TREM2 overexpression attenuates neuroinflammation and protects dopaminergic neurons in experimental models of Parkinson's disease.

Abstract:

: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-κB 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.

journal_name

Exp Neurol

journal_title

Experimental neurology

authors

Ren M,Guo Y,Wei X,Yan S,Qin Y,Zhang X,Jiang F,Lou H

doi

10.1016/j.expneurol.2018.01.016

subject

Has Abstract

pub_date

2018-04-01 00:00:00

pages

205-213

eissn

0014-4886

issn

1090-2430

pii

S0014-4886(18)30023-2

journal_volume

302

pub_type

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