Our earlier immuno-confocal and electron microscopy studies have shown that dysfunction in pre-autophagosome formation, ER tubulation, mitochondrial dynamics, autophagy degradation, and ubiquitin proteasome systems occurs at different time points during amyloid plaque growth in 5xFAD and PA mouse brains, resulting in sequential accumulation of proteins, such as ATG9A, RTN3, RAB7, and ubiquitin, in three layers of DNs in surrounding amyloid plaques [11]. Here, ATG9A is linked to amyloidosis.