As the receptor for advanced glycation end products (RAGE) has been found to mediate amyloid-β influx and microglial activation at the blood-brain barrier, this may also represent a future pharmacological target in humans, with data from mouse models of Alzheimer’s disease showing effective control of amyloid-β accumulation and amyloid-β-mediated cellular stress using RAGE inhibitors [84]. Here, AGER is linked to early-onset autosomal dominant Alzheimer disease.