In AD patient-derived neurons and triple transgenic (3xTg-AD, carrying mutated forms of APP, PSEN1, and MAPT/tau) mouse model, inhibition of HDAC3 (Class I) decreases pathological tau phosphorylation and acetylation, reduces Aβ protein expression, increases Aβ degradation, improves learning and memory and normalizes several AD-related genes [83]. Here, APP is linked to Alzheimer disease.