Nevertheless, the present study is the first to demonstrate that G. tsugae significantly attenuates D-gal-induced cognitive impairment and pathological neural damage; increases the activities of SOD-1, catalase, and BDNF; decreases the concentration of AGEs and the expression of inflammatory cytokines and 4-HNE; promotes dendritic branching. The gene discussed is SOD1; the disease is Cognitive impairment.