Evidence map›Paper›PMID 30485540›Full record

ArticleGlia2019

Defined astrocytic expression of human amyloid precursor protein in Tg2576 mouse brain.

Tina Heiland, Ulrike Zeitschel, Maja A Puchades, Peer-Hendrik Kuhn, Stefan F Lichtenthaler, Jan G Bjaalie, Maike Hartlage-Rübsamen, Steffen Roßner, Corinna Höfling

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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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

9 authors at 4 institutions in 2 countries.

Tina HeilandPaul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany.
Ulrike ZeitschelPaul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany.
Maja A PuchadesNeural Systems Laboratory, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Peer-Hendrik KuhnInstitute of Pathology, Technical University of Munich, Munich, Germany.
Stefan F LichtenthalerDeutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Munich, Germany.
Jan G BjaalieNeural Systems Laboratory, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Maike Hartlage-RübsamenPaul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany.
Steffen RoßnerPaul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany.ORCID 0000-0002-9959-283X
Corinna HöflingPaul Flechsig Institute for Brain Research, University of Leipzig, Leipzig, Germany.
Leipzig University · DEUniversity of Oslo · NOGerman Center for Neurodegenerative Diseases · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transgenic Tg2576 mice expressing human amyloid precursor protein (hAPP) with the Swedish mutation are among the most frequently used animal models to study the amyloid pathology related to Alzheimer's disease (AD). The transgene expression in this model is considered to be neuron-specific. Using a novel hAPP-specific antibody in combination with cell type-specific markers for double immunofluorescent labelings and laser scanning microscopy, we here report that-in addition to neurons throughout the brain-astrocytes in the corpus callosum and to a lesser extent in neocortex express hAPP. This astrocytic hAPP expression is already detectable in young Tg2576 mice before the onset of amyloid pathology and still present in aged Tg2576 mice with robust amyloid pathology in neocortex, hippocampus, and corpus callosum. Surprisingly, hAPP immunoreactivity in cortex is restricted to resting astrocytes distant from amyloid plaques but absent from reactive astrocytes in close proximity to amyloid plaques. In contrast, neither microglial cells nor oligodendrocytes of young or aged Tg2576 mice display hAPP labeling. The astrocytic expression of hAPP is substantiated by the analyses of hAPP mRNA and protein expression in primary cultures derived from Tg2576 offspring. We conclude that astrocytes, in particular in corpus callosum, may contribute to amyloid pathology in Tg2576 mice and thus mimic this aspect of AD pathology.

Indexed as

Age FactorsAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsAstrocytesBrainCalcium-Binding ProteinsCells, CulturedDisease Models, AnimalGene Expression RegulationGlial Fibrillary Acidic ProteinGlutathione S-Transferase piHumansMiceMice, Inbred C57BLMicrofilament ProteinsAif1 protein, mouseAmyloid beta-Protein PrecursorCalcium-Binding ProteinsGlial Fibrillary Acidic ProteinGlutathione S-Transferase piGstp1 protein, ratMicrofilament ProteinsMuscle ProteinsPhosphopyruvate HydrataseRNA, MessengerTransforming Growth Factor betatransgelinAlzheimer's diseaseastrocyteshuman APP Swedishmicrogliaoligodendrocytesprimary neuronal and glial culturesTg2576 mice

Identifiers

PMID30485540
PMCPMC6588085
OpenAlexW2903093553

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.