Although the physiological role of TREM2 is still under investigation, it is thought to be protective in the context of AD since TREM2 deficiency in the 5XFAD mouse model causes increased amyloid deposition (Wang et al., 2015), whereas overexpression of TREM2 in the Amyloid precursor protein/Presenilin-1 (APP)/(PS1) mouse ameliorates neuropathology (Jiang et al., 2014). This evidence concerns the gene APP and Alzheimer disease.