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Dynamic complexity of the microglial activation response in transgenic models of amyloid deposition: implications for Alzheimer therapeutics
Morgan D, Gordon MN, Tan J, Wilcock D, Rojiani AM.. Journal of neuropathology and experimental neurology, 2005-09-01
Topic: Brain proteins, microglia and lab models
The presence of activated microglia in postmortem Alzheimer disease specimens is used to support the argument that inflammation contributes to Alzheimer pathogenesis. Transgenic mice overexpressing the amyloid precursor protein (APP) gene form amyloid plaques that are accompanied by local activation of microglia/macrophages in a manner similar to the human disease. Many markers of microglial activation and inflammation increase in an age-dependent manner in these mice.
Key findings
- Transgenic mice overexpressing the amyloid precursor protein (APP) gene form amyloid plaques that are accompanied by local activation of microglia/macrophages in a manner similar to the human disease.
- Many markers of microglial activation and inflammation increase in an age-dependent manner in these mice.
- However, manipulation of these inflammatory reactions can lead to unexpected outcomes with several instances of reduced pathology when microglia/macrophages are activated further.
- In particular, anti-Abeta immunotherapy in amyloid-depositing transgenic mice causes a complex series of changes in microglial markers, negating the implicit belief that such activation is monotonic and represented equally well by any of several "activation" markers.
Why it matters
This review of transgenic mouse models notes that microglial activation and inflammation increase with age alongside amyloid plaques, but that boosting these inflammatory reactions sometimes reduced pathology rather than worsening it. It is based on animal models and reports no treatment, cure or prevention for people.
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Study details
- Evidence strengthLow
How this study scored 40/100
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 (Journal of neuropathology and experimental neurology) |
| Journal's citation record | 2 / 4 | Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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 | 2005 — older than 20 years, still counted |
| 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 “transgenic”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 179 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.8 citations a year over 23 year(s) since 2005 |
| Impact for its field and year | 4 / 6 | Cited 8.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 8 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 | 2 / 4 | Last-listed author Amyn M. Rojiani: h-index 46 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of South Florida: institution h-index 806 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 16141783) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 40 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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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
Morgan, D., Gordon, M. N., Tan, J., Wilcock, D., & Rojiani, A. M. (2005). Dynamic complexity of the microglial activation response in transgenic models of amyloid deposition: implications for Alzheimer therapeutics. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/01.jnen.0000178444.33972.e0
Vancouver
Morgan D, Gordon MN, Tan J, Wilcock D, Rojiani AM. Dynamic complexity of the microglial activation response in transgenic models of amyloid deposition: implications for Alzheimer therapeutics. Journal of neuropathology and experimental neurology. 2005. doi:10.1097/01.jnen.0000178444.33972.e0. PMID: 16141783.
BibTeX
@article{morgan2005-16141783,
author = {Morgan, D. and Gordon, M. N. and Tan, J. and Wilcock, D. and Rojiani, A. M.},
title = {{Dynamic complexity of the microglial activation response in transgenic models of amyloid deposition: implications for Alzheimer therapeutics}},
journal = {Journal of neuropathology and experimental neurology},
year = {2005},
doi = {10.1097/01.jnen.0000178444.33972.e0},
pmid = {16141783},
url = {https://doi.org/10.1097/01.jnen.0000178444.33972.e0}
}
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