Evidence regarding the overexpression of tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and transforming growth factor-β (TGF-β) in the brain of affected patients and transgenic animal models for AD [1,2,3], the association of some genetic polymorphisms of these mediators and the disease manifestation [4], in addition to the neuroprotective impact attributed to anti-inflammatory drugs [5], have accumulated to support the involvement of neuroinflammation in the pathogenesis of neurodegenerative diseases. This evidence concerns the gene IL1B and neurodegenerative disease.