The CNS is presumably exposed mainly to Aβ generated within the CNS, rather than Aβ generated peripherally and entering across the BBB (although Aβ transfer in this direction is possible via the receptor for advanced glycation end products (RAGE) [32]), Consequently, the rise of CNS Aβ concentration that occurs in AD depends not only on the rate of Aβ production, but also on the rate at which it is enzymatically degraded within and removed from the CNS [108]. Here, AGER is linked to Alzheimer disease.