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.
Keywords: amyloid precursor protein, AD brains, neurofibrillary tangles, endothelin 1, blood-brain barrier
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