P-glycoprotein deficiency at the blood-brain barrier increases amyloid-beta deposition in an Alzheimer disease mouse model.

By John R. Cirrito, R. Deane, Anne M. Fagan, Michael L. Spinner, Maia Parsadanian, M. Finn, Hong Jiang, Julie L. Prior, A. Sagare, K. Bales and 4 more. Journal of Clinical Investigation, 2005

650 citations recorded by the source corpus.

Subfields: Oncology, Pediatrics, Perinatology and Child Health, Physiology

View Paper: https://www.semanticscholar.org/paper/e00ebded7b1f3680f3b9d2495a4857477deb5672

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Citations in the corpus

Impairment of Glymphatic Pathway Function Promotes Tau Pathology after Traumatic Brain Injury (2014, background): “Mannitol and inulin were selected as interstitial tracers because neither are cleared across the blood– brain barrier, and both are cleared from the brain by convective bulk flow (Cirrito et al., 2005; Syková and Nicholson, 2008).”
apoE isoform-specific disruption of amyloid beta peptide clearance from mouse brain. (2008, background): “Clearance of Alzheimer’s amyloid β(1-40)-peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier.”
Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “Animal work has shown that each of these proteins can enhance either Aβ degradation (Leissring et al. 2003) or Aβ transport (Cirrito et al. 2005, Deane et al. 2004).”
Classification and basic pathology of Alzheimer disease (2009, background): “[292] or with P-glycoprotein [67] to cross the blood–brain barrier.”
The Role of Apolipoprotein E in Alzheimer’s Disease (2009, background): “At the BBB, soluble Aβ is predominantly transported from the interstitial fluid into the bloodstream via LRP1 and P-glycoprotein (Cirrito et al., 2005; Zlokovic, 2008).”
The blood–brain barrier in health and disease: Important unanswered questions (2020, background): “Blood–brain barrier review https://doi.org/10.1084/jem.20190062 clearance rate in half and increases CNS Aβ deposition (Cirrito et al., 2005), and Aβ40 triggers ubiquitination and internalization of PGP (Hartz et al., 2016), suggesting a dangerous feedback cycle.”
A blood–brain barrier overview on structure, function, impairment, and biomarkers of integrity (2020, background): “In an animal model of AD, ABC transporters are affected, which leads to the accumulation of amyloid β-peptide (Aβ) in the brain [127].”
Xenobiotic, Bile Acid, and Cholesterol Transporters: Function and Regulation (2010, background): “Furthermore, administration of a Pgp inhibitor to transgenic mice that over- express amyloid precursor protein stimulates accumulation of amyloid beta in the brain (Cirrito et al., 2005).”
Blood–brain Barrier: Structural Components and Function Under Physiologic and Pathologic Conditions (2006, background): “P-gp expression was shown to correlate inversely with deposition of β-amyloid in Alzheimer’s disease (Cirrito et al. 2005).”