Evidence map›Paper›PMID 40210700›Full record

ArticleGene therapy2025

Expression of anti-amyloid CARs in microglia promotes efficient and selective phagocytosis of Aβ1‒42.

Christina N Heiss, Rebecca Riise, Eric Hanse, Stefanie Fruhwürth, Henrik Zetterberg, Andreas Björefeldt

Erratum issuedAbstract read
In one paragraph

Article in Gene therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Christina N Heiss *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Rebecca Riise *Sahlgrenska Center for Cancer Research, Institute of Clinical Sciences, University of Gothenburg, Gothenburg, Sweden.
Eric HanseDepartment of Physiology, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Stefanie FruhwürthDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Andreas BjörefeldtDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden. andreas.bjorefeldt@gu.se.ORCID 0000-0002-1230-3610

Funding

Alzheimerfonden AF-939887, AF-993056EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) 101053962Hjärnfonden (Swedish Brain Foundation) FO2021-0023University of Gothenburg | Sahlgrenska Akademin (Sahlgrenska Academy) GU2020/2376Vetenskapsrådet (Swedish Research Council) 2020-00878Vetenskapsrådet (Swedish Research Council) 2023-00356, 2022-01018, 2019-02397
6 · The paper itself

Abstract

Genetic engineering of microglial cells is a promising therapeutic avenue emerging with advancements in gene delivery techniques. Using a recently developed AAV capsid for efficient in vitro transduction we report the engineering of microglia with CARs (CAR-Mic) targeting phagocytosis of amyloid beta 1‒42 (Aβ42). Functional screening of seven CAR constructs in human iPSC-derived microglia revealed up to 6-fold increases in internalized Aβ relative to viral control. CAR-driven phagocytic enhancement was selective for Aβ, dependent on intracellular domain signaling, and was confirmed in primary mouse microglia. These findings highlight the potential of using this approach to target dysfunctional microglia in Alzheimer's disease and other CNS disorders.

Indexed as

Amyloid beta-PeptidesMicrogliaPeptide FragmentsPhagocytosisReceptors, Chimeric AntigenAlzheimer DiseaseAnimalsCells, CulturedDependovirusHumansInduced Pluripotent Stem CellsMiceAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide FragmentsReceptors, Chimeric Antigen

Identifiers

PMID40210700
PMCPMC12310543

What OpenQuestion holds

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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.