Alzheimer’s disease (AD) is now the most common neurodegenerative disease. As drugs approved are not very effective, the brain-mediated monochromatic phototherapy is one of therapeutic candidate approaches. The cellular model studies of AD have been conducted in our laboratory and will be reviewed in this paper. Genetic studies have shown that dysfunction of amyloid-β (Aβ) or tau is sufficient to cause AD. Aβ or hydrogen peroxide (H2O2) induced neuron apoptosis might be a cellular model of AD. We found red light at 640±15 nm from light emitting diode array (RLED640) might inhibit PC12 cell apoptosis induced by Aβ25-35 and apoptosis of differentiated PC12 cell (dPC12) induced by H2O2, which might be mediated by cAMP and tyrosine hydroxylase, respectively. The dysfunction of tau might be mimicked by colchicine. We found H2O2 and colchicines might lead to dPC12 abortive apoptosis, and the abortive apoptosis might be inhibited with RLED640. The rhythm dysfunction in AD might be mimicked by tumor necrosis factor α(TNF-α). We also found low intensity 810 nm laser irradiation might rehabilitate inhibition of circadian gene expression of NIH 3T3 fibroblasts induced by the TNF-α.