On the contrary, a recent study showed that promoting the interaction between APP and CD2AP via introduction of a lactyl-mimicking mutation in the APP protein (K612 T) accelerates the endosomal-lysosomal degradation pathway of APP, reduces the load of Aβ produced in neurons and even slows down cognitive deficits in a APP23/PS45 double-transgenic mouse model of amyloidosis [114]. This evidence concerns the gene APP and amyloidosis.