Specifically, while levels of a key transporter of the substrate for RA (STRA6) were decreased in the aged hippocampus independent of cognitive status, changes in other components of the RA signaling pathway, including but not limited to synthesis and catabolism of RA (RALDH1, CYP26B1, RARα, FMRP, and GluR1), were selectively increased among aged animals with memory impairment. The gene discussed is CYP26B1; the disease is memory impairment.