IL1B and Alzheimer disease: NF-κB activation triggers gene transcription, releasing proinflammatory cytokines like tumor necrosis factor-α (TNF-α) and interleukin- 1β (IL-1β), which increase angiotensin-converting enzyme (ACE) levels [12] and promote AD pathogenesis by increasing amyloid precursor protein expression and Aβ formation [13].