Turning On Lights to Stop Neurodegeneration: The Potential of Near Infrared Light Therapy in Alzheimer's and Parkinson's Disease

Daniel M Johnstone, Cécile Moro, Jonathan Stone, Alim-Louis Benabid, John Mitrofanis, Daniel M Johnstone, Cécile Moro, Jonathan Stone, Alim-Louis Benabid, John Mitrofanis

Abstract

Alzheimer's and Parkinson's disease are the two most common neurodegenerative disorders. They develop after a progressive death of many neurons in the brain. Although therapies are available to treat the signs and symptoms of both diseases, the progression of neuronal death remains relentless, and it has proved difficult to slow or stop. Hence, there is a need to develop neuroprotective or disease-modifying treatments that stabilize this degeneration. Red to infrared light therapy (λ = 600-1070 nm), and in particular light in the near infrared (NIr) range, is emerging as a safe and effective therapy that is capable of arresting neuronal death. Previous studies have used NIr to treat tissue stressed by hypoxia, toxic insult, genetic mutation and mitochondrial dysfunction with much success. Here we propose NIr therapy as a neuroprotective or disease-modifying treatment for Alzheimer's and Parkinson's patients.

Keywords: amyloid plaques; disease-modifying; neuroprotection; photobiomodulation; tau protein.

Figures

Figure 1
Figure 1
The major brain sites of pathology in Alzheimer's and Parkinson's patients. For Alzheimer's disease, green shade indicates major regions of cell loss and β-amyloid plaques and tau pathology, while in Parkinson's disease, red shade indicates sites of major cell loss and α-synuclein pathology.
Figure 2
Figure 2
The putative NIr protective mechanisms in the brain. (A) Direct NIr stimulation of the mitochondria of the damaged neurons or endothelial cells. This stimulation would repair the damage leading to neuronal protection. NIr may also stimulate neurogenesis in the hippocampus and/or synaptogenesis in the damaged neurons (B) indirect (remote) stimulation via circulating immune cells and/or bone marrow stem cells leading to neuronal protection. The latter is similar to the so-called “abscopal” effect in the treatment of cancer metastasis. We suggest that the primary mechanism is the direct effect, of neurons and/or of endothelial cells, while the systemic indirect effect forms a secondary supportive mechanism.
Figure 3
Figure 3
Potential NIr applications in Alzheimer's and Parkinson's patients. For effective neuroprotection, NIr could be applied extracranially in Alzheimer's disease (e.g., in the form of a helmet) and intracranially in Parkinson's disease (e.g., in the form of an optical fiber linked to a LED or laser source). NIr would be delivered very close to the diseased cells in the neocortex (for Alzheimer's) and brainstem SNc (for Parkinson's). In Parkinson's patients selected for deep brain stimulation, the NIr optical fiber could be implanted surgically at the same time, for neuroprotection of remaining dopaminergic cells (see text for details).

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