In the light of increasing evidence supporting an involvement of PARylation in normal neuronal functions as well as in neurodegeneration and neuropathology [12,51], we reasoned that PARP-1 could represent a new interesting pharmacological target in AD, and PARP-1 inhibitors could become the objects of a drug-repurposing evaluation to identify a new beneficial treatment for AD. This evidence concerns the gene PARP1 and Alzheimer disease.