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Soluble TREM2 in CSF and its association with other biomarkers and cognition in autosomal-dominant Alzheimer's disease: a longitudinal observational study
Morenas-Rodríguez E, Li Y, Nuscher B, Franzmeier N, Xiong C, Suárez-Calvet M, Fagan AM, Schultz S et al.. The Lancet. Neurology, 2022-04-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Although studies in animal models suggest that TREM2 is protective against Alzheimer's pathology, its effect on tau pathology and its potential beneficial role in people with Alzheimer's disease is still unclear. Augmented annual rates of increase in soluble TREM2 were associated with a diminished rate of decrease in amyloid deposition, as measured by Aβ42 in CSF (r=0·56 [0·22], p=0·011), in presymptomatic carriers of pathogenic variants, and with diminished annual rate of increase in PiB-PET (r=-0·67 [0·25], p=0·0060) in symptomatic carriers of pathogenic variants. Interpretation Our findings in autosomal dominant Alzheimer's disease position the TREM2 response within the amyloid cascade immediately after the first pathological changes in Aβ aggregation and further support the role of TREM2 on Aβ plaque deposition and compaction. Furthermore, these findings underpin a beneficial effect of TREM2 on Aβ deposition, Aβ-dependent tau pathology, cortical shrinkage, and cognitive decline.
What this study adds
Evidence grade: Moderate
This is a follow-up (cohort) study of 155 participants. In people with autosomal-dominant Alzheimer disease, faster increases in soluble TREM2 in spinal fluid were linked to slower amyloid buildup, suggesting a possibly beneficial role for TREM2. This is an observational biomarker study and does not test any treatment, cure, or prevention.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Morenas-Rodríguez, E., Li, Y., Nuscher, B., Franzmeier, N., Xiong, C., Suárez-Calvet, M., et al. (2022). Soluble TREM2 in CSF and its association with other biomarkers and cognition in autosomal-dominant Alzheimer's disease: a longitudinal observational study. The Lancet. Neurology. https://doi.org/10.1016/s1474-4422(22)00027-8
Vancouver
Morenas-Rodríguez E, Li Y, Nuscher B, Franzmeier N, Xiong C, Suárez-Calvet M, et al. Soluble TREM2 in CSF and its association with other biomarkers and cognition in autosomal-dominant Alzheimer's disease: a longitudinal observational study. The Lancet. Neurology. 2022. doi:10.1016/s1474-4422(22)00027-8. PMID: 35305339.
BibTeX
@article{morenasrodriguez2022-35305339,
author = {Morenas-Rodríguez, E. and Li, Y. and Nuscher, B. and Franzmeier, N. and Xiong, C. and Suárez-Calvet, M. and Fagan, A. M. and Schultz, S. and others},
title = {{Soluble TREM2 in CSF and its association with other biomarkers and cognition in autosomal-dominant Alzheimer's disease: a longitudinal observational study}},
journal = {The Lancet. Neurology},
year = {2022},
doi = {10.1016/s1474-4422(22)00027-8},
pmid = {35305339},
url = {https://doi.org/10.1016/s1474-4422(22)00027-8}
}
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
- Although studies in animal models suggest that TREM2 is protective against Alzheimer's pathology, its effect on tau pathology and its potential beneficial role in people with Alzheimer's disease is still unclear.
- Augmented annual rates of increase in soluble TREM2 were associated with a diminished rate of decrease in amyloid deposition, as measured by Aβ42 in CSF (r=0·56 [0·22], p=0·011), in presymptomatic carriers of pathogenic variants, and with diminished annual rate of increase in PiB-PET (r=-0·67 [0·25], p=0·0060) in symptomatic carriers of pathogenic variants.
- Interpretation Our findings in autosomal dominant Alzheimer's disease position the TREM2 response within the amyloid cascade immediately after the first pathological changes in Aβ aggregation and further support the role of TREM2 on Aβ plaque deposition and compaction.
- Furthermore, these findings underpin a beneficial effect of TREM2 on Aβ deposition, Aβ-dependent tau pathology, cortical shrinkage, and cognitive decline.
Why it matters
In people with autosomal-dominant Alzheimer disease, faster increases in soluble TREM2 in spinal fluid were linked to slower amyloid buildup, suggesting a possibly beneficial role for TREM2. This is an observational biomarker study and does not test any treatment, cure, or prevention.
New to this subject? Start with our plain-English guide: Brain scans & tests →
Study details
- Study designlongitudinal study
- Participants155
- Evidence strengthModerate
How this study scored 71/100
Published in a leading specialty journal, and it is a longitudinal study following the same people over time. Scored zero for effect reported and randomized / 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 68 of the 96 points we could judge it on, which is 71 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (The Lancet. Neurology) |
| Journal's citation record | 3 / 4 | The Lancet Neurology: journal h-index 457 (OpenAlex, 2026-10-29) |
| Study design | 7 / 12 | A longitudinal study following the same people over time |
| Strength of evidence | 3 / 5 | Rated “moderate” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 3 / 5 | 2022 — within 6 year(s) of the newest study here |
| Sample size | 2 / 4 | 155 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) |
| Randomized / blinded | 0 / 2 | No randomization 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 | 4 / 5 | 29.8 citations a year over 6 year(s) since 2022 |
| Impact for its field and year | 4 / 6 | Cited 19.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 20 other studies in this library |
| Still being cited | 3 / 4 | Cited 111 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 | University College London: institution h-index 2,029 (OpenAlex) |
| Multicenter collaboration | 3 / 3 | OpenAlex lists 18 institution(s) in 5 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 35305339) |
| Free to read | 2 / 2 | Free to read |
| Points | 68 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 68 of the 96 points we could judge it on is 71 out of 100. |
| Total | 71 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/s1474-4422(22)00027-8
- PubMed: 35305339
- Original source →
- Free full text: The Lancet Neurology →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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