Evidence map›Paper›PMID 28197095›Full record

ArticleFrontiers in aging neuroscience2017

Increase of TREM2 during Aging of an Alzheimer's Disease Mouse Model Is Paralleled by Microglial Activation and Amyloidosis.

Matthias Brendel, Gernot Kleinberger, Federico Probst, Anna Jaworska, Felix Overhoff, Tanja Blume, Nathalie L Albert, Janette Carlsen, Simon Lindner, Franz Josef Gildehaus and 8 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 67 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

18 authors at 5 institutions in 3 countries.

Matthias BrendelDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität München Munich, Germany.
Gernot KleinbergerDepartment of Biochemistry, Biomedical Center (BMC), Ludwig-Maximilians-Universität MünchenMunich, Germany; Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilians-Universität MünchenMunich, Germany.
Federico ProbstDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität München Munich, Germany.
Anna JaworskaDZNE-German Center for Neurodegenerative DiseasesMunich, Germany; Laboratory of Neurodegeneration, International Institute of Molecular and Cell BiologyWarsaw, Poland.
Felix OverhoffDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität München Munich, Germany.
Tanja BlumeDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität München Munich, Germany.
Nathalie L AlbertDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität München Munich, Germany.
Janette CarlsenDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität München Munich, Germany.
Simon LindnerDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität München Munich, Germany.
Franz Josef GildehausDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität München Munich, Germany.
Laurence OzmenRoche Pharma Research and Early Development, Neuroscience Discovery, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd. Basel, Switzerland.
Marc Suárez-CalvetDepartment of Biochemistry, Biomedical Center (BMC), Ludwig-Maximilians-Universität MünchenMunich, Germany; DZNE-German Center for Neurodegenerative DiseasesMunich, Germany.
Peter BartensteinDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität MünchenMunich, Germany; Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilians-Universität MünchenMunich, Germany.
Karlheinz BaumannRoche Pharma Research and Early Development, Neuroscience Discovery, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd. Basel, Switzerland.
Michael EwersDZNE-German Center for Neurodegenerative Diseases Munich, Germany.
Jochen HermsMunich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilians-Universität MünchenMunich, Germany; DZNE-German Center for Neurodegenerative DiseasesMunich, Germany.
Christian HaassDepartment of Biochemistry, Biomedical Center (BMC), Ludwig-Maximilians-Universität MünchenMunich, Germany; Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilians-Universität MünchenMunich, Germany; DZNE-German Center for Neurodegenerative DiseasesMunich, Germany.
Axel RomingerDepartment of Nuclear Medicine, Ludwig-Maximilians-Universität MünchenMunich, Germany; Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilians-Universität MünchenMunich, Germany.
Ludwig-Maximilians-Universität München · DEGerman Center for Neurodegenerative Diseases · DEMunich Cluster for Systems Neurology · DERoche (Switzerland) · CHInternational Institute of Molecular and Cell Biology · PL

Funding

European Research Council 321366
6 · The paper itself

Abstract

Heterozygous missense mutations in the triggering receptor expressed on myeloid cells 2 (TREM2) have been reported to significantly increase the risk of developing Alzheimer's disease (AD). Since TREM2 is specifically expressed by microglia in the brain, we hypothesized that soluble TREM2 (sTREM2) levels may increase together with

Indexed as

Alzheimer’s diseaseamyloid-PETneuroinflammationTREM2TSPO-PET

Identifiers

PMID28197095
PMCPMC5282474
OpenAlexW2584772033

What OpenQuestion holds

Textmetadata
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.