For example, while in aforementioned genetic models of AD [20,256] or after 192 IgG-saporin injection [250] (a common pharmacological model of AD cholinergic deficits [257,258]) IGF-2-dependent IGF2R stimulation or endogenous IGF2R expression increase were associated with neuroprotection, there are some data indicating that an excess of IGF2R may be harmful for the cell and may even lead to Aβ accumulation. This evidence concerns the gene IGF2 and Alzheimer disease.