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Part of the oxygen that is metabolized produces reactive oxygen species (ROS) as a natural by-product. ROS are chemically active molecules that play an important role in cell signaling, regulation of cell cycle progression, enzyme activation, and nucleic acid and protein synthesis. Within the cell, there is strong evidence to suggest that LLLT acts on the mitochondria 15 to increase adenosine tri- phosphate (ATP) production 16, modulation of reactive oxygen species (ROS), and the induction of transcription factors 17. These transcription factors then cause protein synthesis that triggers further effects down- stream, such as increased cell proliferation and migration, modulation in the levels of cytokines, growth factors and inflammatory mediators, and increased tissue oxygenation 18. Dosimetry in LLLT is highly complicated. The large of number of interrelated parameters has meant that there has not yet been a comprehensive study reported that examined the effect of varying all the individual parameters one by one, and it is unlikely there will ever be such a study carried out. This considerable level of complexity has meant that the choice of parameters has often depended on the experimenter’s or the practitioner’s personal preference or experience rather than on a consensus statement by an authoritative body. Nevertheless, the World Association of Laser Therapy (WALT) has attempted to provide dosage guidelines (http://www.walt.nu/dosage-recommendations.html). In vitro studies, animal experiments and clinical studies have all tended to indicate that LLLT with fluences of red or NIR as low as 3 to 5 J/cm2 will be beneficial in vivo, but a large dose like 50 to 100 J/cm2 will lose the beneficial effect and may even become detrimental. LLLT is also being considered as a viable treatment for serious neurological conditions such as traumatic brain injury (TBI), stroke, spinal cord injury, and degenerative central nervous system disease. Further experiments have tried to pinpoint the mechanism underlying these results. As expected, increased mitochondrial activity has been found in brain cells irradiated with LLLT 19, indicating that the increased respiration and ATP production that usually follow laser therapy are at least partly responsible for the improvement shown in stroke patients. However, there is still the possibility that LLLT has other effects specific to the brain. Several groups have suggested that the improvements in patient outcomes are because of the promotion of neurogenesis, and migration of neurons 20. This hypothesis is supported by the fact that the benefits of LLLT following a stroke may take 2– 4 weeks to manifest, reflecting the time necessary for new neurons to form and gather at the damaged site in the brain 21 22. However, the exact processes underlying the effects of LLLT in a stroke patient are still poorly understood. The RPE is the major local source of Complement Factor H (CFH) at the retina/choroid interface. Mutations or down regulation of CFH may increase the chance of RPE cells being attacked by activated complement systems. Damage caused by oxidative stress and inflammation lead to progressive loss of cell functionPDF Image | dry Age-related Macular Degeneration Photobiomodulation
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