Diminishing eIF2α phosphorylation via fore-brain-specific conditional deletion, genetic haploinsufficiency, or pharmacological manipulation of PERK mitigates cerebral Aβ accumulation by reducing BACE1 levels and ameliorates cognition deficits in AD transgenic mice (Ma et al., 2013; Zhu et al., 2013b; Devi and Ohno, 2014). This evidence concerns the gene EIF2A and Alzheimer disease.