Indeed, unlike the selective lesion of cholinergic cells with p75NTR targeting neurotoxin (IgG192-saporin) in AD APPswe/PS1dE9 mice, exhibiting cognitive deficit and enhanced deposition of Aβ in several cortical regions, genetic deletion of p75NTR without ablation of cholinergic neurons led to enhanced cortical Aβ loading in the absence of cognitive deficit. This evidence concerns the gene NGFR and Cognitive impairment.