TREM2 function impedes tau seeding in neuritic plaques
Nature neuroscience, 2019•nature.com
Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) have been
associated with increased risk for sporadic, late-onset Alzheimer's disease. Here we show
that germline knockout of Trem2 or the TREM2 R47H variant reduces microgliosis around
amyloid-β plaques and facilitates the seeding and spreading of neuritic plaque tau
aggregates. These findings demonstrate a key role for TREM2 and microglia in limiting the
development of peri-plaque tau pathologies.
associated with increased risk for sporadic, late-onset Alzheimer's disease. Here we show
that germline knockout of Trem2 or the TREM2 R47H variant reduces microgliosis around
amyloid-β plaques and facilitates the seeding and spreading of neuritic plaque tau
aggregates. These findings demonstrate a key role for TREM2 and microglia in limiting the
development of peri-plaque tau pathologies.
Abstract
Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) have been associated with increased risk for sporadic, late-onset Alzheimer’s disease. Here we show that germline knockout of Trem2 or the TREM2R47H variant reduces microgliosis around amyloid-β plaques and facilitates the seeding and spreading of neuritic plaque tau aggregates. These findings demonstrate a key role for TREM2 and microglia in limiting the development of peri-plaque tau pathologies.
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