Faculty Opinions recommendation of TREM2 function impedes tau seeding in neuritic plaques.

Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) have been associated with increased risk for sporadic, late-onset Alzheimer's disease (AD).Here we show that germline knockout of Trem2 or the TREM2 R47H variant reduce microgliosis around amyloid-β (Aβ) plaques and facilitate the seeding and spreading of neuritic plaque (NP) tau aggregates.These findings demonstrate a key role for TREM2 and microglia in limiting development of peri-plaque tau pathologies.Rare variants conferring a partial loss of function in TREM2, a cell surface receptor specifically found on microglia in the brain, increase AD-risk 2-4-fold. 1In addition, TREM2 variant carriers have a faster rate of cognitive decline, suggesting TREM2 also influences disease progression. 2Previous studies by our group and others have characterized the effects of TREM2 deficiency on Aβ plaques, hypothesized to be an initiator of AD, 3 and Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research,