Investigating the role of BDNF in modulation of APP β‐cleavage and BACE1 subcellular distribution

Acute treatment with BDNF may decrease β-cleavage of APP by altering the subcellular distribution of BACE1, increasing recruitment/retention of BACE1 at the plasma membrane and decreasing BACE1 endocytosis. This effect appears to be independent of clathrin-mediated endocytosis, as PitStop2 treatment increases α-cleavage of APP but does not reduce β-cleavage independent of BDNF treatment. Hence, BDNF may reduce production of Aβ by altering BACE1 distribution, decreasing upstream β-cleavage.