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Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease
Fonseca MI, Ager RR, Chu SH, Yazan O, Sanderson SD, LaFerla FM, Taylor SM, Woodruff TM et al.. Journal of immunology (Baltimore, Md. : 1950), 2009-06-26
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is an age-related dementia, characterized by amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss in the brain. Components of the complement system, known to produce a local inflammatory reaction, are associated with the plaques and tangles in AD brain, and thus a role for complement-mediated inflammation in the acceleration or progression of disease has been proposed. A complement activation product, C5a, is known to recruit and activate microglia and astrocytes in vitro by activation of a G protein-coupled cell-surface C5aR.
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APA 7th
Fonseca, M. I., Ager, R. R., Chu, S. H., Yazan, O., Sanderson, S. D., LaFerla, F. M., et al. (2009). Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease. Journal of immunology (Baltimore, Md. : 1950). https://doi.org/10.4049/jimmunol.0901005
Vancouver
Fonseca MI, Ager RR, Chu SH, Yazan O, Sanderson SD, LaFerla FM, et al. Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease. Journal of immunology (Baltimore, Md. : 1950). 2009. doi:10.4049/jimmunol.0901005. PMID: 19561098.
BibTeX
@article{fonseca2009-19561098,
author = {Fonseca, M. I. and Ager, R. R. and Chu, S. H. and Yazan, O. and Sanderson, S. D. and LaFerla, F. M. and Taylor, S. M. and Woodruff, T. M. and others},
title = {{Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease}},
journal = {Journal of immunology (Baltimore, Md. : 1950)},
year = {2009},
doi = {10.4049/jimmunol.0901005},
pmid = {19561098},
url = {https://doi.org/10.4049/jimmunol.0901005}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- Components of the complement system, known to produce a local inflammatory reaction, are associated with the plaques and tangles in AD brain, and thus a role for complement-mediated inflammation in the acceleration or progression of disease has been proposed.
- A complement activation product, C5a, is known to recruit and activate microglia and astrocytes in vitro by activation of a G protein-coupled cell-surface C5aR.
- Here, oral delivery of a cyclic hexapeptide C5a receptor antagonist (PMX205) for 2-3 mo resulted in substantial reduction of pathological markers such as fibrillar amyloid deposits (49-62%) and activated glia (42-68%) in two mouse models of AD.
- The reduction in pathology was correlated with improvements in a passive avoidance behavioral task in Tg2576 mice.
Why it matters
In mouse models of Alzheimer's disease, oral delivery of the C5a receptor antagonist PMX205 decreased pathology and improved behavioral performance. This is animal research and does not yet show that the treatment would work in people.
Study details
- Evidence strengthLow
How this study scored 47/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of immunology (Baltimore, Md. : 1950)) |
| Journal's citation record | 4 / 4 | The Journal of Immunology: journal h-index 531 (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 | 2009 — 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 “murine”) — scores zero |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 266 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 14.0 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 4 / 6 | Cited 10.7× 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 | 2 / 4 | Cited 42 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Andrea J. Tenner: h-index 77 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | The University of Queensland: institution h-index 1,516 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19561098) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 47 / 100 | — |
What each of these 20 components measures, and what this score is not →
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