In agreement, the memory deficits and the increased inflammatory mediators, such as TNF-α and IL-1β, were observed by Gao et al. in D-gal-induced AD rats, which was closely associated with SIRT1/NF-κB signaling pathway [38], further indicating that DHM may ameliorate the cognitive functions and inhibit the neuroinflammatory responses through activation of AMPK/SIRT1 signaling pathway to down-regulate NF-κB p65. The gene discussed is IL1B; the disease is Alzheimer disease.