ArticleFrontiers in aging neuroscience2016
Green-Fluorescent Protein(+) Astrocytes Attach to Beta-Amyloid Plaques in an Alzheimer Mouse Model and Are Sensitive for Clasmatodendrosis.
Article in Frontiers in aging neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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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.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Tanycytic degeneration impairs tau clearance and contributes to Alzheimer's disease pathology.Cell press blue · 2026Article
- Three-dimensional organotypic mouse brain slices to study Alzheimer's disease pathologies: a review.Frontiers in dementia · 2025Review
- Long-term live-cell imaging of GFAP+ astroglia and laminin+ vessels in organotypic mouse brain slices using microcontact printing.Frontiers in cellular neuroscience · 2025Article
- Astrocytes in human central nervous system diseases: a frontier for new therapies.Signal transduction and targeted therapy · 2023Review
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- Article
- The phenomenon of clasmatodendrosis.Heliyon · 2021Review
- Spreading of Beta-Amyloid in Organotypic Mouse Brain Slices and Microglial Elimination and Effects on Cholinergic Neurons.Biomolecules · 2021Article
- Intranasal Delivery of Collagen-Loaded Neprilysin Clears Beta-Amyloid Plaques in a Transgenic Alzheimer Mouse Model.Frontiers in aging neuroscience · 2021Article
- Production of transgenic pigs using aJournal of veterinary science · 2018Article
- Deciphering the Astrocyte Reaction in Alzheimer's Disease.Frontiers in aging neuroscience · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is pathologically characterized by beta-amyloid (Aβ) plaques and Tau pathology. It is well-established that Aβ plaques are surrounded by reactive astrocytes, highly expressing glial fibrillary acidic protein (GFAP). In order to study the cellular interaction of reactive astrocytes with Aβ plaques, we crossbred mice overexpressing amyloid precursor protein (APP) with the Swedish-Dutch-Iowa mutations (APP-SweDI) with mice expressing green fluorescent protein (GFP) under the GFAP-promotor. Three-dimensional confocal microscopy revealed a tight association and intense sprouting of astrocytic finely branched processes towards Aβ plaques in 12 month old mice. In order to study phagocytosis, 110 μm thick brain slices from 12 month old crossbred mice were cultured overnight, however, we found that the GFP fluorescence faded, distal processes degenerated and a complete loss of astrocytic morphology was seen (clasmatodendrosis). In summary, our data show that GFP(+) reactive astrocytes make intense contact with Aβ plaques but these cells are highly vulnerable for degeneration.
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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.