Since genetically decreasing TREM2 function increases Aβ-induced tau seeding, we hypothesized that chronically increasing TREM2 signaling would decrease amyloid-induced tau-seeding and spreading. Thus, microglia and TREM2 are at a critical intersection of Aβ and tau pathologies in AD. Genetic loss of or decreased TREM2 function impairs the microglial response to amyloid-β (Aβ) plaques, resulting in more diffuse Aβ plaques and increased peri-plaque neuritic dystrophy and AD-tau seeding. Variants in the triggering receptor expressed on myeloid cells 2 ( TREM2) gene are associated with increased risk for late-onset AD.
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