Recent works have demonstrated a rare functional variant (R47H) in triggering 
receptor expressed on myeloid cells (TREM) 2 gene, encoding TREM2 protein, 
increase susceptibility to late-onset Alzheimer's disease (AD), with an odds 
ratio similar to that of the apolipoprotein E ε4 allele. The reduced function of 
TREM2 was speculated to be the main cause in the pathogenic effects of this risk 
variant, and TREM2 is highly expressed in white matter, as well as in the 
hippocampus and neocortex, which is partly consistent with the pathological 
features reported in AD brain, indicating the possible involvement of TREM2 in 
AD pathogenesis. Emerging evidence has demonstrated that TREM2 could suppress 
inflammatory response by repression of microglia-mediated cytokine production 
and secretion, which may prevent inflammation-induced bystander damage of 
neurons. TREM2 also participates in the regulation of phagocytic pathways that 
are responsible for the removal of neuronal debris. In this article, we review 
the recent epidemiological findings of TREM2 that related with late-onset AD and 
speculate the possible roles of TREM2 in progression of this disease. Based on 
the potential protective actions of TREM2 in AD pathogenesis, targeting TREM2 
might provide new opportunities for AD treatment.