Given the similarity in BACE1 enrichment at these AP-4 dystrophies to that observed at amyloid plaques (Zhao et al., 2007; Gowrishankar et al., 2015), and the potential for increased APP processing and Aβ production at these sites, we predicted that the axonal pathology arising from AP-4 complex loss, i.e., occurrence of AP-4 dystrophies, would lead to a worsening of the amyloid plaque pathology. The gene discussed is APP; the disease is amyloidosis.