In both AD and PD, mitochondrial dysfunction, reactive oxygen species (ROS)-mediated macromolecular damage, and microglial overactivation—leanding to the release of pro-inflammatory cytokines [e.g., tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β)] collectively exacerbate neurodegeneration in both AD and PD (32). The gene discussed is IL1B; the disease is Alzheimer disease.