Clearance of Alzheimer's amyloid-ss(1-40) peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier.

By Masayoshi Shibata, S. Yamada, S. R. Kumar, M. Calero, J. Bading, B. Frangione, D. Holtzman, C. Miller, D. Strickland, J. Ghiso and 1 more. Journal of Clinical Investigation, 2000

1,466 citations recorded by the source corpus.

Subfields: Nutrition and Dietetics, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/e906d48815458443a6f62b00f62b3ef8cf23891d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Nutrition and Dietetics

1. Berislav Zlokovic

In Oncology

1. Berislav Zlokovic
2. D. Holtzman
3. G. Bu
4. R. Bell
5. C. Iadecola
6. R. Daneman

In Physiology

1. Berislav Zlokovic
2. D. Holtzman
3. C. Iadecola
4. R. Bell
5. A. Sagare
6. G. Bu
7. J. Herz
8. R. Daneman

Citations in the corpus

• The pathobiology of vascular dementia (2013, positive): “The vascular pathway is estimated to be a major route of removal of Ab from the brain (Castellano et al., 2012; Shibata et al., 2000).”
• Neurovascular mechanisms and blood–brain barrier disorder in Alzheimer’s disease (2009, background): “LRP is the major cell surface Ab clearance receptor that transports Ab out of the brain across the BBB [9, 25, 80] and promotes Ab clearance on VSMC [87] (Fig.”
• LRP: a multifunctional scavenger and signaling receptor. (2001, background): “At the same time, the Aβ peptide binds avidly to LRP ligands, such as α2M and apoE, and LRP-mediated clearance of these ligands complexed to Aβ contributes to a reduction in Aβ levels (45, 48).”
• Impairment of paravascular clearance pathways in the aging brain (2014, background): “In addition to paravascular pathways of Ab clearance, the clearance of Ab by BBB transporters such as low-density lipoprotein receptor–related protein 1 are major contributors to Ab efflux from the brain.(15) We surmise that these are likely overlapping processes.”
• Therapeutics of Alzheimer's disease: Past, present and future. (2014, background): “With age, LRP expression decreases, impairing Ab efflux contributing to prolonged Ab stay in the brain (Shibata et al., 2000).”
• Classification and basic pathology of Alzheimer disease (2009, background): “[292] or with P-glycoprotein [67] to cross the blood–brain barrier.”
• P-glycoprotein deficiency at the blood-brain barrier increases amyloid-beta deposition in an Alzheimer disease mouse model. (2005, background): “The latter, representing efflux across the BBB into the periphery, appears to be a substantial pathway for elimination of CNS-derived Aβ (5).”
• Alzheimer’s Disease and the β-Amyloid Peptide (2010, neutral): “Soluble A β is exchanged across the BBB by two principle mechanisms, the low-density lipoprotein receptor-related protein (LRP) on the abluminal (brain) side [65], and the receptor for advanced glycation end products (RAGE) on the luminal (blood) side [66].”
• The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics (2011, background): “Amyloid-β is trafficked via the interstitial fluid (ISF) into the cerebrospinal fluid (CSF) via bulk flow; however, this has been shown to be a minor route for amyloid-β clearance in mice, as it only accounts for approximately 10% of amyloid-β clearanc”
• The blood–brain barrier in health and disease: Important unanswered questions (2020, background): “Substrate-specific solute transporters can also be important for removing molecules from the CNS; lipoprotein receptor-related protein-1 (LRP1) is a critical transporter for eliminating β-amyloid (Shibata et al., 2000; Storck et al., 2016).”
• Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease. (2012, background): “Recombinant RAP and LRP1 antibody also reduce Ab efflux from mouse brain (Shibata et al. 2000).”