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Green-Fluorescent Protein(+) Astrocytes Attach to Beta-Amyloid Plaques in an Alzheimer Mouse Model and Are Sensitive for Clasmatodendrosis
Daschil N, Humpel C.. Frontiers in aging neuroscience, 2016-04-08
Topic: Brain proteins, microglia and lab models
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.
Key findings
- 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).
Why it matters
In an Alzheimer mouse model, astrocytes were found to make close contact with amyloid plaques but were highly vulnerable to degeneration in cultured brain slices. This is animal and laboratory work and does not test any treatment, cure, or prevention in humans.
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Study details
- Evidence strengthLow
How this study scored 37/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in aging neuroscience) |
| Journal's citation record | 2 / 4 | Frontiers in Aging Neuroscience: journal h-index 174 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2016 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 17 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.4 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 1 / 6 | Cited 0.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 1 / 4 | Cited 4 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Christian Humpel: h-index 51 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Universität Innsbruck: institution h-index 803 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27092076) |
| Free to read | 2 / 2 | Free to read |
| Total | 37 / 100 | — |
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Read the original
- DOI: 10.3389/fnagi.2016.00075
- PubMed: 27092076
- Original source →
- Free full text: Frontiers in Aging Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Daschil, N., & Humpel, C. (2016). Green-Fluorescent Protein(+) Astrocytes Attach to Beta-Amyloid Plaques in an Alzheimer Mouse Model and Are Sensitive for Clasmatodendrosis. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2016.00075
Vancouver
Daschil N, Humpel C. Green-Fluorescent Protein(+) Astrocytes Attach to Beta-Amyloid Plaques in an Alzheimer Mouse Model and Are Sensitive for Clasmatodendrosis. Frontiers in aging neuroscience. 2016. doi:10.3389/fnagi.2016.00075. PMID: 27092076.
BibTeX
@article{daschil2016-27092076,
author = {Daschil, N. and Humpel, C.},
title = {{Green-Fluorescent Protein(+) Astrocytes Attach to Beta-Amyloid Plaques in an Alzheimer Mouse Model and Are Sensitive for Clasmatodendrosis}},
journal = {Frontiers in aging neuroscience},
year = {2016},
doi = {10.3389/fnagi.2016.00075},
pmid = {27092076},
url = {https://doi.org/10.3389/fnagi.2016.00075}
}
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