Abstract

Transcranial photobiomodulation (tPBM) was tested for efficacy in a mouse model of Alzheimer’s disease (AD) using a near infrared 810nm laser system. Photobiomodulation (PBM) is thought to stimulate ATP production, increase mitochondrial activity, and help maintain neuronal function. Studies were performed to determine the effect of tPBM in an amyloid-beta protein precursor (AβPP) transgenic mouse model. tPBM was administered 3 times/week at various doses, starting at 3 months of age, and was compared to a control group (no PBM treatment). Treatment was continued for a total of 6 months. Animals were examined for amyloid load, inflammatory markers, brain amyloid-β (Aβ) levels, plasma Aβ levels, cerebrospinal fluid Aβ levels, soluble AβPP (sAβPP) levels, and behavioral changes. The numbers of Aβ plaques were significantly reduced in the brain with administration of tPBM in a dose-dependent fashion. Administration of tPBM was associated with a dose-dependent reduction in amyloid load. All tPBM doses mitigated the behavioral effects seen with advanced amyloid deposition and reduced the expression of inflammatory markers in the AβPP transgenic mice. All PBM doses produced an increase in sAβPPα and a decrease in CTFβ levels consistent with inhibition of the β-secretase activity. In addition, PBM showed an increase in ATP levels, mitochondrial function, and c-fos suggesting an overall improvement in neurological function. These studies suggest that tPBM is a potential candidate for treatment of AD.

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