Evidence map›Paper›PMID 32630447›Full record

ArticleInternational journal of molecular sciences2020

IPSC-Derived Neuronal Cultures Carrying the Alzheimer's Disease Associated

Soraia Martins, Andreas Müller-Schiffmann, Lars Erichsen, Martina Bohndorf, Wasco Wruck, Kristel Sleegers, Christine Van Broeckhoven, Carsten Korth, James Adjaye

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Roles of TREM2 in Alzheimer's disease.Translational neurodegeneration · 2025
    Review
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  5. Article
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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 2 institutions in 2 countries.

Soraia MartinsInstitute for Stem Cell Research and Regenerative Medicine, Medical Faculty, Heinrich-Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0002-7894-6539
Andreas Müller-SchiffmannDepartment of Neuropathology, Heinrich-Heine University, 40225 Düsseldorf, Germany.
Lars ErichsenInstitute for Stem Cell Research and Regenerative Medicine, Medical Faculty, Heinrich-Heine University, 40225 Düsseldorf, Germany.
Martina BohndorfInstitute for Stem Cell Research and Regenerative Medicine, Medical Faculty, Heinrich-Heine University, 40225 Düsseldorf, Germany.
Wasco WruckInstitute for Stem Cell Research and Regenerative Medicine, Medical Faculty, Heinrich-Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0002-9153-7051
Kristel SleegersNeurodegenerative Brain Diseases Group, VIB-Center for Molecular Neurology, University of Antwerp, 20610 Antwerp, Belgium.
Christine Van BroeckhovenNeurodegenerative Brain Diseases Group, VIB-Center for Molecular Neurology, University of Antwerp, 20610 Antwerp, Belgium.ORCID 0000-0003-0183-7665
Carsten KorthDepartment of Neuropathology, Heinrich-Heine University, 40225 Düsseldorf, Germany.
James AdjayeInstitute for Stem Cell Research and Regenerative Medicine, Medical Faculty, Heinrich-Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0002-6075-6761
Heinrich Heine University Düsseldorf · DEUniversity of Antwerp · BE

Funding

Seventh Framework Programme 305299
6 · The paper itself

Abstract

Genes associated with immune response and inflammation have been identified as genetic risk factors for late-onset Alzheimer´s disease (LOAD). The rare R47H variant within triggering receptor expressed on myeloid cells 2 (TREM2) has been shown to increase the risk for developing Alzheimer's disease (AD) 2-3-fold. Here, we report the generation and characterization of a model of late-onset Alzheimer's disease (LOAD) using lymphoblast-derived induced pluripotent stem cells (iPSCs) from patients carrying the TREM2 R47H mutation, as well as from control individuals without dementia. All iPSCs efficiently differentiated into mature neuronal cultures, however AD neuronal cultures showed a distinct gene expression profile. Furthermore, manipulation of the iPSC-derived neuronal cultures with an Aβ-S8C dimer highlighted metabolic pathways, phagosome and immune response as the most perturbed pathways in AD neuronal cultures. Through the construction of an Aβ-induced gene regulatory network, we were able to identify an Aβ signature linked to protein processing in the endoplasmic reticulum (ER), which emphasized ER-stress, as a potential causal role in LOAD. Overall, this study has shown that our AD-iPSC based model can be used for in-depth studies to better understand the molecular mechanisms underlying the etiology of LOAD and provides new opportunities for screening of potential therapeutic targets.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesBrainCell DifferentiationEndoplasmic ReticulumFemaleGene Regulatory NetworksGenetic Predisposition to DiseaseGenetic VariationHumansMaleMembrane GlycoproteinsModels, BiologicalMutationMyeloid CellsAmyloid beta-PeptidesMembrane GlycoproteinsReceptors, ImmunologicTREM2 protein, humanAβS8C dimeriPSC-derived neuronal cultureslate onset Alzheimer’s diseaseTREM2 R47H

Identifiers

PMID32630447
PMCPMC7350255
OpenAlexW3038108579

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.