Neuroscience

Biology

Senile plaques

Receptor

Tauopathy

Amyloid (mycology)

Neurodegeneration

Alzheimer's disease

Knockout mouse

Immunology

Microglia

TREM2

Inflammation

Internal medicine

Medicine

Disease

Pathology

Nature Neuroscience

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.

TREM2 function impedes tau seeding in neuritic plaques