In vitro experiments further suggested that PARP16 silencing mitigated Aβ‐induced neuronal damage and ER stress. Mechanistically, PARP16 functions as an RNA‐binding protein that stabilizes amyloid precursor protein (APP) mRNA, thereby preventing APP degradation and elevating protein levels, which exacerbate Alzheimer's disease pathology [65, 149]. Here, APP is linked to early-onset autosomal dominant Alzheimer disease.