The potential of light therapy in Parkinson's disease

Abstract:

Parkinson’s disease is a movement disorder with cardinal signs of resting tremor, akinesia, and rigidity. These manifest after a progressive death of many dopaminergic neurons of the midbrain. Unfortunately, the progression of this neuronal death has proved difficult to slow and impossible to reverse despite an intense search for the specific causes and for treatments that address the causes. There is a corresponding need to develop approaches that regulate the self-repair mechanisms of neurons, independent of the specific causes of the damage that leads to their death. Red to infrared light therapy (λ=600–1,070 nm) is emerging as an effective, repair-oriented therapy that is capable of stabilizing dying neurons. Initially a space-age anecdote, light therapy has become a treatment for tissue stressed by the known causes of age-related diseases: hypoxia, toxic environments, and mitochondrial dysfunction. Here we focus on several issues relating to the use of light therapy for Parkinson’s disease: 1) What is the evidence that it is neuroprotective? We consider the basic science and clinical evidence; 2) What are the mechanisms of neuroprotection? We suggest a primary mechanism acting directly on the neuron’s mitochondria (direct effect) as well as a secondary, supportive mechanism acting indirectly through systemic systems (indirect effect); 3) Could this be effective in humans? We discuss the pros and cons of this treatment in humans, including the development of a new surgical method of delivery; and 4) What are the advantages of using light therapy? We explore the features that make this therapy a promising potential treatment. In summary, early evidence indicates that light regulates specific neuronal functions and is neuroprotective in animal models of Parkinson’s disease. The stage is set for detailed and rigorous explorations into its use on Parkinson’s disease patients, in particular, whether light slows the disease progression rather than simply mitigating signs.

Keywords::

• infrared
• near infrared
• neuroprotection
• photobiomodulation
• substantia nigra

Acknowledgments

We are forever grateful to Tenix corp, Salteri family, Sir Zelman Cowen Universities Fund, Foundation Philanthropique Edmond J Safra, France Parkinson, Michael J Fox Foundation, Fight for Sight, International Retinal Research Foundation, and the French National Research Agency (ANR Carnot Institute) for funding our work. We thank Sharon Spana, Rat Venceslas, Vincente Di Calogero, Christophe Gaude, Caroline Meunier, and the Leti-DTBS staff for excellent technical assistance for many of the experiments. Many thanks also to Glen Jeffery (University College London) for his critical analysis of our manuscript. We dedicate this work to our dear friend and esteemed colleague, Gary Baker, who passed away during the early stages of the preparation of this review.

Disclosure

The authors report no conflict of interest concerning the use of light therapy. KC, CM, NT, DMJ, JTE, KA, JS, ALB, and JM are members of staff at their respective institutions. DMJ is supported by a National Health and Medical Research Council of Australia (NHMRC) Early Career Fellowship. JS is a director of Clear Sight Clear Mind (CSCM) Pty Ltd. All authors contributed to the writing of the manuscript. The authors report no other conflicts of interest in this work.