While many of these features have been described in AD brains and transgenic animal models throughout the literature (e.g., aberrant cell cycle activity, p16INK4A co‐localization with NFTs (Arendt, Rodel, Gartner, & Holzer, 1996), decreased lamin B1, and heterochromatin relaxation (Frost, Bardai, & Feany, 2016); a role for cellular senescence in AD‐associated neurodegeneration has not been investigated. Here, LMNB1 is linked to Alzheimer disease.