| First Author | Ren M | Year | 2018 |
| Journal | Exp Neurol | Volume | 302 |
| Pages | 205-213 | PubMed ID | 29407460 |
| Mgi Jnum | J:305994 | Mgi Id | MGI:6152919 |
| Doi | 10.1016/j.expneurol.2018.01.016 | Citation | Ren M, et al. (2018) TREM2 overexpression attenuates neuroinflammation and protects dopaminergic neurons in experimental models of Parkinson's disease. Exp Neurol 302:205-213 |
| abstractText | Triggering receptor expressed on myeloid cells-2 (TREM2) was a newly identified receptor expressed on microglia. Several observations support the hypothesis that TREM2 variation may confer susceptibility to Parkinson''s disease (PD). Therefore, in this paper, we explored the role of TREM2 in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Our results revealed that overexpression of TREM2 remarkably reduced MPTP-induced neuropathology including the dopaminergic neurodegeneration and neuroinflammation in vivo. Further mechanistic study revealed that TREM2 inhibited neuroinflammation by negatively regulating the TRAF6/TLR4-mediated activation of the MAPK and NF-kappaB signaling pathways. Taken together, our data suggest that TREM2 may have important neuroprotective effects against PD by critically modulating neuroinflammatory responses. These findings provide insights into the role of TREM2 in PD pathogenesis, and highlight TREM2 as a potential therapeutic target for this kind of disease. |
