Though I am not an expert in this area by any stretch of the imagination, and I can't answer your question regarding lasers, I will refer to the presentation given to me by Berman. If you have further questions, I suggest contacting him directly.

1072nm light provides the greatest penetration with the least amount of heat. Because bone is porous, it is translucent and allows infrared light to penetrate into the out layers of the cortex. Most of the IR light is absorped by the skin, with 6-8% of the light being absorbed by the cortex (3-4cm). In addition, because the posterior IR light is shined at an angle, it is postulated that it will pass through the occipital bone/foramen magnum of the skull to stimulate the cerebellum:



Many articles have been written about the benefits of other wavelengths, and I included a link to an article that shows 680nm has significant therapeutic effects on mice with Parkinson's. I imagine that 1072nm is used in humans due to the thickness of the skull, and thus offers greater depth of penetration to reach the underlying cortex.

Here is the research I've found on the topic of IR and alpha-synuclein so far:

Non-invasive infra-red therapy (1072 nm) reduces b-amyloid protein levels
in the brain of an Alzheimer’s disease mouse model, TASTPM

http://www.ncbi.nlm.nih.gov/pubmed/23603448

Here is a PDF of that research:

http://stevekbaker.com/wp-content/up...ouse-model.pdf

-------------

Therapeutic effect of near infrared (NIR) light on Parkinson's disease models

http://www.ncbi.nlm.nih.gov/pubmed/22201916

Link to full paper:

https://www.bioscience.org/2012/v4e/af/421/2.htm

"The mice were sacrificed after six days, and the brains were processed for tyrosine hydroxylase immunochemistry. Dopaminergic cells from two regions were studied, the substantia nigra pars compacta (SNc) and the zona incerta-hypothalamus (ZI-Hyp). The SNc is the region showing the main loss of dopaminergic cells seen in Parkinson's disease. The major finding was the presence of significantly more dopaminergic cells in the MPTP NIR light-treated animals as compared to MPTP alone animals. In contrast, the ZI-Hyp samples showed no significant difference between these groups. In addition, cell survival was MPTP dose dependent. After the higher MPTP dose, the magnitude of cell loss was similar in the two regions, while cell loss was greater in the SNc than the ZI-Hyp after the lower dose. This neuroprotection of dopaminergic cells by NIR light therapy, more evident in the PD relevant SNc, has clear clinical applications in the treatment of Parkinson's disease.

7.2. Transgenic mice

The study of alpha-synuclein point mutations has been expanded from the neuroblastoma cell model to a transgenic mouse model by investigating the protective effects of NIR light therapy in transgenic mice expressing the A53T human alpha-synuclein point mutation (31). A53T transgenic mice received NIR light treatment at 670 nm and 7.5 J/cm2 three times per week beginning at eight weeks of age. At phenotype onset mice received NIR light once per day until they exhibited signs of extreme distress. Onset and severity of disease phenotype were analyzed.

NIR light therapy delayed disease progression and attenuated the severity of the disease phenotype. The median age of disease phenotype onset was 455 days for non-NIR light treated mice and 535 days for NIR light-treated mice. At 500 days, significantly fewer NIR light treated mice developed the disease phenotype. Also, of those mice that developed the disease phenotype, NIR light treated mice demonstrated delayed progression of disease measured from time of phenotype onset to sacrifice. Utilizing a grading scale developed to score disease phenotype, the median scores of NIR light treated mice was 1, whereas non-NIR light treated A53T mice had a median score of 2. These findings support the neuroprotective actions of NIR light therapy in an established animal model of Parkinson's disease.

8. PERSPECTIVE

The PD models detailed in this review allow us a way to test a promising new therapy for neurodegenerative diseases using near infrared radiation. As the cellular mechanisms and processes involved when using NIR light therapy are unraveled, against a background of established PD models, we can work out the details of the necessary light exposure and the changes we expect to see. Work has been pushed forward to include rodent models and actual behavioral measures, which brings us closer to our goal of an effective therapy relevant to the needs of actual human Parkinson's sufferers. As current Parkinson's treatments revolve around counteracting the effect of neuronal loss, we are still in the stage of trying to make the surviving neurons "work harder". A more elegant, and possibly more effective, goal would be to prevent the loss of dopaminergic neurons in the first place. Although this would not reverse any degeneration that may have occurred already, we may be able, for the first time, to actually arrest, or at least slow down, further neuronal degeneration and perhaps halt disease progress. As Parkinson's patients do not normally present until the disease stage is well advanced, this is perhaps the best course we can offer.

------------

Low-Intensity Light Therapy (1068 nm) Protects CAD Neuroblastoma Cells
from β-Amyloid-Mediated Cell Death

http://omicsonline.com/open-access/l...s1-1000003.pdf