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Increased cerebrospinal fluid soluble TREM2 concentration in Alzheimer's disease
Heslegrave A, Heywood W, Paterson R, Magdalinou N, Svensson J, Johansson P, Öhrfelt A, Blennow K et al.. Molecular neurodegeneration, 2016-01-12
Topic: Brain proteins, microglia and lab models
Background The discovery that heterozygous missense mutations in the gene encoding triggering receptor expressed on myeloid cells 2 (TREM2) are risk factors for Alzheimer's disease (AD), with only the apolipoprotein E (APOE) ε4 gene allele conferring a higher risk, has led to increased interest in immune biology in the brain. TREM2 is expressed on microglia, the resident immune cells of the brain and has been linked to phagocytotic clearance of amyloid β (Aβ) plaques. Soluble TREM2 (sTREM2) has previously been measured in cerebrospinal fluid (CSF) by ELISA but in our hands commercial kits have proved unreliable, suggesting that other methods may be required.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Heslegrave, A., Heywood, W., Paterson, R., Magdalinou, N., Svensson, J., Johansson, P., et al. (2016). Increased cerebrospinal fluid soluble TREM2 concentration in Alzheimer's disease. Molecular neurodegeneration. https://doi.org/10.1186/s13024-016-0071-x
Vancouver
Heslegrave A, Heywood W, Paterson R, Magdalinou N, Svensson J, Johansson P, et al. Increased cerebrospinal fluid soluble TREM2 concentration in Alzheimer's disease. Molecular neurodegeneration. 2016. doi:10.1186/s13024-016-0071-x. PMID: 26754172.
BibTeX
@article{heslegrave2016-26754172,
author = {Heslegrave, A. and Heywood, W. and Paterson, R. and Magdalinou, N. and Svensson, J. and Johansson, P. and Öhrfelt, A. and Blennow, K. and others},
title = {{Increased cerebrospinal fluid soluble TREM2 concentration in Alzheimer's disease}},
journal = {Molecular neurodegeneration},
year = {2016},
doi = {10.1186/s13024-016-0071-x},
pmid = {26754172},
url = {https://doi.org/10.1186/s13024-016-0071-x}
}
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
- TREM2 is expressed on microglia, the resident immune cells of the brain and has been linked to phagocytotic clearance of amyloid β (Aβ) plaques.
- Soluble TREM2 (sTREM2) has previously been measured in cerebrospinal fluid (CSF) by ELISA but in our hands commercial kits have proved unreliable, suggesting that other methods may be required.
- We developed a mass spectrometry method using selected reaction monitoring for the presence of a TREM2 peptide, which can be used to quantify levels of sTREM2 in CSF.
- Findings We examined CSF samples from memory clinics in Sweden and the UK.
Why it matters
The authors found that commercial ELISA kits for soluble TREM2 (sTREM2), a protein shed from the brain's immune cells (microglia), were "unreliable" in their hands. So they developed a mass spectrometry method to measure it in spinal fluid, and used it on samples "from memory clinics in Sweden and the UK". The title reports that sTREM2 is increased in Alzheimer's disease, but our record holds no group sizes, effect size or statistics, so how large or consistent the increase is cannot be checked here. It is a measurement study and does not test any treatment, cure or prevention.
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Study details
- Participants37
- Evidence strengthModerate
How this study scored 60/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular neurodegeneration) |
| Journal's citation record | 2 / 4 | Molecular Neurodegeneration: journal h-index 164 (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 | 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 | 1 / 5 | 2016 — within 20 year(s) of the newest study here |
| Sample size | 1 / 4 | 37 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 | 6 / 7 | Cited 305 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 25.4 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 4 / 6 | Cited 14.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 67 other studies in this library |
| Still being cited | 3 / 4 | Cited 81 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Henrik Zetterberg: h-index 196 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University College London: institution h-index 2,029 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 26754172) |
| Free to read | 2 / 2 | Free to read |
| Total | 60 / 100 | — |
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Read the original
- DOI: 10.1186/s13024-016-0071-x
- PubMed: 26754172
- Original source →
- Free full text: Molecular Neurodegeneration →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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