| First Author | Zhu C | Year | 2015 |
| Journal | Neurobiol Aging | Volume | 36 |
| Issue | 5 | Pages | 1994-2003 |
| PubMed ID | 25816748 | Mgi Jnum | J:222427 |
| Mgi Id | MGI:5644601 | Doi | 10.1016/j.neurobiolaging.2015.02.019 |
| Citation | Zhu C, et al. (2015) Triggering receptor expressed on myeloid cells-2 is involved in prion-induced microglial activation but does not contribute to prion pathogenesis in mouse brains. Neurobiol Aging 36(5):1994-2003 |
| abstractText | Dysfunctional variants of the innate immune cell surface receptor TREM2 (triggering receptor expressed on myeloid cells-2) were identified as major genetic risk factors for Alzheimer's disease and other neurodegenerative conditions. Here we assessed a possible involvement of TREM2 in prion disease. We report that TREM2 expression by microglia is significantly up-regulated upon prion infection. However, depletion of TREM2 did not affect disease incubation time and survival after intracerebral prion infection. Interestingly, markers of microglial activation were attenuated in prion-infected TREM2(-/-) mice, suggesting an involvement of TREM2 in prion-induced microglial activation. Further phenotype profiling of microglia revealed that TREM2 deficiency did not change microglial phenotypes. We conclude that TREM2 is involved in prion-induced microglial activation but does not noticeably modulate the pathogenesis of experimental prion infections. |
