Mechanisms underlying its anti-AD effects include but are not limited to preventing antioxidant enzyme activity, increasing the synthesis of BDNF, reducing the levels of ROS, TNF-α, IL-1β, IL-6, malondialdehyde (MDA) [136, 137], and affecting the aggregation of tau and amyloid proteins [138, 139]. The gene discussed is IL1B; the disease is Alzheimer disease.