Overexpression of C/EBPβ increased AEP expression and accelerated the AD pathologies, leading to the aggravation of cognitive deficits in young 3 × Tg mice; and conversely, depletion of C/EBPβ in old 5 × FAD or 3 × Tg mice down-regulated AEP and diminished the pathological features, ultimately ameliorating cognitive dysfunctions in these AD experimental models [26]. Here, LGMN is linked to Alzheimer disease.