Shi Du Yan

TL;DR: Evidence is presented that the 'receptor for advanced glycation end products' (RAGE) is such a receptor, and that it mediates effects of the peptide on neurons and microglia and indicates that it is relevant to the pathogenesis of neuronal dysfunction and death.

TL;DR: RAGE is a new member of the immunoglobulin superfamily of cell surface molecules and shares significant homology with MUC 18, NCAM, and the cytoplasmic domain of CD20 and could potentially mediate cellular effects of this class of glycosylated proteins.

TL;DR: These findings suggest that vascular RAGE is a target for inhibiting pathogenic consequences of Aβ-vascular interactions, including development of cerebral amyloidosis.

TL;DR: It is demonstrated here that physiologically relevant CML modifications of proteins engage cellular RAGE, thereby activating key cell signaling pathways such as NF-κB and modulating gene expression, and triggers processes intimately linked to accelerated vascular and inflammatory complications that typify disorders in which inflammation is an established component.

TL;DR: The CypD-mediated mitochondrial permeability transition pore is directly linked to the cellular and synaptic perturbations observed in the pathogenesis of Alzheimer's disease.