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Microglial immunoreceptor tyrosine-based activation and inhibition motif signaling in neuroinflammation
Linnartz B, Wang Y, Neumann H.. International journal of Alzheimer's disease, 2010-06-22
Topic: Brain proteins, microglia and lab models
Elimination of extracellular aggregates and apoptotic neural membranes without inflammation is crucial for brain tissue homeostasis. In the mammalian central nervous system, essential molecules in this process are the Fc receptors and the DAP12-associated receptors which both trigger the microglial immunoreceptor tyrosine-based activation motif- (ITAM-) Syk-signaling cascade. Microglial triggering receptor expressed on myeloid cells-2 (TREM2), signal regulatory protein-beta1, and complement receptor-3 (CD11b/CD18) signal via the adaptor protein DAP12 and activate phagocytic activity of microglia.
Key findings
- In the mammalian central nervous system, essential molecules in this process are the Fc receptors and the DAP12-associated receptors which both trigger the microglial immunoreceptor tyrosine-based activation motif- (ITAM-) Syk-signaling cascade.
- Microglial triggering receptor expressed on myeloid cells-2 (TREM2), signal regulatory protein-beta1, and complement receptor-3 (CD11b/CD18) signal via the adaptor protein DAP12 and activate phagocytic activity of microglia.
- Microglial ITAM-signaling receptors are counter-regulated by immunoreceptor tyrosine-based inhibition motif- (ITIM-) signaling molecules such as sialic acid-binding immunoglobulin superfamily lectins (Siglecs).
- Siglecs can suppress the proinflammatory and phagocytic activity of microglia via ITIM signaling.
Why it matters
This review describes microglial immunoreceptor ITAM and inhibition motif signaling in neuroinflammation, including TREM2 signaling via DAP12 to activate phagocytosis. It is a review of mechanisms and reports no treatment, cure or prevention for Alzheimer's disease.
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Study details
- Evidence strengthLow
How this study scored 41/100
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 (International journal of Alzheimer's disease) |
| Journal's citation record | 0 / 4 | International Journal of Alzheimer s Disease: journal h-index 73 (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 | 2010 — 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 | 4 / 7 | Cited 87 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.8 citations a year over 18 year(s) since 2010 |
| Impact for its field and year | 3 / 6 | Cited 3.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 10 other studies in this library |
| Still being cited | 1 / 4 | Cited 7 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 | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 20721346) |
| Free to read | 2 / 2 | Free to read |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.4061/2010/587463
- PubMed: 20721346
- Original source →
- Free full text: International Journal of Alzheimer s Disease →
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
Linnartz, B., Wang, Y., & Neumann, H. (2010). Microglial immunoreceptor tyrosine-based activation and inhibition motif signaling in neuroinflammation. International journal of Alzheimer's disease. https://doi.org/10.4061/2010/587463
Vancouver
Linnartz B, Wang Y, Neumann H. Microglial immunoreceptor tyrosine-based activation and inhibition motif signaling in neuroinflammation. International journal of Alzheimer's disease. 2010. doi:10.4061/2010/587463. PMID: 20721346.
BibTeX
@article{linnartz2010-20721346,
author = {Linnartz, B. and Wang, Y. and Neumann, H.},
title = {{Microglial immunoreceptor tyrosine-based activation and inhibition motif signaling in neuroinflammation}},
journal = {International journal of Alzheimer's disease},
year = {2010},
doi = {10.4061/2010/587463},
pmid = {20721346},
url = {https://doi.org/10.4061/2010/587463}
}
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