The M1 phenotype is induced by lipopolysaccharide (LPS) or interferon-gamma (IFN-γ), resulting in the production of pro-inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and reactive oxygen species (ROS), which contribute to neurotoxicity and chronic neuroinflammation in conditions such as Alzheimer’s disease (AD) and PD [8,9]. This evidence concerns the gene IL1B and Alzheimer disease.