Use of Mitochondrial Delayed Luminescence Measurements From Brain Tissue to Optimize Photobiomodulation Prarameters in Alzheimer's Disease Mice.

Abstract

The therapeutic potential of photobiomodulation (PBM) for Alzheimer's disease (AD) was evaluated by examining β-amyloid accumulation, microglial activation, and memory function. Mitochondrial delayed luminescence (m-DL), an indirect mitochondrial marker, was measured by irradiating 2 J/cm² of 808 nm near-infrared light to the exposed brain surface of anesthetized 5XFAD mice. Based on m-DL findings, behavioral PBM was applied transcranially to the intact scalp using the same fluence at 30, 40, and 80 Hz with respective duty cycles and durations. The 80 Hz setting produced the longest m-DL decay time and selectively improved recognition memory. Immunofluorescence revealed a significant 0.27-fold decrease in β-amyloid and 0.13-fold decrease in microglial activation without changes in neuronal density. Limitations include the small sample size, short duration, and the need to validate m-DL with established bioenergetic assays. Despite these, findings suggest that optimized PBM may offer a promising noninvasive intervention for AD, warranting further long-term investigation.