Protein synthesis has been reported to be impaired in early-stage Alzheimer's disease (AD). Previously, we found that oxygen supplementation improved cognitive function and reduced mitochondrial damage in AD model mice. In the present study, we examined the effects of supplemental oxygen treatment on protein synthesis and oxidative damage. The synthesis of numerous proteins involved in mRNA splicing, transcription regulation, and translation was found to be significantly upregulated in cortex tissues of AD model mice given a supplemental oxygen treatment (OT group), relative to those of non-treated control AD model mice (Ctrl group), suggesting that impairment in protein synthesis may be alleviated by increased oxygen inhalation. Methionine oxidation and oxidation levels in general were similar between the OT and Ctrl groups, indicating that the oxygen supplementation treatment did not cause increases in peptide oxidation levels. On the contrary, the OT group exhibited upregulation of several proteins associated with antioxidant defense. These results support further exploration into the development of supplementary oxygen treatment as a potential therapy for AD.
Keywords: Alzheimer’s disease; Antioxidant defense; Oxidative stress; Oxygen; Protein synthesis; Quantitative proteomics.