ArticleGlia2025
Three-dimensional view of microglia-amyloid plaque interactions.
Article in Glia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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.
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.
Who cites it
8 citing papers in PubMed.
- DeepPlaque: a scalable multimodal platform for Aβ pathology and cell analysis in Alzheimer's disease.EMBO molecular medicine · 2026Article
- PLGA Nanoparticle-based Anti-TLR2 scFv Gene Delivery for the Treatment of Alzheimer's Disease.Experimental neurobiology · 2026Article
- Early abstinence in severe alcohol use disorder: MCP-1 decline, choroid plexus shrinkage, and region-specific grey-matter volume changes.Translational psychiatry · 2026Article
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Making tracks: microglia and the extracellular matrix.Molecular neurodegeneration · 2025Review
- Chemerin 15 enhances microglial phagocytosis to attenuate cerebral ischemia-reperfusion injury through the ChemR23/p38 MAPK pathway.iScience · 2025Article
- Neuroinflammation and hypoxia promote astrocyte phenotypic transformation and propel neurovascular dysfunction in brain arteriovenous malformation.Journal of neuroinflammation · 2025Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Recent gene expression studies have revealed about 10 different states of microglia, some of which are characteristic for Alzheimer-like amyloid plaque pathology. However, it is not presently known how these translate into morphological features that would reflect microglia interaction with amyloid plaques. With optimized conditions for confocal microscopy in amyloid plaque forming APP/PS1 transgenic mice we reveal new details of how microglia processes interact with amyloid plaques. The microglia contacts differed drastically between purely diffuse plaque and those with a fibrillar core. We identified microglia that extend their enlarged processes through the diffuse shell of the amyloid plaques and cover the fibrillar plaque core with snowplow-like expanded end-feet. These end-feet were filled with the lysosomal marker CD68, while both non-fibrillar and fibrillar amyloid was found in perinuclear vesicles of some "snowplower" microglia. In the organized dense-core plaques, we consistently saw a layer of Apolipoprotein E (ApoE) between the fibrillar core and the microglial end-feet. ApoE covered also loose fibrillar amyloid and diffuse amyloid plaques that were about 10 μm or larger in diameter. These findings are compatible with both amyloid plaque phagocytosis and compaction by microglia. Further, they support a chemotactic role of ApoE for microglia contacts with amyloid plaques.
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Identifiers
What OpenQuestion holds
Registered trials
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.