Is it time to consider photobiomodulation as a drug equivalent?

The question of whether photobiomodulation should be used as a drug equivalent arose in my mind after listening to presentations at the recent conference of the World Association for Laser Therapy (WALT)-2012 (Gold Cost City, Australia), and later at home when searching MEDLINE® for the years 2009–2012. Photobiomodulation (earlier terms: low level laser therapy, LLLT, laser biostimulation) has been used in clinical practice for >40 years by now, and its action mechanisms on cellular and molecular levels have been studied for >30 years. Enthusiastic medical specialists successfully used photobiomodulation in treating healing-resistant wounds and ulcers (e.g., chronic diabetic ulcers), in pain management, and in spinal cord and nervous system injuries when other methods had had limited success.1 However, photobiomodulation is still not a part of mainstream medicine. The goal of the present Editorial is to highlight some important recent developments in clinical applications and in studies of cellular and molecular mechanisms behind the clinical findings.

One of the impressive and perspective challenges for photobiomodulation is its use in cases of Parkinson’s disease. Research in recent years evidenced that neuroprotective treatment with red and near infrared radiation (NIR) prevented mitochondrial dysfunction and dopamine loss in Parkinson’s disease patients.2 In another set of experiments, NIR normalized mitochondrial movement and axon transport, as well as stimulating respiration in cytoplasmic hybrid (“cybrid”) neurons.3,4 It is important to recall that reduced axonal transport contributes substantially to the degeneration of neuronal processes in Parkinson’s disease.