Evidence map›Paper›PMID 30876953›Full record

ArticleJournal of controlled release : official journal of the Controlled Release Society2019

Dual-drug loaded nanoparticles of Epigallocatechin-3-gallate (EGCG)/Ascorbic acid enhance therapeutic efficacy of EGCG in a APPswe/PS1dE9 Alzheimer's disease mice model.

Amanda Cano, Miren Ettcheto, Jui-Hsien Chang, Emma Barroso, Marta Espina, Britta A Kühne, Marta Barenys, Carmen Auladell, Jaume Folch, Eliana B Souto and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of controlled release : official journal of the Controlled Release Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 1 pooled it
20.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

142 citing papers in PubMed, 1 synthesis or guideline pooled it, 322 citations in OpenAlex.

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82 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 6 institutions in 4 countries.

Amanda CanoDepartment of Pharmacy, Pharmaceutical Technology and Physical Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain; Institute of Nanoscience and Nanotechnology (IN2UB), Barcelona, Spain; Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain; UCL Institute of Ophthalmology, University College of London, United Kingdom.
Miren EttchetoBiomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain; Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain; Unit of Biochemistry and Pharmacology, Faculty of Medicine and Health Sciences, University of Rovira i Virgili, Reus, Tarragona, Spain.
Jui-Hsien ChangUCL Institute of Ophthalmology, University College of London, United Kingdom.
Emma BarrosoDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain; Biomedical Research Center in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Health Institute Carlos III, Barcelona, Spain; Research Institute-Hospital Sant Joan de Déu, Esplugues de Llobregat, Barcelona, Spain.
Marta EspinaDepartment of Pharmacy, Pharmaceutical Technology and Physical Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain; Institute of Nanoscience and Nanotechnology (IN2UB), Barcelona, Spain.
Britta A KühneDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain.
Marta BarenysDepartment of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain.
Carmen AuladellDepartment of Cellular Biology, Physiology and Immunology, Faculty of Biology, University of Barcelona, Spain.
Jaume FolchBiomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain; Unit of Biochemistry and Pharmacology, Faculty of Medicine and Health Sciences, University of Rovira i Virgili, Reus, Tarragona, Spain.
Eliana B SoutoDepartment of Pharmaceutical Technology, Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal; REQUIMTE/LAQV, Group of Pharmaceutical Technology, Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal.
Antoni CaminsBiomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain; Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain.
Patric TurowskiUCL Institute of Ophthalmology, University College of London, United Kingdom.. Electronic address: p.turowski@ucl.ac.uk.
Maria Luisa GarcíaDepartment of Pharmacy, Pharmaceutical Technology and Physical Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, Spain; Institute of Nanoscience and Nanotechnology (IN2UB), Barcelona, Spain. Electronic address: marisagarcia@ub.edu.
Biomedical Research Networking Center on Neurodegenerative Diseases · ESUniversitat de Barcelona · ESUniversity College Hospital · GBInstitut de Nanociència i Nanotecnologia de la Universitat de BarcelonaHospital Sant Joan de Déu Barcelona · ESRede de Química e Tecnologia · PT

Funding

British Heart Foundation FS/16/26/32193
6 · The paper itself

Abstract

Epigallocatechin-3-gallate (EGCG) is a candidate for treatment of Alzheimer's disease (AD) but its inherent instability limits bioavailability and effectiveness. We found that EGCG displayed increased stability when formulated as dual-drug loaded PEGylated PLGA nanoparticles (EGCG/AA NPs). Oral administration of EGCG/AA NPs in mice resulted in EGCG accumulation in all major organs, including the brain. Pharmacokinetic comparison of plasma and brain accumulation following oral administration of free or EGCG/AA NPs showed that, whilst in both cases initial EGCG concentrations were similar, long-term (5-25 h) concentrations were ca. 5 fold higher with EGCG/AA NPs. No evidence was found that EGCG/AA NPs utilised a specific pathway across the blood-brain barrier (BBB). However, EGCG, empty NPs and EGCG/AA NPs all induced tight junction disruption and opened the BBB in vitro and ex vivo. Oral treatment of APPswe/PS1dE9 (APP/PS1) mice, a familial model of AD, with EGCG/AA NPs resulted in a marked increase in synapses, as judged by synaptophysin (SYP) expression, and reduction of neuroinflammation as well as amyloid β (Aβ) plaque burden and cortical levels of soluble and insoluble Aβ

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAntioxidantsAscorbic AcidBrainCatechinDisease Models, AnimalDrug CarriersDrug LiberationEndothelial CellsMaleMice, Inbred C57BLMice, TransgenicNanoparticlesPolyethylene GlycolsAmyloid beta-PeptidesAntioxidantsAscorbic AcidCatechinDrug Carriersepigallocatechin gallatePolyethylene GlycolsPolylactic Acid-Polyglycolic Acid CopolymerAlzheimer's diseaseAPP/PS1 miceEGCGEpigallocatechin gallatePLGA-PEGPolymeric nanoparticles

Identifiers

PMID30876953
PMCPMC6510952
OpenAlexW2920901214

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.