DIAPH1 and Alzheimer disease: In the same study, Coelho and colleagues demonstrated that suppression of fitness-based removal of Aβ42-damaged neurons by knockdown of azot, the fitness checkpoint gene, and overexpression of DIAP1 exacerbated AD-like phenotypes of Aβ42-expressing flies, including degenerative vacuoles, a decreased lifespan, a locomotory defect, and a memory defect.