Overexpression of SREBP-2 in APP/PS1 mice results in Aβ deposition and tau aggregation typical of AD [104], and inhibiting SREBP-2 improves neurodegenerative pathology by significantly reducing Aβ production, abundance, and aggregation, as well as restoring synaptic function and alleviating cognitive and memory deficits [105]. Here, APP is linked to Alzheimer disease.