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Key Aging-Associated Alterations in Primary Microglia Response to Beta-Amyloid Stimulation
Caldeira C, Cunha C, Vaz AR, Falcão AS, Barateiro A, Seixas E, Fernandes A, Brites D.. Frontiers in aging neuroscience, 2017-08-31
Topic: Brain proteins, microglia and lab models
Alzheimer's disease (AD) is characterized by a progressive cognitive decline and believed to be driven by the self-aggregation of amyloid-β (Aβ) peptide into oligomers and fibrils that accumulate as senile plaques. It is widely accepted that microglia-mediated inflammation is a significant contributor to disease pathogenesis; however, different microglia phenotypes were identified along AD progression and excessive Aβ production was shown to dysregulate cell function. As so, the contribution of microglia to AD pathogenesis remains to be elucidated.
Key findings
- It is widely accepted that microglia-mediated inflammation is a significant contributor to disease pathogenesis; however, different microglia phenotypes were identified along AD progression and excessive Aβ production was shown to dysregulate cell function.
- As so, the contribution of microglia to AD pathogenesis remains to be elucidated.
- In this study, we wondered if isolated microglia cultured for 16 days in vitro (DIV) would react differentially from the 2 DIV cells upon treatment with 1000 nM Aβ 1-42 for 24 h.
- No changes in cell viability were observed and morphometric alterations associated to microglia activation, such as volume increase and process shortening, were obvious in 2 DIV microglia, but less evident in 16 DIV cells.
Why it matters
This study compared how microglia cultured for different lengths of time respond to beta-amyloid stimulation. It is an in-vitro laboratory study, so it does not show any treatment, cure or prevention for Alzheimer's disease in people.
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Study details
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people 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 | 2 / 5 | 2017 — within 10 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 117 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 10.6 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 3 / 6 | Cited 3.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 5 other studies in this library |
| Still being cited | 2 / 4 | Cited 43 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Dora Maria Tuna Oliveira Brites: h-index 59 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | University of Lisbon: institution h-index 605 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28912710) |
| Free to read | 2 / 2 | Free to read |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fnagi.2017.00277
- PubMed: 28912710
- 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. The record names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
APA 7th
Caldeira, C., Cunha, C., Vaz, A. R., Falcão, A. S., Barateiro, A., Seixas, E., et al. (2017). Key Aging-Associated Alterations in Primary Microglia Response to Beta-Amyloid Stimulation. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2017.00277
Vancouver
Caldeira C, Cunha C, Vaz AR, Falcão AS, Barateiro A, Seixas E, et al. Key Aging-Associated Alterations in Primary Microglia Response to Beta-Amyloid Stimulation. Frontiers in aging neuroscience. 2017. doi:10.3389/fnagi.2017.00277. PMID: 28912710.
BibTeX
@article{caldeira2017-28912710,
author = {Caldeira, C. and Cunha, C. and Vaz, A. R. and Falcão, A. S. and Barateiro, A. and Seixas, E. and Fernandes, A. and Brites, D.},
title = {{Key Aging-Associated Alterations in Primary Microglia Response to Beta-Amyloid Stimulation}},
journal = {Frontiers in aging neuroscience},
year = {2017},
doi = {10.3389/fnagi.2017.00277},
pmid = {28912710},
url = {https://doi.org/10.3389/fnagi.2017.00277}
}
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