Attenuation Aβ(1-42)-induced neurotoxicity in neuronal cell by 660nm and 810nm LED light irradiation

Oligomeric amyloid-β 1–42 (Aβ(1–42)) has a close correlation with neurodegenerative disorder especially Alzheimer’s disease (AD). It induces oxidative stress and mitochondrial damage in neurons. Therefore, it is used to generate AD-like in vitro model for studying neurotoxicity and neuroprotection against amyloid-β. A low-level light therapy (LLLT) is a non-invasive method that has been used to treat several neurodegenerative disorders. In this study, the red wavelength (660nm) and near infrared wavelength (810nm) at energy densities of 1, 3, and 5 J/cm(2) were used to modulate biochemical processes in the neural cells. The exposure of Aβ(1–42) resulted in cell death, increased intracellular reactive oxygen species (ROS), and retracted neurite outgrowth. We showed that both of LLLT wavelengths could protect neurons form Aβ(1-42)-induced neurotoxicity in a biphasic manner. The treatment of LLLT at 3 J/cm(2) potentially alleviated cell death and recovered neurite outgrowth. In addition, the treatment of LLLT following Aβ(1–42) exposure could attenuate the intracellular ROS generation and Ca(2+) influx. Interestingly, both wavelengths could induce minimal level of ROS generation. However, they did not affect cell viability. In addition, LLLT also stimulated Ca(2+) influx, but not altered mitochondrial membrane potential. This finding indicated LLLT may protect neurons through the stimulation of secondary signaling messengers such as ROS and Ca(2+). The increase of these secondary messengers was in a functional level and did not harmful to the cells. These results suggested the use of LLLT as a tool to modulate the neuronal toxicity following Aβ(1–42) accumulation in AD’s brain.