Mice predisposed to aggressive Alzheimer’s disease (through beta amyloid plaquing upregulation) shows improvement in amyloid accumulation, neuron loss, and brain inflammation (microgliosis) through light therapy (photobiomodulation). Light therapy could be used as a form of treatment for neurological disorders.
Photobiomodulation using low-level light-emitting diode (LED) can be rapidly applied in neurological and physiological disorders safely and non-invasively. Photobiomodulation is effective for chronic diseases due to fewer side effects than drugs. Here we investigated the effects of photobiomodulation using LED on amyloid plaques, gliosis, and neuronal loss to prevent and/or recover cognitive impairment, and optimal timing of photobiomodulation initiation for recovering cognitive function in a mouse model of Alzheimer’s disease (AD). 5XFAD mice were used as an AD model. Animals receiving photobiomodulation treatment were divided into two groups: an early group starting photobiomodulation at 2 months of age (5XFAD+Early), and a late group starting photobiomodulation at 6 months of age (5XFAD+Delay). Both groups received photobiomodulation 20 minutes per session three times per week for 14 weeks. The Morris water maze, passive avoidance, and elevated plus maze tests were performed at 10 months of age. Immunohistochemistry and western blot were performed after behavioral evaluation. The results showed that photobiomodulation treatment at early stages reduced amyloid accumulation, neuronal loss, and microgliosis and alleviated the cognitive dysfunction in 5XFAD mice, possibly by increasing insulin degrading enzyme (IDE) related to amyloid-beta (Aβ) degradation. Photobiomodulation may be an excellent candidate for advanced preclinical AD research.