That is highlighted by several examples: (i) Aβ oligomers induce dendritic spine loss and aberrant dendritic spine formation in primary hippocampal neurons [90,91]; (ii) Tg2576 mice exhibit reduced spine density in CA1 and dentate gyrus, correlating with cognitive decline [92,93]; (iii) the overexpression of human APP in AD animal models leads to substantial spine loss and neurite dystrophy around amyloid plaques, disrupting neuronal circuits and causing cognitive decline [94,95,96]. Here, APP is linked to Alzheimer disease.