Interleukin-1β (IL-1β) is the key molecule involved in the neuroinflammation observed in cases of AD, as IL-1β drives the release of multiple inflammatory mediators by activated microglia, leading to a self-propagating cycle of neuroinflammation, which results in direct neurotoxicity and contributes to promoting the formation of dystrophic neurites [4]. This evidence concerns the gene IL1B and Alzheimer disease.