Photobiomodulation (PBM) has been reported to have effects on respiratory burst of polymorphonuclear neutrophils (PMNs), but little focus was on the individual differences of human PMNs. The latter was investigated in this study. The PMNs were isolated from peripheral blood of 13 volunteers (10 ordinary persons, 3 athletes) and treated by red light (640 ± 15 nm) from light emitting diodes (RLED) at 50, 100, 300, 500 and 1000 J/m2 for 100 seconds, respectively. Blood samples of athletes were extracted at different running stages in 10 km non-interrupted long-distance running, before running, 1 hour after running began, just finishing the running, resting for 1 hour and 2 hours after running. The PMN respiratory burst was assessed by the nitroblue tetrazolium test. It was found that there were three types of RLED PBM on the respiratory burst of 3 types of PMNs, respectively, inducing for the subactivated PMNs, inhibiting for the overactivated PMNs and none for the PMNs in homeostasis. It was then concluded that there may be RLED PBM on dysfunctional human PMNs while none on those in homeostasis, and RLED at 300 J/m2 for 100 seconds may have bi-direction modulation on PMN respiratory burst.

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 2 O 2 ) 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. KEYWORDS: Alzheimer's disease (AD), PhotobiomodulationAlzheimer's disease (AD), the most common cause of dementia in the elderly, with more than 20 million cases worldwide, is characterized by progressive and insidious neurodegeneration of the central nervous system leading to a gradual decline of cognitive function and dementia [1] . The major neuropathological features of AD are synaptic and neuronal degeneration and the presence of amyloid plaques and neurofibrillary tangles (NFTs) [2] . There is a century since the first AD description in 1907 by Alois Alzheimer [3] . Over the past 25 years, it has become clear that the proteins forming the deposits are central to the disease process. Two hypothetical models are proposed, in which beta-amyloid (Aβ) and tau represent the key element. Aβ and tau make up the amyloid plaques and NFTs of AD, where these normally soluble proteins assemble into amyloid-like filaments. Genetic studies have shown that dysfunction of Aβ or tau is sufficient to cause dementia [4] . Despite approval of several drugs for AD, the disease continues to rob millions of their memories and their lives. The lack of treatments with a major impact might be discouraging. Fortunately, basic research is identifying many of the pathways that contribute to this devastating disease, providing unprecedented opportunities for