Taken together, the Aβ pathology in these AD-like monkeys may be attributed to either increased Aβ accumulation driven by APP- or BACE-containing endosomes trapped by phosphorylated tau on disrupted microtubules [69–71], or decreased Aβ clearance due to impaired perivascular drainage and glymphatic system caused by tau-induced astrocytic AQP4 depolarization [72, 73]. Here, APP is linked to Alzheimer disease.