Neuroprotective Potential of Photobiomodulation Therapy: Mitigating Amyloid-Beta Accumulation and Modulating Acetylcholine Levels in an In Vitro Model of Alzheimer’s Disease

Abstract

Objective: To investigate the effects of photobiomodulation therapy (PBMT) at 660 and 810 nm on amyloid-beta (Ab)42-induced toxicity in differentiated SH-SY5Y cells and to assess its impact on Ab42 accumulation and cholinergic neurotransmission. Background: Alzheimer’s disease (AD) is characterized by the accumulation of Ab peptides, leading to neurodegeneration, cholinergic deficit, and cognitive decline. PBMT has emerged as a potential therapeutic approach to mitigate Ab-induced toxicity and enhance cholinergic function. Methods: Differentiated neurons were treated with 1 lM Ab42 for 1 day, followed by daily PBMT at wavelengths of 660 and 810 nm for 7 days. Treatments used LEDs emitting continuous wave light at a power density of 5 mW/cm2 for 10 min daily to achieve an energy density of 3 J/cm2. Results: Differentiated SH-SY5Y cells exhibited increased Ab42 aggregation, neurite retraction, and reduced cell viability. PBMT at 810 nm significantly mitigated the Ab42-induced toxicity in these cells, as evidenced by reduced Ab42 aggregation, neurite retraction, and improved cell viability and neuronal morphology. Notably, this treatment also restored acetylcholine levels in the neurons exposed to Ab42. Conclusions: PBMT at 810 nm effectively reduces Ab42-induced toxicity and supports neuronal survival, highlighting its neuroprotective effects on cholinergic neurons. By shedding light on the impact of low-level light therapy on Ab42 accumulation and cellular processes. These findings advocate for further research to elucidate the mechanisms of PBMT and validate its clinical relevance in AD management.