Attenuation A?1-42-induced neurotoxicity in neuronal cell by 660nm and 810nm LED light irradiation

Abstract

Oligomeric amyloid-? 1-42 (A?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-?. 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/cm2 were used to modulate biochemical processes in the neural cells. The exposure of A?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 A?1-42-induced neurotoxicity in a biphasic manner. The treatment of LLLT at 3 J/cm2 potentially alleviated cell death and recovered neurite outgrowth. In addition the treatment of LLLT following A?1-42 exposure could attenuate the intracellular ROS generation and Ca2+ influx. Interestingly both wavelengths could induce minimal level of ROS generation. However they did not affect cell viability. In addition LLLT also stimulated Ca2+ 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 Ca2+. 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 A?1-42 accumulation in AD s brain. ? 2023 Thammasart et al. This is an open access article distributed under the terms of the Creative Commons Attribution License which permits unrestricted use distribution and reproduction in any medium provided the original author and source are credited.