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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cerebral Cortex / pathology
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Membrane Glycoproteins / genetics*
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Membrane Glycoproteins / metabolism*
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Mice
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Mice, Knockout
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Microglia / pathology
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Plaque, Amyloid / genetics*
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Plaque, Amyloid / metabolism*
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Receptors, Immunologic / genetics*
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Receptors, Immunologic / metabolism*
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Tauopathies / genetics*
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Tauopathies / metabolism*
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tau Proteins / genetics*
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tau Proteins / metabolism*
Substances
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Membrane Glycoproteins
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Receptors, Immunologic
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Trem2 protein, mouse
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tau Proteins