Similarly to the other groups we found that IGF-1 signaling reduction protected the mice from AD-associated memory and orientation impairments, mitigated the rates of neuro-inflammation, and largely prevented neuronal and synaptic losses.53 Although the total Aβ quantities as well as the levels of APP processing enzymes were similar in APPswe/PS1ΔE9 and in APPswe/PS1ΔE9/Igf1r+/− mice, Aβ plaques were smaller in size and of higher density in AD-model mice with reduced IGF-1 signaling compared to their litter-mates which exhibited natural levels of IGF-1 signaling. The gene discussed is IGF1R; the disease is Alzheimer disease.