Shi Du Yan, Xi Chen, Douglas G. Walker, Ann Marie Schmidt, Ottavio Arancio and Lih-Fen Lue Pages 735 - 742 ( 8 )
This review focuses on the current findings regarding interaction between amyloid β peptide (Aβ) and receptor for advanced glycation endproducts (RAGE) and its roles in the pathogenesis of Alzheimers disease (AD). As a ubiquitously expressed cell surface receptor, RAGE mediates the effects of Aβ on microglia, blood-brain barrier (BBB) and neurons through activating different signaling pathways. Data from autopsy brain tissues, in vitro cell cultures and transgenic mouse models suggest that Aβ-RAGE interaction exaggerates neuronal stress, accumulation of Aβ, impaired learning memory, and neuroinflammation. Blockade of RAGE protects against Aβ-mediated cellular perturbation. These findings may have an important therapeutic implication for neurodegenerative disorders relevant to AD.
amyloid precursor protein, AD brains, neurofibrillary tangles, endothelin 1, blood-brain barrier
Department of Pathology,Surgery, and the Taub Institute for Research on Alzheimer's disease and the Aging Brain, College of Physicians&Surgeons,Columbia University, 650 West 168th Street, Black Building, Room 17-07, New York, NY 10032, USA.