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.

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.

Previous studies examining the focal application of photobiomodulation (PBM) on nerves have consistently yielded reductions in small-diameter fiber activity lasting multiple days. Experiments demonstrating that PBM applied to the sciatic nerve following selective small-diameter fiber excitation would provide further evidence that PBM reduces sensitivity of small-diameter fibers. To investigate this, focal PBM was applied to the rat sciatic nerve, a capsaicin solution was injected into the hind paw, and behavioral data were collected following PBM application. Small fiber heat sensitivities were reduced by over 20% for days following treatment, but mechanical sensitivities were only reduced for one day. To understand translational opportunities, we measured additional effects: focal PBM’s effect on tissue temperature, and PBM’s effect on motor fiber output of the gastrocnemius. Focal PBM application to the sciatic nerve caused an average temperature change of 5oC, and the force generation of the gastrocnemius did not vary following PBM application. Taken together, these data support focal PBM’s translational appeal as a non-addictive, prolonged, pain-reducing therapy.

Photobiomodulation (PBM) with low-power near-infrared (NIR) light has shown diverse beneficial effects. Recent studies report that PBM also increases bioavailable nitric oxide (NO), which is a critical gaseous mediator for various physiological processes and could be used to treat cardiovascular and cerebrovascular diseases with suppressed endothelial NO production. We explored using NIR-II light (1000-1700 nm) for PBM. NIR-II laser treatment efficiently enhanced NO generation in endothelial cells. Since impaired NO production is also associated with neurological diseases, this novel therapy could be further explored to treat diseases such as traumatic brain injury, sleep disorders, and Alzheimer's disease.

Current methods to treat pain have several limitations (e.g., addiction, limited efficacy, etc.) and new options are sorely needed. Photobiomodulation (PBM) at 808 nm has been shown to reduce small fiber axon sensitivities in both human and animal models when applied for the purposes of action potential block. A study using a pulsed light dosing scheme was conducted to determine the viability of using commercially available IPGs for a potential implanted system. Results showed a reduction in pain lasting about 8 days, indicating that this method of delivery has promise for an implanted system.

Recently, attention of many scientists has been focused on the assessment of photobiomodulation to increase wound healing in various cells and animal models. Zebrafish have important and unique features that can make them one of the most informative models used for investigation of regenerative mechanisms. One of these features is their interesting capability to regenerate an amputated fin. The zebrafish model have become increasingly important in scientific research as its characteristics allow for being the smart model of investigation of many human injuries. Twenty juvenile zebrafish had caudal fin was amputated under anesthesia. The zebrafish were randomly and equally divided into two groups including negative control group in which the caudal fin was monitored until fully regenerated, and the intervention group in which the amputated fin was irradiated with laser This study showed that our experimental conditions of laser irradiation had benefits and can be considered as regenerative stimulator for the amputated zebrafish caudal fin. and was significantly different when compared with the control group.

BACKGROUND Oral Mucositis is a common and often severe side effect of radiotherapy in head and neck cancer (HNC) patients. It is a painful inflammatory and ulcerative condition of the mouth, leading to difficulty eating, drinking, and swallowing. Many patients require expensive analgesics, nasogastric tube insertion or PEG or RIG feeding, requiring some time in the hospital. OBJECTIVE Evaluate the Cost-effectiveness of Photobiomodulation (PBM) for treating and preventing Oral Mucositis in head and neck cancer patients. METHODS A comprehensive search was conducted on PubMed using the terms (Photobiomodulation OR Low-Level Laser OR LLLT OR Cold Laser OR Laser Biostimulation) AND (Cost-effectiveness OR Cost Benefit OR Economic). Additionally, hand-searching references and exploring other internet sources were employed to identify cost-effectiveness studies on Photobiomodulation for treating and preventing Oral Mucositis in head and neck cancer patients. This process yielded 13 papers. However, eight of these were excluded for not meeting the inclusion criteria, leaving a total of five papers for in-depth review. The evaluation focused on the cost per patient, taking into account the expenses associated with the PBM device, its administration, consumables, analgesics, nutritional support, and hospitalization. RESULTS In all but one study, PBM was found to decrease the incidence and severity of Oral Mucositis, along with associated costs for consumables, analgesics, nutritional support, and hospitalization. However, the expense related to the PBM device and its administration typically outweighed these savings. The exception was one study where patient self-administration using an LED Lollipop device resulted in a cost saving of $3,850 per patient. CONCLUSION Photobiomodulation (PBM) was found to decrease the incidence and severity of Oral Mucositis, along with associated costs. However, the expense related to the PBM device and its administration typically outweighed these savings. One exception was a study where patients self-administered using an LED Lollipop device, resulting in a cost saving of $3,850 per patient.

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.

BACKGROUND: Photobiomodulation therapy (PBMT) is recommended for the prevention of oral mucositis (OM) in cancer patients. Transcutaneous, extraoral delivery of PBMT with LED arrays, versus intraoral delivery with laser, may be more effective for treatment of at-risk sites and better tolerated by patients. The objective was to develop an evidence-based extraoral PBMT treatment protocol. METHODS: We previously demonstrated that Monte Carlo modeling accurately simulates in vivo transmittance measurements. Archival MRI studies (n=18) were used to determine anatomical structures along the trajectories of 850 nm light through the cheek, lip, mandible angle and neck. Optical properties of skin, fat, muscle, cartilage, and blood were obtained from literature, and Monte Carlo modeling was performed for skin types I and VI. Simulation results were used to determine the treatment time needed to deliver a median dose between 1 and 6 J/cm2 to the mucosa. RESULTS: Cheek had greatest variability in thickness (13-29 mm) corresponding to a 25-fold difference in the mucosal fluence rate. Despite tissue differences, fluence attenuation is primarily determined by the overall thickness of all tissue

Previous studies have shown a decrease in sensitivity to noxious thermal stimuli to the limb following focal photobiomodulation (PBM) of the sural nerve. The mechanism by which PBM blocks nociceptive transmission in the sural nerve is unknown. We tested two possible theories for neural inhibition using computational models (NEURON simulation environment). First, the beading phenomenon known as varicosities observed with PBM and second, the observations that nitric oxide or other reactive oxygen species are increased following PBM. Other groups have shown that nitric oxide can block unmyelinated and demyelinated axons by blocking sodium current. We hypothesize that the size increase observed with PBM in vivo is not sufficient to block action potentials, and the results indicate that increasing the axon diameter to block action potentials requires diameter increases much larger than those observed in vivo, suggesting varicosities cannot be solely responsible for the block phenomenon. However, the role of nitric oxide on sodium current is expected to reduce the action potential magnitude enough to cause the block effect, and this mechanism of block merits further investigation.

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.

Photobiomodulation (PBM) of both oxidative stress and microglia metabolism associated with the activation of metabolic processes by 808 nm near-infrared light is carried out on microglia cells treated with β-amyloid. The light induces a metabolic shift from glycolysis to mitochondrial activity in pro-inflammatory microglia affected by Aβ. Thereby, the level of anti-inflammatory microglia increases. This process is accompanied by a decrease in pro-inflammatory cytokines and an activation of phagocytosis. Light exposure decreases the Aβ-induced activity of glucose-6-phosphate dehydrogenase, an enzyme that regulates the rate of the pentose phosphate pathway, which activates nicotinamide adenine dinucleotide phosphate oxidases to further produce ROS. During co-cultivation of neurons with microglia, light prevents the death of neurons, which is caused by ROS produced by Aβ-altered microglia. These original data clarify reasons for how PBM protects against neurodegeneration and support the use of light for therapeutic research in the treatment of Alzheimer's disease.