Evidence map›Paper›PMID 33153231›Full record

ArticleInternational journal of molecular sciences2020

Brain Distribution of Dual ABCB1/ABCG2 Substrates Is Unaltered in a Beta-Amyloidosis Mouse Model.

Thomas Wanek, Viktoria Zoufal, Mirjam Brackhan, Markus Krohn, Severin Mairinger, Thomas Filip, Michael Sauberer, Johann Stanek, Thomas Pekar, Jens Pahnke and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

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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

11 authors at 3 institutions in 4 countries.

Thomas WanekPreclinical Molecular Imaging, AIT Austrian Institute of Technology GmbH, 2444 Seibersdorf, Austria.ORCID 0000-0002-0404-4452
Viktoria ZoufalPreclinical Molecular Imaging, AIT Austrian Institute of Technology GmbH, 2444 Seibersdorf, Austria.
Mirjam BrackhanDepartment of Neuro-/Pathology, University of Oslo (UiO) and Oslo University Hospital (OUS), 0424 Oslo, Norway.
Markus KrohnDepartment of Neuro-/Pathology, University of Oslo (UiO) and Oslo University Hospital (OUS), 0424 Oslo, Norway.ORCID 0000-0002-5345-9048
Severin MairingerPreclinical Molecular Imaging, AIT Austrian Institute of Technology GmbH, 2444 Seibersdorf, Austria.ORCID 0000-0001-5094-9351
Thomas FilipPreclinical Molecular Imaging, AIT Austrian Institute of Technology GmbH, 2444 Seibersdorf, Austria.
Michael SaubererPreclinical Molecular Imaging, AIT Austrian Institute of Technology GmbH, 2444 Seibersdorf, Austria.
Johann StanekPreclinical Molecular Imaging, AIT Austrian Institute of Technology GmbH, 2444 Seibersdorf, Austria.
Thomas PekarBiomedical Analytics, University of Applied Sciences Wiener Neustadt, 2700 Wiener Neustadt, Austria.
Jens PahnkeDepartment of Neuro-/Pathology, University of Oslo (UiO) and Oslo University Hospital (OUS), 0424 Oslo, Norway.ORCID 0000-0001-7355-4213
Oliver LangerPreclinical Molecular Imaging, AIT Austrian Institute of Technology GmbH, 2444 Seibersdorf, Austria.
Austrian Institute of Technology · ATOslo University Hospital · NOFachhochschule Wiener Neustadt · AT

Funding

Austrian Science Fund FWF I 1609
6 · The paper itself

Abstract

backgroundABCB1 (P-glycoprotein) and ABCG2 (breast cancer resistance protein) are co-localized at the blood-brain barrier (BBB), where they restrict the brain distribution of many different drugs. Moreover, ABCB1 and possibly ABCG2 play a role in Alzheimer's disease (AD) by mediating the brain clearance of beta-amyloid (Aβ) across the BBB. This study aimed to compare the abundance and activity of ABCG2 in a commonly used β-amyloidosis mouse model (APP/PS1-21) with age-matched wild-type mice.

methodsThe abundance of ABCG2 was assessed by semi-quantitative immunohistochemical analysis of brain slices of APP/PS1-21 and wild-type mice aged 6 months. Moreover, the brain distribution of two dual ABCB1/ABCG2 substrate radiotracers ([

resultsImmunohistochemical analysis revealed a significant reduction (by 29-37%) in the number of ABCG2-stained microvessels in the brains of APP/PS1-21 mice. Partial ABCG2 inhibition significantly increased the brain distribution of [

conclusionsDespite a reduction in the abundance of cerebral ABCG2 and ABCB1 in APP/PS1-21 mice, the brain distribution of two dual ABCB1/ABCG2 substrates was unaltered. Our results suggest that the brain distribution of clinically used ABCB1/ABCG2 substrate drugs may not differ between AD patients and healthy people.

Indexed as

Amyloid beta-PeptidesAmyloidosisAnimalsATP Binding Cassette Transporter, Subfamily B, Member 1ATP Binding Cassette Transporter, Subfamily G, Member 2Blood-Brain BarrierBrainDisease Models, AnimalFemaleMiceMice, Inbred C57BLMice, TransgenicPositron-Emission TomographyQuinolinesTissue DistributionAbcg2 protein, mouseAmyloid beta-PeptidesATP Binding Cassette Transporter, Subfamily B, Member 1ATP Binding Cassette Transporter, Subfamily G, Member 2QuinolinestariquidarABCB1ABCG2Alzheimer’s diseasebeta-amyloidblood-brain barriererlotinibPETtariquidar

Identifiers

PMID33153231
PMCPMC7663372
OpenAlexW3097850956

What OpenQuestion holds

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LicenceCC BY
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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.