Notably, PARP-1 inhibition had no effect on TE expression (except for opus) in control flies, but strongly suppressed Aβ42-induced TE dysregulation in elav-Gal4 > Aβ42 AD flies, indicating again that the functional correlation between PARP-1 activity and TE expression could be crucial in determining the AD pathological phenotype. The gene discussed is PARP1; the disease is Alzheimer disease.