Author: ["Rashid Deane","Shi Du Yan","Ram Kumar Submamaryan","Barbara LaRue","Suzana Jovanovic","Elizabeth Hogg","Deborah Welch","Lawrence Manness","Chang Lin","Jin Yu","Hong Zhu","Jorge Ghiso","Blas Frangione","Alan Stern","Ann Marie Schmidt","Don L Armstrong","Bernd Arnold","Birgit Liliensiek","Peter Nawroth","Florence Hofman","Mark Kindy","David Stern","Berislav Zlokovic"]
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Abstract
Amyloid-β peptide (Aβ) interacts with the vasculature to influence Aβ levels in the brain and cerebral blood flow, providing a means of amplifying the Aβ-induced cellular stress underlying neuronal dysfunction and dementia. Systemic Aβ infusion and studies in genetically manipulated mice show that Aβ interaction with receptor for advanced glycation end products (RAGE)-bearing cells in the vessel wall results in transport of Aβ across the blood-brain barrier (BBB) and expression of proinflammatory cytokines and endothelin-1 (ET-1), the latter mediating Aβ-induced vasoconstriction. Inhibition of RAGE-ligand interaction suppresses accumulation of Aβ in brain parenchyma in a mouse transgenic model. These findings suggest that vascular RAGE is a target for inhibiting pathogenic consequences of Aβ-vascular interactions, including development of cerebral amyloidosis.Cite this article
Deane, R., Du Yan, S., Submamaryan, R. et al. RAGE mediates amyloid-β peptide transport across the blood-brain barrier and accumulation in brain. Nat Med 9, 907–913 (2003). https://doi.org/10.1038/nm890 