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TREM2-transduced myeloid precursors mediate nervous tissue debris clearance and facilitate recovery in an animal model of multiple sclerosis
Takahashi K, Prinz M, Stagi M, Chechneva O, Neumann H.. PLoS medicine, 2007-04-01
Topic: Brain proteins, microglia and lab models
Background In multiple sclerosis, inflammation can successfully be prevented, while promoting repair is still a major challenge. Microglial cells, the resident phagocytes of the central nervous system (CNS), are hematopoietic-derived myeloid cells and express the triggering receptor expressed on myeloid cells 2 (TREM2), an innate immune receptor. Myeloid cells are an accessible source for ex vivo gene therapy.
Key findings
- Microglial cells, the resident phagocytes of the central nervous system (CNS), are hematopoietic-derived myeloid cells and express the triggering receptor expressed on myeloid cells 2 (TREM2), an innate immune receptor.
- Myeloid cells are an accessible source for ex vivo gene therapy.
- We investigated whether myeloid precursor cells genetically modified to express TREM2 affect the disease course of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis.
- Methods and findings EAE was induced in mice by immunization with a myelin autoantigen.
Why it matters
This 2007 mouse study tested whether immune precursor cells genetically modified to carry TREM2, a receptor found on the brain's clean-up cells (microglia), change the course of an animal model of multiple sclerosis. Its title reports that the modified cells "mediate nervous tissue debris clearance and facilitate recovery" in that model; the abstract stored here stops before the results, so no numbers are available. It is an animal study of multiple sclerosis, not Alzheimer's disease, and says nothing about treating people.
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Study details
- Evidence strengthLow
How this study scored 52/100
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 (PLoS medicine) |
| Journal's citation record | 3 / 4 | PLoS Medicine: journal h-index 350 (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 | 6 / 7 | Cited 415 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 19.8 citations a year over 21 year(s) since 2007 |
| Impact for its field and year | 4 / 6 | Cited 11.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 71 other studies in this library |
| Still being cited | 3 / 4 | Cited 50 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Harald Neumann: h-index 73 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Bonn: institution h-index 1,072 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 17425404) |
| Free to read | 2 / 2 | Free to read |
| Total | 52 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1371/journal.pmed.0040124
- PubMed: 17425404
- Original source →
- Free full text: PLoS Medicine →
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. Check the citation against the original before you use it.
APA 7th
Takahashi, K., Prinz, M., Stagi, M., Chechneva, O., & Neumann, H. (2007). TREM2-transduced myeloid precursors mediate nervous tissue debris clearance and facilitate recovery in an animal model of multiple sclerosis. PLoS medicine. https://doi.org/10.1371/journal.pmed.0040124
Vancouver
Takahashi K, Prinz M, Stagi M, Chechneva O, Neumann H. TREM2-transduced myeloid precursors mediate nervous tissue debris clearance and facilitate recovery in an animal model of multiple sclerosis. PLoS medicine. 2007. doi:10.1371/journal.pmed.0040124. PMID: 17425404.
BibTeX
@article{takahashi2007-17425404,
author = {Takahashi, K. and Prinz, M. and Stagi, M. and Chechneva, O. and Neumann, H.},
title = {{TREM2-transduced myeloid precursors mediate nervous tissue debris clearance and facilitate recovery in an animal model of multiple sclerosis}},
journal = {PLoS medicine},
year = {2007},
doi = {10.1371/journal.pmed.0040124},
pmid = {17425404},
url = {https://doi.org/10.1371/journal.pmed.0040124}
}
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