Alzheimer's disease (AD) is now the most common neurodegenerative disease. Despite approval of several drugs
for AD, the disease continues to rob millions of their memories and their lives. We have studied the cellular models of
brain-mediated phototherapy on AD, and the studies will be reviewed in this paper. Genetic studies have shown that
dysfunction of amyloid β-protein (Aβ) or tau is sufficient to cause AD. Aβ or Aβ induced redox stress induced neuron
apoptosis might be as a cellular model of AD. We found red light at 640±15 nm from light emitting diode array
(RLED640) might inhibit Aβ 25-35 induced PC12 cell apoptosis, which is mediated by cyclic adenosine monophosphate,
and it might inhibit hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) induced differentiated PC12 cell (dPC12) apoptosis, which is mediated by
tyrosine hydroxylase. There is rhythm dysfunction in AD. We found low intensity 810 nm laser irradiation might
rehabilitate TNF-alpha induced inhibition of clock gen expression of NIH 3T3 fibroblasts. Our studies provide a
foundation for photobiomodulation on brain to rehabilitate AD.
Much research showed that there is phtotobiomodulation on cell apoptosis. The membrane receptor mediated signal transduction mechanism (STM) on photobiomodulation was suggested by Liu et al, and verified by successful applications. In this paper, it was used to study photobiomodulation on cell apoptosis. As the frequency of the absorption light of membrane receptors is greater than the visible light, the membrane absorption of the light is non-resonant, and its transition rate is extraordinarily small, but can be amplified by the coherent state of the identical and independent membrane receptors. The activation coherent states of receptors will activate signal transduction pathway, which was called collective phototransduction. It was shown that collective phototransduction mediated STM was one of the possible mechanisms of photobiomodulation on cell apoptosis.