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Essential role of the microglial triggering receptor expressed on myeloid cells-2 (TREM2) for central nervous tissue immune homeostasis
Neumann H, Takahashi K.. Journal of neuroimmunology, 2007-01-18
Topic: Brain proteins, microglia and lab models
While there is a strong evidence for neural tissue destruction mediated by adaptive autoimmune responses, it is still debated how innate immune responses contribute to neuroinflammatory and neurodegenerative diseases such as multiple sclerosis and Alzheimer's disease. Recently, it was shown that loss-of-function mutations of the innate microglial immune receptor triggering receptor expressed on myeloid cells-2 (TREM2) led to a chronic neurodegenerative disease, named Nasu-Hakola disease or polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL). PLOSL is a recessively inherited disease characterized by early onset adult dementia associated with bone cysts.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Neumann, H., & Takahashi, K. (2007). Essential role of the microglial triggering receptor expressed on myeloid cells-2 (TREM2) for central nervous tissue immune homeostasis. Journal of neuroimmunology. https://doi.org/10.1016/j.jneuroim.2006.11.032
Vancouver
Neumann H, Takahashi K. Essential role of the microglial triggering receptor expressed on myeloid cells-2 (TREM2) for central nervous tissue immune homeostasis. Journal of neuroimmunology. 2007. doi:10.1016/j.jneuroim.2006.11.032. PMID: 17239445.
BibTeX
@article{neumann2007-17239445,
author = {Neumann, H. and Takahashi, K.},
title = {{Essential role of the microglial triggering receptor expressed on myeloid cells-2 (TREM2) for central nervous tissue immune homeostasis}},
journal = {Journal of neuroimmunology},
year = {2007},
doi = {10.1016/j.jneuroim.2006.11.032},
pmid = {17239445},
url = {https://doi.org/10.1016/j.jneuroim.2006.11.032}
}
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Key findings
- Recently, it was shown that loss-of-function mutations of the innate microglial immune receptor triggering receptor expressed on myeloid cells-2 (TREM2) led to a chronic neurodegenerative disease, named Nasu-Hakola disease or polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL).
- PLOSL is a recessively inherited disease characterized by early onset adult dementia associated with bone cysts.
- Since microglial cells are the major TREM2-producing cell type in the central nervous system (CNS), they appear to be plausible candidates for the neurodegenerative pathogenesis of PLOSL.
- Indeed, TREM2 of microglia fulfils important function of tissue debris clearance and resolution of latent inflammatory reactions.
Why it matters
This 2007 review brings together earlier work showing that loss-of-function mutations in TREM2, an immune receptor made mainly by microglia in the brain, cause Nasu-Hakola disease (PLOSL), a rare recessively inherited condition with early-onset adult dementia and bone cysts. The authors argue that microglia are "plausible candidates" for causing the brain damage in PLOSL, because microglial TREM2 helps clear tissue debris and resolve inflammation. It reports no new data and no treatment, and it does not test a link to Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 44/100
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. We have no data on senior author's track record, so that was left out: it earned 42 of the 96 points we could judge it on, which is 44 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuroimmunology) |
| Journal's citation record | 2 / 4 | Journal of Neuroimmunology: journal h-index 192 (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 | 2007 — 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 | 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 249 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.9 citations a year over 21 year(s) since 2007 |
| Impact for its field and year | 3 / 6 | Cited 4.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 48 other studies in this library |
| Still being cited | 2 / 4 | Cited 18 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 | 1 / 3 | University of Bonn: institution h-index 1,072 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 17239445) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 42 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 42 of the 96 points we could judge it on is 44 out of 100. |
| Total | 44 / 100 | — |
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