Since APOE4, an apolipoprotein E variant with increased risk of AD71, disrupts FABP7 interaction with sortilin, (an APOE receptor similar to Sorl1), to interfere with neuroprotective lipid signaling72, this suggests circadian variation in local translation of CPEB-mediated polyadenylation of target mRNAs may be a generalizable mechanism that modulates AD susceptibility through downstream lipid pathways. Here, SORL1 is linked to Alzheimer disease.