ArticleThe Journal of pharmacy and pharmacology2011
Up-regulation of P-glycoprotein reduces intracellular accumulation of beta amyloid: investigation of P-glycoprotein as a novel therapeutic target for Alzheimer's disease.
Article in The Journal of pharmacy and pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 71 citations in OpenAlex.
- The relationship between amyloid-beta and brain capillary endothelial cells in Alzheimer's disease.Neural regeneration research · 2022Review
- AGE-TXNIP axis drives inflammation in Alzheimer's by targeting Aβ to mitochondria in microglia.Cell death & disease · 2022Article
- Quantification of P-Glycoprotein in the Gastrointestinal Tract of Humans and Rodents: Methodology, Gut Region, Sex, and Species Matter.Molecular pharmaceutics · 2021Observational
- Disease-Induced Modulation of Drug Transporters at the Blood-Brain Barrier Level.International journal of molecular sciences · 2021Review
- The Interplay of ABC Transporters in Aβ Translocation and Cholesterol Metabolism: Implicating Their Roles in Alzheimer's Disease.Molecular neurobiology · 2021Review
- Repurposing Licensed Drugs for Use Against Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2021Review
- Warm, Sweetened Milk at the Twilight of Immunity - Alzheimer's Disease - Inflammaging, Insulin Resistance,Frontiers in immunology · 2021Review
- Article
- New Evidence for P-gp-Mediated Export of Amyloid-β PEPTIDES in Molecular, Blood-Brain Barrier and Neuronal Models.International journal of molecular sciences · 2020Article
- The effects of oral administration of Cola nitida on the pharmacokinetic profile of metoclopramide in rabbits.BMC pharmacology & toxicology · 2020Article
- Verapamil and Alzheimer's Disease: Past, Present, and Future.Frontiers in pharmacology · 2020Review
- Plasma Rich in Growth Factors (PRGF) Disrupt the Blood-Brain Barrier Integrity and Elevate Amyloid Pathology in the Brains of 5XFAD Mice.International journal of molecular sciences · 2019Article
- Potential microRNA-related targets in clearance pathways of amyloid-β: novel therapeutic approach for the treatment of Alzheimer's disease.Cell & bioscience · 2019Review
- Cellular Models and In Vitro Assays for the Screening of modulators of P-gp, MRP1 and BCRP.Molecules (Basel, Switzerland) · 2017Review
- Amyloid-β and Astrocytes Interplay in Amyloid-β Related Disorders.International journal of molecular sciences · 2016Review
- Olive Oil and the Hallmarks of Aging.Molecules (Basel, Switzerland) · 2016Review
- Evidence against a role of P-glycoprotein in the clearance of the Alzheimer's disease Aβ1-42 peptides.Cell stress & chaperones · 2015Article
- Reduced Alzheimer's disease pathology by St. John's Wort treatment is independent of hyperforin and facilitated by ABCC1 and microglia activation in mice.Current Alzheimer research · 2013Article
- Olive-oil-derived oleocanthal enhances β-amyloid clearance as a potential neuroprotective mechanism against Alzheimer's disease: in vitro and in vivo studies.ACS chemical neuroscience · 2013Article
- The changing landscape of voltage-gated calcium channels in neurovascular disorders and in neurodegenerative diseases.Current neuropharmacology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesSeveral studies have suggested the efflux transporter P-glycoprotein (P-gp) to play a role in the etiology of Alzheimer's disease through the clearance of amyloid beta (Aβ) from the brain. In this study, we aimed to investigate the possibility of P-gp as a potential therapeutic target for Alzheimer's disease by examining the impact of P-gp up-regulation on the clearance of Aβ, a neuropathological hallmark of Alzheimer's disease.
methodsUptake studies for ¹²⁵I-radiolabelled Aβ₁₋₄₀, and fluorescent immunostaining technique for P-gp and fluorescent imaging of Aβ₁₋₄₀ were carried out in LS-180 cells following treatment with drugs known to induce P-gp expression. KEY
findingsApproximately 10-35% decrease in ¹²⁵I-Aβ₁₋₄₀ intracellular accumulation was observed in cells treated with rifampicin, dexamethasone, caffeine, verapamil, hyperforin, β-estradiol and pentylenetetrazole compared with control. Also, fluorescent micrographs showed an inverse relationship between levels of P-gp expression and 5-carboxyfluorescein labelled Aβ (FAM-Aβ₁₋₄₀) intracellular accumulation. Quantitative analysis of the micrographs revealed that the results were consistent with those of the uptake studies using ¹²⁵I-Aβ₁₋₄₀.
conclusionsThe investigated drugs were able to improve the efflux of Aβ₁₋₄₀ from the cells via P-gp up-regulation compared with control. Our results elucidate the importance of targeting Aβ clearance via P-gp up-regulation, which will be effective in slowing or halting the progression of Alzheimer's disease.
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