Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. α2AAR-mediated G protein activation in brain homogenates prepared from WT or APP-KI mice at 7.5 months of age.
  • Fig. S2. α2AAR density measured by radioligand-binding assays in AD models.
  • Fig. S3. α2AAR-mediated G protein activation and receptor density tested in brain homogenates prepared from nTg or APP/PS1 mice at 5 weeks of age.
  • Fig. S4. Profiling of Aβ42 peptide oligomerization by fluorescent size-exclusion chromatography.
  • Fig. S5. α2AAR-mediated G protein activation in WT mouse brain homogenates in the presence of human TBS extracts with or without Aβ depletion.
  • Fig. S6. Cell-surface expression of HA-tagged receptors tested by fluorescence-activated cell sorting.
  • Fig. S7. AβO was detected on the surface of cells expressing WT but not 3eL-9A mutant α2AAR.
  • Fig. S8. Binding of an orthosteric ligand to WT or mutant α2AARs.
  • Fig. S9. Full blots of the AKT pathway phosphorylation arrays.
  • Fig. S10. Naturally secreted oligomeric Aβ induced GSK3β dephosphorylation/activation in neurons in the presence of clonidine.
  • Fig. S11. Quantitation of tau phosphorylation and GSK3β expression.
  • Fig. S12. Proposed model of Aβ hijacking NE signaling through α2AAR to induce activation of GSK3β/tau cascade.
  • Fig. S13. Idazoxan treatment reduces Aβ pathology in APP-KI mouse brains.
  • Fig. S14. Idazoxan treatment reduces GSK3β activity and tau hyperphosphorylation in APP-KI mouse brains.
  • Fig. S15. Open-field and elevated zero maze tests in nTg and APP/PS1 mice.
  • Fig. S16. Open-field and elevated zero maze tests in APP-KI mice.
  • Table S1. Information of human samples used in Fig. 1A.
  • Table S2. Extracted data used in Fig. 1 (B and C).
  • Table S3. Information of antibodies used in this study.
  • Legend for data file S1
  • References (2729, 31, 38, 4665)

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