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Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease
Alexandrov PN, Pogue A, Bhattacharjee S, Lukiw WJ.. Neuroreport, 2011-08-01
Topic: Brain proteins, microglia and lab models
Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution of β-amyloid precursor protein (βAPP), Aβ42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology. In this report, we have studied the levels of βAPP, Aβ40 and Aβ42 peptide, as well as the innate immune and inflammatory response-regulator complement factor H in the brain and retina in four different Tg-AD models including Tg2576, PSAPP, 3xTg-AD, and 5xFAD. Aged, symptomatic 5xFAD mice showed the highest retinal abundance of Aβ42 peptides and the highest deficits in complement factor H.
Key findings
- In this report, we have studied the levels of βAPP, Aβ40 and Aβ42 peptide, as well as the innate immune and inflammatory response-regulator complement factor H in the brain and retina in four different Tg-AD models including Tg2576, PSAPP, 3xTg-AD, and 5xFAD.
- Aged, symptomatic 5xFAD mice showed the highest retinal abundance of Aβ42 peptides and the highest deficits in complement factor H.
- This may be a useful model to study the mechanisms of amyloid-mediated inflammatory degeneration.
- The superior colliculus and retina obtained from late-stage Alzheimer's disease revealed upregulated amyloidogenic and inflammatory signaling along the anteroposterior axis of the retinal-primary visual cortex pathway.
Why it matters
In several transgenic mouse models of Alzheimer's disease, aged symptomatic 5xFAD mice showed the highest retinal amyloid-beta 42 and the lowest complement factor H. This is animal work and does not establish a treatment, cure or prevention for people.
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Study details
- Evidence strengthLow
How this study scored 41/100
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 (Neuroreport) |
| Journal's citation record | 2 / 4 | Neuroreport: journal h-index 242 (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 | 2011 — 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 “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 128 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.5 citations a year over 17 year(s) since 2011 |
| Impact for its field and year | 3 / 6 | Cited 3.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 7 other studies in this library |
| Still being cited | 1 / 4 | Cited 11 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Walter J. Lukiw: h-index 75 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Louisiana State University: institution h-index 856 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 21734608) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 41 / 100 | — |
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Read the original
- DOI: 10.1097/wnr.0b013e3283497334
- PubMed: 21734608
- Original source →
- Free full text: PubMed Central →
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
Alexandrov, P. N., Pogue, A., Bhattacharjee, S., & Lukiw, W. J. (2011). Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease. Neuroreport. https://doi.org/10.1097/wnr.0b013e3283497334
Vancouver
Alexandrov PN, Pogue A, Bhattacharjee S, Lukiw WJ. Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease. Neuroreport. 2011. doi:10.1097/wnr.0b013e3283497334. PMID: 21734608.
BibTeX
@article{alexandrov2011-21734608,
author = {Alexandrov, P. N. and Pogue, A. and Bhattacharjee, S. and Lukiw, W. J.},
title = {{Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease}},
journal = {Neuroreport},
year = {2011},
doi = {10.1097/wnr.0b013e3283497334},
pmid = {21734608},
url = {https://doi.org/10.1097/wnr.0b013e3283497334}
}
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