ABSTRACT
This chapter aims to investigate the protective effects of Selenomethionine (SeMet) supplementation against D-gal-induced memory impairment in mice and explore the potential mechanisms related to the beneficial effects. SeMet, a major organic form of Selenium (Se), has greater bioavailability and less toxicity than inorganic Se. Cognitive deficits are the most common phenotypes in normal aging, including the decline of episodic memory, spatial memory, and attention. D-gal induced behavioral and neurochemical changes can mimic many characters of the natural brain aging process, such as cognitive dysfunction and neurons cell death, which is widely considered as a typical aging model. D-gal-treated-alone mice dramatically increased the mean escape latency compared to the control group during trial session, while such an alteration was significantly reversed by SeMet treatment. While SeMet treatment partially rescued the reduction of the superoxide dismutase, glutathione peroxidase and catalase activities, decreased malondialdehyde level, implying that SeMet could alleviate oxidative damage caused by D-gal in aging mice.
