Haploinsufficiency of the IGF-1 receptor (IGF-1R) (IGF-1R+/- mice) as well as neuronal deficiency of the insulin receptor (IR) (nIR-/- mice) or IGF-1R (nIGF-1R-/- mice) leads to delayed Aβ accumulation when crossed with mouse models for AD. The gene discussed is IGF1R; the disease is Alzheimer disease.