It has been described that using noninvasive exposure to 40-Hz white light LED reduces amyloid-beta, a peptide thought to initiate neurotoxic events in Alzheimer's disease (AD). However, the mechanisms remain to be identified. Since AD impairs mitochondrial potassium channels and respiratory chain activity, the objectives of the current study were to determine the effect of 40-Hz white light LED on structure-function of mitoK channel and brain mitochondrial respiratory chain activity, production of reactive oxygen species (ROS), and ΔΨ in AD. Single mitoK channel was considered using a channel incorporated into the bilayer lipid membrane and expression of mitoK-Kir6.1 subunit as a pore-forming subunit of the channel was determined using a western blot analysis in Aβ1-42 toxicity and light-treated rats. Our results indicated a severe decrease in mito-K channel permeation and Kir6.1 subunit expression coming from the Aβ1-42-induced neurotoxicity. Furthermore, we found that Aβ1-42-induced neurotoxicity decreased activities of complexes I and IV and increased ROS production and ΔΨ. Surprisingly, light therapy increased channel permeation and mitoK-Kir6.1 subunit expression. Noninvasive 40-Hz white light LED treatment also increased activities of complexes I and IV and decreased ROS production and ΔΨ up to ~ 70%. Here, we report that brain mito-K channel and respiratory chain are, at least in part, novel targets of 40-Hz white light LED therapy in AD.