Evidence map›Paper›PMID 30241479›Full record

ArticleJournal of neuroinflammation2018

Microglia prevent peripheral immune cell invasion and promote an anti-inflammatory environment in the brain of APP-PS1 transgenic mice.

M S Unger, P Schernthaner, J Marschallinger, H Mrowetz, L Aigner

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
–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

74 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  10. A common Iba1 antibody labels vasopressin neurons in mice.bioRxiv : the preprint server for biology · 2025
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  13. Review
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  16. Microglial Lyzl4 Facilitates β-Amyloid Clearance in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  17. Review
  18. Article
  19. Article
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14 more citing papers are in PubMed but not listed here.

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

5 authors.

M S UngerInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria.
P SchernthanerInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria.
J MarschallingerInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria.
H MrowetzInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria.
L AignerInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria. ludwig.aigner@pmu.ac.at.

Funding

European Union's Seventh Framework Program HEALTH-F2-2011-278850FWF F4413-B23FWF T736-B24PMU-FFF A-15/01/017-MAR
6 · The paper itself

Abstract

backgroundUndoubtedly, neuroinflammation is a major contributor to Alzheimer's disease (AD) progression. Neuroinflammation is characterized by the activity of brain resident glial cells, in particular microglia, but also by peripheral immune cells, which infiltrate the brain at certain stages of disease progression. The specific role of microglia in shaping AD pathology is still controversially discussed. Moreover, a possible role of microglia in the interaction and recruitment of peripheral immune cells has so far been completely ignored.

methodsWe ablated microglia cells in 12-month-old WT and APP-PS1 transgenic mice for 4 weeks using the CSF1R inhibitor PLX5622 and analyzed its consequences to AD pathology and in particular to peripheral immune cell infiltration.

resultsPLX5622 treatment successfully reduced microglia numbers. Interestingly, it uncovered a treatment-resistant macrophage population (Iba1

conclusionWe conclude that in neurodegenerative conditions, chronically activated microglia might limit CD3

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsAnti-Inflammatory AgentsCalcium-Binding ProteinsDisease Models, AnimalEncephalitisFemaleGene Expression RegulationLymphocytesMaleMaze LearningMiceMice, Inbred C57BLMice, TransgenicMicrofilament ProteinsAif1 protein, mouseAmyloid beta-Protein PrecursorAnti-Inflammatory AgentsCalcium-Binding ProteinsCsf1r protein, mouseMicrofilament ProteinsNerve Tissue ProteinsPresenilin-1Receptors, Granulocyte-Macrophage Colony-Stimulating FactorZap70 protein, mouseZAP-70 Protein-Tyrosine KinaseAlzheimer’s diseaseMacrophagesMicrogliaT-cellsTMEM119

Identifiers

PMID30241479
PMCPMC6151006

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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.