In the animal models of AD, activated microglia and astrocytes not only lead to the loss of synaptic components and decreased synaptic plasticity [16] but also release pro-inflammatory cytokines including interleukin-1α (IL-1α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), thereby accelerating the amyloid β (Aβ) deposition and cognitive decline [17]. This evidence concerns the gene IL6 and Alzheimer disease.