There is a close association between the gut microbiome and metabolic and neurodegenerative diseases, especially in Parkinson’s disease. The potential of photobiomodulation to alleviate motor and non-motor symptoms of Parkinson’s disease has been demonstrated in animal experiments and proof-of-concept clinical trials. We have also previously shown that PBM can alter the gut microbiome in a mouse model, case studies and in a clinical trial of Parkinson’s disease. Here we present a clinical trial documenting changes in the microbiome of Parkinson’s participants with abdominal PBM that parallel changes in the symptoms of Parkinson’s disease and the disruption of the PBM effects by antibiotics.
Renal disease is a severe and increasing problem with chronic kidney disease (CKD) associated with increasing incidence of obesity and metabolic disease. Current treatments for diabetic kidney disease are limited and generally ineffective, highlighting the need for innovative therapeutic strategies. Photobiomodulation is one such potential therapy. PBM is known to modulate cellular function, suppress inflammation, restore balance redox, and improve mitochondrial activity, all of which are hallmarks of CKD. Here we highlight photobiomodulation treatment for CKD in in vitro and in vivo models, with implications for photobiomodulation mechanisms. In vitro results showed that low-dose photobiomodulation resulted in over-expression of fibronectin and tumour necrosis factor and down-regulation of glutathione peroxidase while high-dose photobiomodulation did not. Similarly, in vivo results also showed that low but not high-dose PBM improved kidney function, decreased blood urea, albumin, albumin-creatinine ratio and other markers of CKD. There were significant microbiome changes associated with photobiomodulation treatment.
A number of studies have suggested that PBM can have positive effects on the symptoms of Parkinson’s disease. The objective of this study was to determine the safety and efficacy of transcranial photobiomodulation (tPBM) for Parkinson’s disease symptoms, including motor symptoms, as measured by UPDRS, and sense of smell and patient reported outcomes. A 20+20 double-blind, randomised, sham controlled trial was conducted over 24 weeks, with Group 1 having sham helmet for 12 weeks and then active helmet for 12 weeks and Group 2 having active helmet for 12 weeks and then no treatment for 12 weeks. The clinical trial was conducted entirely remotely during the COVID-19 restrictions. Despite a large placebo effect, the treatment was found to be both safe and effective, with a clinically and statistically significant reduction in UPDRS scores. There were also improvements in some participants sense of smell and quality of life.
We propose that conformational changes to the cytoskeleton is a mechanism of photobiomodulation additional to its other known effects, underlying pain relief by PBM. These conformational changes may lead to secondary effects within nerve cells, such as the slowing of conduction velocity and changes in mitochondrial membrane potentials, both of which are modulated by photobiomodulation. We propose that the mechanism that links photobiomodulation to cytoskeleton changes is the action of light on photoacceptors such as ion channels, with cytoskeletal modulations affecting downstream signalling, resulting in changes to the integrity of cell membrane and overall cell configuration. This proposed mechanism has potential implications for pathologies such as chronic pain, dysregulated immune responses and neurological diseases such as traumatic brain injury and Parkinson’s disease.
The gut microbiome has been increasingly recognised as crucial to health and has been shown to be disrupted in such diverse diseases and conditions as cardiovascular disease, renal disease, liver disease, lung infections, osteoarthritis. In addition, the microbiome-gut-brain axis has been shown to be a vital link in the neurological and neurodegenerative disorders of Alzheimer’s disease, Parkinson’s disease, autism spectrum disorder and depression. We have previously demonstrated the effect that PBM can have on the microbiome of healthy mice. In this presentation, results from a number of case studies from human trials will be presented, suggesting the potential of PBM to influence the microbiome in a positive manner. These changes correspond to improvements in a number of measures of human health in cancer treatment, Parkinson’s disease and metabolic syndrome. The interaction between light and the microbiome will be explored.
Chronic kidney disease (CKD) is a worldwide public health problem, resulting in a significant burden on the health system. PBM is effective in mitigating inflammation, mitochondrial dysfunction, and oxidative stress, all of which are factors inherent in CKD. The aim of this study was to identify the direct effects of PBM in an in-vitro model of CKD. In vitro human proximal tubular cells (HK2 cells) were pre-treated with low (1.38 J/cm2) or high dosage (2.75J/cm2) of PBM. Cells were then incubated with TGF-β1 (2 ng/ml) for 48 hours with or without PBM irradiation every 24 hours. The SHAM groups were processed under the exact same conditions except in the absence of PBM irradiation. The expression levels of inflammatory markers monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), fibrotic marker fibronectin (FN), antioxidative markers superoxide dismutase 1 (SOD1) and SOD2 were measured by qRT-PCR or ELISA The results showed that TGF-β1 significantly increased MCP-1, TNF-α, and fibronectin mRNA expression in HK2 cells, which was significantly reversed by the low dosage of PBM (0.45 J/cm2, P<0.05), but not the higher dosage of PBM (0,9 J/cm2) when compared with the SHAM control group. The dose-response characteristics of PBM observed in this study followed the biphasic pattern. In conclusion, the present study suggests that PBM directly reduced inflammation and fibrosis in kidney tubular cells when used at the appropriate dose.
Oral mucositis (OM) is a common side effect of radiation therapy for cancers, which has major consequences for the patient including severe pain, systemic infections, reduced nutritional intake, and adverse quality of life. The standard care currently available for OM is symptomatic, mainly directed towards pain remission (topical analgesics and parenteral drugs) and the prevention of secondary infection which have effect in the prevention and management of OM. Photobiomodulation therapy (PBMt) has been shown to stimulate tissue regeneration, reduce inflammation and control pain. The National Institute for Health and Care Excellence (NICE) has included PBMt as recommended therapy for preventing OM caused by radiotherapy or chemotherapy, and the Multinational-Association of Supportive Care in Cancer and the International Society for Oral Oncology (MASCC/ISOO) found the evidence for LLLT/PBMt in the prevention of OM in patients to be safe and potentially very effective.
A Quality Assurance study of the efficacy of pre-emptive PBMt to prevent/reduce severity of OM in radiotherapy patients was conducted at the San Hospital in Australia. Patients were given PBMt daily from before radiotherapy and throughout therapy, including home-treatment when the clinic could not be attended.
Results were clinically positive, with no patient in the study developing OM beyond level 1. One participant presented a unique opportunity to compare OM treatments and outcomes, as his twin brother suffered the same cancer and was treated with the same radiation therapy, but without PBMt, a number of years previously. Implications of the therapy will be discussed.
The mechanisms of photobiomodulation, beyond the light interaction with cytochrome C oxidase has been the subject of increasing focus in the past few years, but have yet to be fully elucidated. Research into the non-mitochondrial mechanisms is warranted in order to more fully explain photobiomodulation mechanism in order to garner greater acceptance in the traditional medical non-photobiomodulation field. This is especially important since the currently accepted central mechanism of action, the absorption of wavelengths by cytochrome-C-oxidase and the subsequent release of ROS and production of ATP, is being increasingly questioned. A narrative literature review was conducted across photobiomodulation, photochemistry and photophysical scientific published literature to gather information to integrate potential novel mechanisms of photobiomodulation. This presentation will examine some of these potential mechanisms beyond cytochrome-C-oxidase, including opsins as potential photobiomodulation targets and the associated non-visual phototransduction pathways, the potential of photobiomodulation to produce a photophysical effect to induce mechanotransduction pathways, the potential of photons to interact with proteins in micro-oscillatory cellular effects, including interaction with the cytoskeleton and the role of internally produced light. An overarching hypothesis for an integrated mechanism of light pathways will be presented, with implications for treatment of chronic pain, and neurodegenerative disease, including Parkinson’s and Alzeimer’s diseases.
Despite heavy focus on the photochemical and photoelectrical mechanisms of Photobiomodulation (PBMt) and Photodynamic therapies (PDt), minimal attention has been paid to photophysical pathways. In this presentation, we will discuss non-visual phototransduction pathways including mechanotransduction, biophotonic signalling, and light-indued micro-oscillation mechanisms related to PBMt and PDt. We will also discuss the implications of these mechanisms in pathological conditions such as Parkinson’s disease, migraine with aura, and fibromyalgia, and Crigler-Najjar syndrome, and how PBMt may be effective as a potential therapy.
Myocardial ischemic reperfusion (MIR) injury results from coronary revascularization and cardiac intervention procedures. It is a negative pathophysiological event that may result in cardiac cell apoptosis. The resulting loss of cardiomyocyte cells and the formation of scar tissue, impair heart function and this is a major prognostic determinant of long-term cardiac outcomes. Photobiomodulation (PBM) is potential cardiac surgery intervention that could prevent myocardial ischemic reperfusion related myocardial injury. A growing body of evidence supporting the use of photobiomodulation in myocardial infarct models (tissues, animal models and a limited number of clinical trials) has implicated multiple molecular pathways of PBM action. PBM has been shown to decrease infarct size, both when delivered transthoracically and to remote areas of the body. PBM has also been shown to decrease the complications of hearts surgery including arrhythmias, to reduced restenosis, to accelerate wound healing, both superficial and deep, and to improve subjective well-being.
One important factor in negative impact of injury is the spread of proteotoxic stress across compartments within the cell and across tissues. PBM is known to modify redox stress, to alter membrane ion channel stability, to affect cytoskeleton rescue and catastrophe and to alter the fluidity and stability of membranes and lipid rafts. A simple window into this is erythrocytes stability. The use of this measurement will be discussed, including its relevance to cardiac injury and its modification by PBM and the broader implications of the importance of PBM to cardioprotection and neuroprotection.
Photobiomodulation (PBM) is an effective tool for the management of spinal pain including inflammation of facet joints. Apart from cervical and lumbar joint pain the upper cervical spine facet joint inflammation can result in the CGH (traumatic or atraumatic in origin). This condition affects children, adults and elders and is responsible for 19% of chronic headache and up to 33% of patients in pain clinics. The condition responds well to physiotherapy, facet joint injection, radiofrequency neurotomy and surgery at a rate of 75%. The other 25% being unresponsive to treatment with no identified features of unresponsiveness. In other conditions of chronic unresponsive cervical pain have responded to photobiomodulation at a level of 80% in the short and medium term.
A clinical trial was therefore conducted on a cohort of atraumatic patients from the ages of 5-93 (predominantly Neurologist referred / familial sufferers 2/3 generations vertically and laterally) who had responded to a course of PBM and physiotherapy. The CGH sufferers and their non CGH suffering relatives over these generations were then compared for features that distinguish the two groups. Fifty parameters were tested (anthropmetric, movement and neural tension tests included) and there was a noted difference in tandem stance between the groups (.04 significance with repeated measures).
As this impairment is common to benign ataxia and migrainous vertigo and in these conditions there is an ion channelopathy (especially potassium channelopathy). A postulated mechanism of action of PBM would involve modulation of ion channels and this is discussed in this presentation.
Access to the requested content is limited to institutions that have purchased or subscribe to SPIE eBooks.
You are receiving this notice because your organization may not have SPIE eBooks access.*
*Shibboleth/Open Athens users─please
sign in
to access your institution's subscriptions.
To obtain this item, you may purchase the complete book in print or electronic format on
SPIE.org.
INSTITUTIONAL Select your institution to access the SPIE Digital Library.
PERSONAL Sign in with your SPIE account to access your personal subscriptions or to use specific features such as save to my library, sign up for alerts, save searches, etc.