Microglia modulation with 1070-nm light attenuates Aβ burden and cognitive impairment in Alzheimer's disease mouse model

Photobiomodulation, by utilizing low-power light in the visible and near-infrared spectra to trigger biological responses in cells and tissues, has been considered as a possible therapeutic strategy for Alzheimer's disease (AD), while its specific mechanisms have remained elusive. Here, we demonstrate that cognitive and memory impairment in an AD mouse model can be ameliorated by 1070-nm light via reducing cerebral beta-amyloid (A beta) burden, the hallmark of AD. The glial cells, including microglia and astrocytes, play important roles in A beta clearance. Our results show that 1070-nm light pulsed at 10 Hz triggers microglia rather than astrocyte responses in AD mice. The 1070-nm light-induced microglia responses with alteration in morphology and increased colocalization with A beta are sufficient to reduce A beta load in AD mice. Moreover, 1070-nm light pulsed at 10 Hz can reduce perivascular microglia and promote angiogenesis to further enhance A beta clearance. Our study confirms the important roles of microglia and cerebral vessels in the use of 1070-nm light for the treatment of AD mice and provides a framework for developing a novel therapeutic approach for AD.

Automated summary

Photobiomodulation using 1070-nm light can ameliorate cognitive and memory impairment in AD mouse model by reducing cerebral Aβ burden. The study demonstrates that 1070-nm light triggers microglia responses, leading to decreased Aβ load, and promotes angiogenesis to enhance Aβ clearance in AD mice. This research confirms the important roles of microglia and cerebral vessels in using 1070-nm light for the treatment of AD, and provides a framework for developing a novel therapeutic approach.