If Arc-endosome trafficking and resultant activity-dependent generation of Aβ remained unchecked, it will create a positive feedback mechanism in which the synaptic removal of AMPAR will produce a significant loss of dendritic spines and synaptic activity, resulting in synaptic failure, similar to that observed in AD (Hsieh et al., 2006; Shankar et al., 2007; Li et al., 2010). This evidence concerns the gene ARC and Alzheimer disease.