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TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function.

Neuron | Mar 7, 2018

Mutations in triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to increased Alzheimer's disease (AD) risk. Neurobiological functions of TREM2 and its pathophysiological ligands remain elusive. Here we found that TREM2 directly binds to β-amyloid (Aβ) oligomers with nanomolar affinity, whereas AD-associated TREM2 mutations reduce Aβ binding. TREM2 deficiency impairs Aβ degradation in primary microglial culture and mouse brain. Aβ-induced microglial depolarization, K+ inward current induction, cytokine expression and secretion, migration, proliferation, apoptosis, and morphological changes are dependent on TREM2. In addition, TREM2 interaction with its signaling adaptor DAP12 is enhanced by Aβ, regulating downstream phosphorylation of SYK and GSK3β. Our data demonstrate TREM2 as a microglial Aβ receptor transducing physiological and AD-related pathological effects associated with Aβ.

Pubmed ID: 29518356 RIS Download

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Associated grants

  • Agency: NIA NIH HHS, Id: R01 AG038710
  • Agency: NIA NIH HHS, Id: R01 AG021173
  • Agency: NIA NIH HHS, Id: R21 AG048519
  • Agency: NIA NIH HHS, Id: R01 AG044420
  • Agency: NIA NIH HHS, Id: RF1 AG056114
  • Agency: NINDS NIH HHS, Id: R01 NS046673
  • Agency: NIA NIH HHS, Id: RF1 AG056130

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