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Early changes in CSF sTREM2 in dominantly inherited Alzheimer's disease occur after amyloid deposition and neuronal injury
Suárez-Calvet M, Araque Caballero MÁ, Kleinberger G, Bateman RJ, Fagan AM, Morris JC, Levin J, Danek A et al.. Science translational medicine, 2016-12-01
Topic: Brain proteins, microglia and lab models
Emerging evidence supports a role for innate immunity and microglia in Alzheimer's disease (AD) pathophysiology. However, no marker related to microglia has been included in the temporal evolution models of AD. TREM2 is a transmembrane protein involved in innate immunity and is selectively expressed by microglia and genetically linked to AD and other neurodegenerative disorders.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Suárez-Calvet, M., MÁ, A. C., Kleinberger, G., Bateman, R. J., Fagan, A. M., Morris, J. C., et al. (2016). Early changes in CSF sTREM2 in dominantly inherited Alzheimer's disease occur after amyloid deposition and neuronal injury. Science translational medicine. https://doi.org/10.1126/scitranslmed.aag1767
Vancouver
Suárez-Calvet M, MÁ AC, Kleinberger G, Bateman RJ, Fagan AM, Morris JC, et al. Early changes in CSF sTREM2 in dominantly inherited Alzheimer's disease occur after amyloid deposition and neuronal injury. Science translational medicine. 2016. doi:10.1126/scitranslmed.aag1767. PMID: 27974666.
BibTeX
@article{suarezcalvet2016-27974666,
author = {Suárez-Calvet, M. and MÁ, Araque Caballero and Kleinberger, G. and Bateman, R. J. and Fagan, A. M. and Morris, J. C. and Levin, J. and Danek, A. and others},
title = {{Early changes in CSF sTREM2 in dominantly inherited Alzheimer's disease occur after amyloid deposition and neuronal injury}},
journal = {Science translational medicine},
year = {2016},
doi = {10.1126/scitranslmed.aag1767},
pmid = {27974666},
url = {https://doi.org/10.1126/scitranslmed.aag1767}
}
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
- However, no marker related to microglia has been included in the temporal evolution models of AD.
- TREM2 is a transmembrane protein involved in innate immunity and is selectively expressed by microglia and genetically linked to AD and other neurodegenerative disorders.
- Its ectodomain is released by proteolysis as a soluble variant (sTREM2) and can be detected in the cerebrospinal fluid (CSF).
- In patients with autosomal dominant AD, we tested how many years before the expected symptom onset did CSF sTREM2 increase in mutation carriers (MCs) compared to noncarriers (NCs).
Why it matters
In people with dominantly inherited Alzheimer's disease, changes in a microglia-related marker called sTREM2 in cerebrospinal fluid occurred after amyloid deposition and neuronal injury. This marker may help track the timing of the disease process, but the study did not test any treatment or cure.
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Study details
- Participants218
- Evidence strengthLow
How this study scored 55/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 53 of the 96 points we could judge it on, which is 55 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Science translational medicine) |
| Journal's citation record | 3 / 4 | Science Translational Medicine: journal h-index 365 (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 | 2 / 4 | 218 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 273 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 22.8 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 4 / 6 | Cited 12.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 72 other studies in this library |
| Still being cited | 3 / 4 | Cited 71 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | 2 / 3 | Washington University in St. Louis: institution h-index 1,962 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27974666) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 53 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 53 of the 96 points we could judge it on is 55 out of 100. |
| Total | 55 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1126/scitranslmed.aag1767
- PubMed: 27974666
- 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).
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