Deregulation of ProSAP/Shank has been reported in AD: in patients brains and in transgenic mice models, the accumulation of Aβ oligomers is accompanied by reduction of synaptic scaffold protein levels, such as Shank1 and ProSAP2/Shank3 [115], and disruption of the Homer1b and Shank1 scaffolds [116]. This evidence concerns the gene SHANK3 and Alzheimer disease.