Patients may exhibit Aβ plaque pathology for more than a decade before any clinical diagnosis of AD,29,30 while tau pathology usually occurs downstream from the deposition of Aβ plaques.31 It is thought that deposited Aβ can act as a damage-associated molecular pattern (DAMP) and bind to receptors like toll-like receptors (TLRs), receptor for advanced glycation end products (RAGE), and nucleotide-binding oligomerization domain-like receptors (NLRs). Here, AGER is linked to Alzheimer disease.