RAGE mediates amyloid-β peptide transport across the blood-brain barrier and accumulation in brain
By R. Deane, S. Yan, Ram Kumar Submamaryan, Barbara LaRue, S. Jovanovic, E. Hogg, D. Welch, Lawrence Manness, Chang Lin, Jin Yu and 13 more. Nature Medicine, 2003
1,439 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Oncology, Physiology
View Paper: https://www.semanticscholar.org/paper/e9e0f432fdaa5568ab57545cf04bdaf5bc89b0b6
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Citations in the corpus
- Transport Pathways for Clearance of Human Alzheimer's Amyloid β-Peptide and Apolipoproteins E and J in the Mouse Central Nervous System (2007, methodology): “…shown by microdialysis technique (DeMattos et al, 2003), given the Ab BBB efflux rate as determined in the present study, it would take about 40 secs for LRP1 to clear this Ab pool from brain ISF, assuming Ab central production and re-entry of circulating Ab into the brain (Deane et al, 2003) stop.”
- Neurovascular mechanisms and blood–brain barrier disorder in Alzheimer’s disease (2009, background): “RAGE is the key receptor that transports Ab from the blood into the brain [23], which occurs at a rate that is five- to sixfold lower than the rate determined for the transport of large neutral amino acids [78].”
- Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain aging (2010, methodology): “Perfusion stress and BBB compromise have been associated with neurodegenerative disorders (Zlokovic, 2008), including Alzheimer’s disease (Iadecola et al., 1999; Deane et al., 2003; Chow et al., 2007; Bell et al., 2009) and amyotrophic lateral sclerosis (Zhong et al.”
- The blood-brain barrier in brain homeostasis and neurological diseases. (2009, neutral): “Aβ peptide influx into the brain is mediated by the receptor for advanced glycosylation products (RAGE) [189] and is dependent on Aβ chaperones, apoE and apoJ [190]: apoE2 and apoE3, but not ApoE4, block the transport of Aβ to the brain [191].”
- The blood-brain barrier in health and chronic neurodegenerative disorders. (2008, positive): “In AD and transgenic models of b-amyloidosis, RAGE expression increases in the affected cerebral vessels, microglia, and neurons (Yan et al., 1996; Deane et al., 2003; Donahue et al., 2006).”
- Classification and basic pathology of Alzheimer disease (2009, background): “There is also a flux of Ab peptide from the blood to the cerebral parenchyma mediated by the receptor for advanced glycation endproducts (RAGE) [77].”