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Abstract
Alzheimer's disease (AD) is the most common form of dementia and the 6th leading cause
of death in the US. The neuropathological hallmarks of the disease are extracellular
amyloid-β (Aβ) plaques and intraneuronal hyperphosphorylated tau aggregates. Genetic
variants of TREM2 (triggering receptor expressed on myeloid cells 2), a cell-surface
receptor expressed selectively in myeloid cells, greatly increase the risk of AD,
implicating microglia and the innate immune system as pivotal factors in AD pathogenesis.
Recent studies have advanced our understanding of TREM2 biology and microglial activities
in aging and neurodegenerative brains, providing new insights into TREM2 functions
in amyloid plaque maintenance, microglial envelopment of plaque, microglia viability,
and the identification of novel TREM2 ligands. Our increased understanding of TREM2
and microglia has opened new avenues for therapeutic intervention to delay or prevent
the progression of AD.