Contributions of triggering-receptor-expressed-on-myeloid-cells-2 to neurological diseases
Abstract
Recent laboratory and gene sequencing data suggest that variations in receptors called the "triggering-receptors-expressed-on-myeloid-cells" (TREMs) are implicated in Alzheimer's disease, Parkinson's disease, multiple sclerosis, and frontotemporal lobar degeneration. TREM receptors are thought to play a critical role in regulating the immune system, inflammation, and certain cellular functions. One TREM, in particular, TREM2, is highly expressed on cells of the myeloid lineage. The binding of TREM2 to the adapter protein, DNAX activating protein of 12 kD (DAP12), in microglial cells has been shown to modulate phagocytosis within the nervous system. This review highlights the role of TREM2 in neurological diseases. Moreover, here we consider potential contributions of TREM2 and mechanisms underlying TREM2 activity as contributing to neurodegeneration. These findings may provide novel insights and opportunities to consider, especially for clinicians, as they diagnose and treat certain neurological diseases.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The TREM2 pathway is induced in microglial cells by anti-inflammatory cytokines, is modulated by CD33, and is down-regulated by agonists of TLR2, 4, and 9, as well as by inflammatory stimuli such as lipopolysaccharides and RNA interference; overexpression of TREM2 promotes phagocytosis and reduces the pro-inflammatory response.
“This pathway, induced in the microglial cells by anti-inflammatory cytokines, is modulated by CD33 and is down-regulated by agonists of TLR2, 4, and 9, as well as by inflammatory stimuli such as lipopolysaccharides and RNA interference. An overexpression of TREM2 promotes phagocytosis and reduces the pro-inflammatory response (Han et al., 2017).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Han et al., 2017
Brain homeostasis without inflammation depends on eliminating extracellular aggregates and apoptotic debris, this being mediated by the TREM2/DAP12 receptor complex.
“Brain homeostasis without inflammation depends on eliminating extracellular aggregates and apoptotic debris, this being mediated by the TREM2/DAP12 receptor complex (Han et al., 2017).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Han et al., 2017
The citation lists haven’t been fetched yet
References 78 · Cited by 30
- Authors
- Han, J., Wang, M., Ren, M., & Lou, H.
- Affiliations
- Shandong University (CN)
- Corresponding author
- Lou, Haiyan
- Venue
- International Journal of Neuroscience
- Publisher
- Informa UK Limited
- Published
- 2016-12-06
- Volume
- 127
- Issue
- 4
- Pages
- 368-375
- ISSN
- 0020-7454 (ISSN-L)
- 1543-5245
- OpenAlex
- W2550139391
- Cited by
- 30
- References
- 78
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 5 · 2023: 2 · 2022: 4 · 2021: 1 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 3
- FWCI
- 0.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81274124)
- Shandong Province Science and Technology Program (2014GSF118038, 2016GSF201061)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- TREM2, DAP12, microglia, neuroinflammation, neurodegeneration, Alzheimer's disease, Parkinson's disease, multiple sclerosis, frontotemporal lobar degeneration, phagocytosis, myeloid cells
- MeSH terms
- Humans, Membrane Glycoproteins, Membrane Proteins, Nervous System Diseases, Receptors, Immunologic, Microglia, Adaptor Proteins, Signal Transducing
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
