Introduction: Photobiomodulation – the treatment of tissue with low-intensity light (λ=600–1100nm) – provides neuroprotection to various animal models of neurodegeneration when applied transcranially. In humans, the clinical utility of transcranial photobiomodulation is limited by skull thickness, however evidence suggests that treatment of peripheral tissues may also confer neuroprotection. This ‘indirect’ effect shows promise in the translation of neuroprotective photobiomodulation for clinical use.
Objectives: To determine whether indirect photobiomodulation mitigates amyloid plaque pathology in an APP/PS1 transgenic mouse model of Alzheimer’s disease.
Methods: Male APP/PS1 mice (aged 33wks) were treated with 670nm light (50mW/cm2) from a WARP 10 LED device for 3min/day, 3days/wk. Each 3min treatment equated to a dosage of 8J/cm2. Light was targeted at the dorsum only, with the head shielded by foil. Sham-treated animals were similarly handled, but the LED device not turned on. Following 8wks of treatment (at age 41wks), mice were perfused with formalin and brains harvested and sectioned at 20µm thickness. Sections were stained with Thioflavin S for amyloid plaques, scanned using a Zeiss Axioscan, and images analysed for measures of plaque pathology using ImageJ 2. Statistical analysis was performed in Prism 6, using an unpaired two-tailed t-test with Welch’s correction. Values are given as means ± SEM.
Results: Cortical plaque load (%tissue area) was not significantly different between treated (0.31±0.02%; n=8) and sham-treated animals (0.30±0.03%; n=5) (P=0.86).
Conclusions & future directions: In APP/PS1 mice with established pathology, indirect photobiomodulation did not affect cortical fibrillary amyloid plaque load. This may be due to the advanced age of the animals when treatment was commenced; future studies may investigate whether earlier treatment mitigates disease development. Future analyses will investigate other signs of earlier-stage pathology, including non-fibrillar β-amyloid deposition and markers of mitochondrial function and oxidative damage, as well as comparison with baseline pathology (i.e. at age 33wks).