Abstract
Alzheimer's disease (AD) and dementia are the most worrying health problems faced by people globally today. Although the pathological features of AD consisting of amyloid-beta (Aβ) plaques in the extracellular space (ECS) and intracellular tau tangles are well established, the developed medicines targeting these two proteins have not obtained the expected clinical effects. Photobiomodulation (PBM) describes the therapeutic use of red light (RL) or near-infrared light (NIR) to serve as a noninvasive neuroprotective strategy for brain diseases. The present review discusses the mechanisms of the photoelectric coupling effect (light energy-induced special electronic transition-related alterations in protein structure) of PBM on reducing Aβ toxicity. On the one hand, RL or NIR can directly disassemble Aβ in vitro and in vivo. On the other hand, formaldehyde (FA)-inhibited catalase (CAT) and H(2)O(2)-inactived formaldehyde dehydrogenase (FDH) are formed a vicious circle in AD; however, light energy not only activates FDH to degrade excessive FA (which crosslinks Aβ monomer to form Aβ oligomers and senile plaques) but also sensitizes CAT to reduce hydrogen peroxide levels (H(2)O(2), which can facilitate Aβ aggregation and enhance FA generation). In addition, it also activates mitochondrial cytochrome-c to produce ATP in the neurons. Clinical trials of phototherapeutics or oral coenzyme Q10 have shown positive effects in AD patients. Hence, a promising strategy combined PBM with nanopacked Q10 has been proposed to apply for treating AD.