Fig. 4
From: Death-associated protein kinase 1 as a therapeutic target for Alzheimer's disease
DAPK1 dysregulation triggers APP phosphorylation and enhances the amyloidogenic processing pathway. DAPK1 is able to interact with APP in neurons, and potentiates the JNK3-induced APP phosphorylation at the Thr668 residue. Phosphorylated APP translocates to the endosomes and undergoes the amyloidogenic cleavage by BACE1 and γ-secretases sequentially. The generation of Aβ is thus enhanced, leading to the pronounced formation of amyloid plaques in the brain