BACE1 and Alzheimer disease: A more consistent view is that in AD, NGF/TrkA mainly acts on non-amyloid proteins, and overexpression of NGF regulates TrkA binding to APP and promotes Golgi transport of APP, inhibits APP binding by BACE1, thus reducing Aβ production and eliminating imbalance, in addition to finding that NGF promotes APP transfer to the α-secretase pathway (Aloe et al., 2012).