expression of genes related to the JAK/STAT signalling pathway in wounded and diabetic wounded cells. J Photochem Photobiol B 2020;204:111791.
    Pubmed CrossRef
  29. Evangelista AN, Dos Santos FF, de Oliveira Martins LP, Gaiad TP, Machado ASD, Rocha-Vieira E, et al. Photobiomodulation therapy on expression of HSP70 protein and tissue repair in experimental acute Achilles tendinitis. Lasers Med Sci 2021;36:1201-8.
    Pubmed CrossRef
  30. DiSabato DJ, Quan N, Godbout JP. Neuroinflammation: the devil is in the details. J Neurochem 2016;139(Suppl 2):136-53.
    Pubmed KoreaMed CrossRef
  31. Abijo A, Lee CY, Huang CY, Ho PC, Tsai KJ. The beneficial role of photobiomodulation in neurodegenerative diseases. Biomedicines 2023;11:1828.
    Pubmed KoreaMed CrossRef
  32. Song S, Zhou F, Chen WR. Low-level laser therapy regulates microglial function through Src-mediated signaling pathways: implications for neurodegenerative diseases. J Neuroinflammation 2012;9:219.
    Pubmed KoreaMed CrossRef
  33. Salehpour F, Mahmoudi J, Kamari F, Sadigh-Eteghad S, Rasta SH, Hamblin MR. Brain photobiomodulation therapy: a narrative review. Mol Neurobiol 2018;55:6601-36.
    Pubmed KoreaMed CrossRef
  34. Chitnis T, Weiner HL. CNS inflammation and neurodegeneration. J Clin Invest 2017;127:3577-87.
    Pubmed KoreaMed CrossRef
  35. Zhou T, Ohulchanskyy TY, Qu J. Effect of NIR light on the permeability of the blood-brain barriers in in vitro models. Biomed Opt Express 2021;12:7544-55.
    Pubmed KoreaMed CrossRef
  36. Daneman R, Prat A. The blood-brain barrier. Cold Spring Harb Perspect Biol 2015;7:a020412.
    Pubmed KoreaMed CrossRef
  37. Abbott NJ, Patabendige AA, Dolman DE, Yusof SR, Begley DJ. Structure and function of the blood-brain barrier. Neurobiol Dis 2010;37:13-25.
    Pubmed CrossRef
  38. Lu Y, Wang R, Dong Y, Tucker D, Zhao N, Ahmed ME, et al. Low-level laser therapy for beta amyloid toxicity in rat hippocampus. Neurobiol Aging 2017;49:165-82.
    Pubmed KoreaMed CrossRef
  39. Johnstone DM, Moro C, Stone J, Benabid AL, Mitrofanis J. Turning on lights to stop neurodegeneration: the potential of near infrared light therapy in Alzheimer's and Parkinson's disease. Front Neurosci 2016;9:500.
    Pubmed KoreaMed CrossRef
  40. Bathina S, Das UN. Brain-derived neurotrophic factor and its clinical implications. Arch Med Sci 2015;11:1164-78.
    Pubmed KoreaMed CrossRef
  41. Wang S, Bray P, McCaffrey T, March K, Hempstead BL, Kraemer R. p75(NTR) mediates neurotrophin-induced apoptosis of vascular smooth muscle cells. Am J Pathol 2000;157:1247-58.
    Pubmed KoreaMed CrossRef
  42. Huang Z, Hamblin MR, Zhang Q. Photobiomodulation in experimental models of Alzheimer's disease: state-of-the-art and translational perspectives. Alzheimers Res Ther 2024;16:114.
    Pubmed KoreaMed CrossRef
  43. Berman MH, Halper JP, Nichols TW, Jarrett H, Lundy A, Huang JH. Photobiomodulation with near infrared light helmet in a pilot, placebo controlled clinical trial in dementia patients testing memory and cognition. J Neurol Neurosci 2017;8:176.
    Pubmed KoreaMed CrossRef
  44. Zein R, Selting W, Hamblin MR. Review of light parameters and photobiomodulation efficacy: dive into complexity. J Biomed Opt 2018;23:1-17.
    Pubmed KoreaMed CrossRef
  45. Bicknell B, Liebert A, Herkes G. Parkinson's disease and photobiomodulation: potential for treatment. J Pers Med 2024;14:112.
    Pubmed KoreaMed CrossRef
  46. Alrouji M, Al-Kuraishy HM, Al-Gareeb AI, Saad HM, Batiha GE. A story of the potential effect of non-steroidal anti-inflammatory drugs (NSAIDs) in Parkinson's disease: beneficial or detrimental effects. Inflammopharmacology 2023;31:673-88.
    Pubmed CrossRef
  47. Peoples C, Spana S, Ashkan K, Benabid AL, Stone J, Baker GE, et al. Photobiomodulation enhances Nigral dopaminergic cell survival in a chronic MPTP mouse model of Parkinson's disease. Parkinsonism Relat Disord 2012;18:469-76.
    Pubmed CrossRef
  48. Cheng XT, Huang N, Sheng ZH. Programming axonal mitochondrial maintenance and bioenergetics in neurodegeneration and regeneration. Neuron 2022;110:1899-923.
    Pubmed KoreaMed CrossRef
  49. Liebert A, Bicknell B, Laakso EL, Jalilitabaei P, Tilley S, Kiat H, et al. Remote photobiomodulation treatment for the clinical signs of Parkinson's disease: a case series conducted during COVID-19. Photobiomodul Photomed Laser Surg 2022;40:112-22.
    Pubmed CrossRef
  50. Herkes G, McGee C, Liebert A, Bicknell B, Isaac V, Kiat H, et al. A novel transcranial photobiomodulation device to address motor signs of Parkinson's disease: a parallel randomised feasibility study. EClinicalMedicine 2023;66:102338.
    Pubmed KoreaMed CrossRef
  51. Ahrabi B, Tabatabaei Mirakabad FS, Niknazar S, Payvandi AA, Ahmady Roozbahany N, Ahrabi M, et al. Photobiomodulation therapy and cell therapy improved Parkinson's diseases by neuro-regeneration and tremor inhibition. J Lasers Med Sci 2022;13:e28.
    Pubmed KoreaMed CrossRef
  52. Bonafede R, Mariotti R. ALS pathogenesis and therapeutic approaches: the role of mesenchymal stem cells and extracellular vesicles. Front Cell Neurosci 2017;11:80.
    Pubmed KoreaMed CrossRef
  53. Longo L, Postiglione M, Gabellini M, Longo D. Amyotrophic Lateral Sclerosis (ALS) treated with Low Level LASER Therapy (LLLT): a case report. AIP Conf Proc 2009;1142:72-4.
    CrossRef
  54. Dubbioso R, Provitera V, Pacella D, Santoro L, Manganelli F, Nolano M. Autonomic dysfunction is associated with disease progression and survival in amyotrophic lateral sclerosis: a prospective longitudinal cohort study. J Neurol 2023;270:4968-77.
    Pubmed KoreaMed CrossRef
  55. Bathini M, Raghushaker CR, Mahato KK. The molecular mechanisms of action of photobiomodulation against neurodegenerative diseases: a systematic review. Cell Mol Neurobiol 2022;42:955-71.
    Pubmed KoreaMed CrossRef
  56. Salehpour F, Cassano P, Rouhi N, Hamblin MR, De Taboada L, Farajdokht F, et al. Penetration profiles of visible and near-infrared lasers and light-emitting diode light through the head tissues in animal and human species: a review of literature. Photobiomodul Photomed Laser Surg 2019;37:581-95.
    Pubmed CrossRef


This Article


Cited By Articles
  • CrossRef (0)
  • Download (44)

Author ORCID Information

Services

Social Network Service

e-submission

Archives