Evidence map›Paper›PMID 37198381›Full record

ArticleCellular and molecular neurobiology2023

Acute and Chronic Macrophage Differentiation Modulates TREM2 in a Personalized Alzheimer's Patient-Derived Assay.

Nicoleta-Carmen Cosma, Neriman Eren, Berk Üsekes, Susanna Gerike, Isabella Heuser, Oliver Peters, Julian Hellmann-Regen

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Roles of TREM2 in Alzheimer's disease.Translational neurodegeneration · 2025
    Review
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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

7 authors at 1 institution in 1 country.

Nicoleta-Carmen Cosma *Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Psychiatry and Psychotherapy, Section Clinical Neurobiology, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany. nicoleta-carmen.cosma@charite.de.ORCID http://orcid.org/0000-0002-2656-8046
Neriman Eren *Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Psychiatry and Psychotherapy, Section Clinical Neurobiology, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Berk ÜsekesCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Psychiatry and Psychotherapy, Section Clinical Neurobiology, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Susanna GerikeCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Psychiatry and Psychotherapy, Section Clinical Neurobiology, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Isabella HeuserCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Psychiatry and Psychotherapy, Section Clinical Neurobiology, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Oliver PetersCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Psychiatry and Psychotherapy, Section Clinical Neurobiology, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Julian Hellmann-RegenCharité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Psychiatry and Psychotherapy, Section Clinical Neurobiology, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Humboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation plays a pivotal role in the pathogenesis of Alzheimer`s disease (AD). Brain macrophage populations differentially modulate the immune response to AD pathology according to the disease stage. Triggering receptor expressed on myeloid cells 2 (TREM2) is known to play a protective role in AD and has been postulated as a putative therapeutic target. Whether, and to which extent TREM2 expression can be modulated in the aged macrophage population of the brain is unknown, emphasizing the need for a human, patient-specific model. Using cells from AD patients and matched controls (CO) we designed an assay based on monocyte-derived macrophages to mimic brain-infiltrating macrophages and to assess the individualized TREM2 synthesis in vitro. We systematically assessed the effects of short-term (acute-2 days) and long-term (chronic-10 days) M1- (LPS), M2- (IL-10, IL-4, TGF-β), and M0- (vehicle) macrophage differentiation on TREM2 synthesis. Moreover, the effects of retinoic acid (RA), a putative TREM2 modulator, on individualized TREM2 synthesis were assessed. We report increased TREM2 synthesis after acute M2- compared to M1-differentiation in CO- but not AD-derived cells. Chronic M2- and M0-differentiation however resulted in an increase of TREM2 synthesis in both AD- and CO-derived cells while chronic M1-differentiation increased TREM2 in AD-derived cells only. Moreover, chronic M2- and M0-differentiation improved the amyloid-β (Aβ) uptake of the CO-derived whereas M1-differentiation of the AD-derived cells. Interestingly, RA-treatment did not modulate TREM2. In the age of personalized medicine, our individualized model could be used to screen for potential drug-mediated treatment responses in vitro. Triggering receptor expressed on myeloid cells 2 (TREM2) has been postulated as a putative therapeutic target in Alzheimer's disease (AD). Using cells from AD patients and matched controls (CO), we designed a monocyte-derived macrophages (Mo-MФs) assay to assess the individualized TREM2 synthesis in vitro. We report increased TREM2 synthesis after acute M2- compared to M1- macrophage differentiation in CO- but not AD-derived cells. Chronic M2- and M0- differentiation however resulted in an increase of TREM2 synthesis in both AD- and CO-derived cells while chronic M1-differentiation increased TREM2 in AD-cells only.

Indexed as

Alzheimer DiseaseAgedAmyloid beta-PeptidesBrainCell DifferentiationHumansMacrophagesMembrane GlycoproteinsMicrogliaReceptors, ImmunologicAmyloid beta-PeptidesMembrane GlycoproteinsReceptors, ImmunologicTREM2 protein, humanLOADMonocyte-derived macrophagesPatient-derived personalized assayRetinoic acidTREM2

Identifiers

PMID37198381
PMCPMC10333375
OpenAlexW4376959542

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.