Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. Tau pathology progression in rTg4510 transgenic mice.
  • Fig. S2. PHF-1 immunoreactivity is reduced by lonafarnib treatment.
  • Fig. S3. Acute treatment of lonafarnib does not alter tau pathology in aged rTg4510 transgenic mice.
  • Fig. S4. Effect of lonafarnib in macroautophagy and CMA.
  • Fig. S5. Farnesyltransferase activity inhibition activates autophagy.
  • Fig. S6. Sumo and ubiquitin are reduced by lonafarnib and Rhes-miR treatments.
  • Fig. S7. Lonafarnib’s effect on Rhes localization.
  • Fig. S8. Degradation of Rhes is insensitive to lysosomal proteolysis blocking.
  • Fig. S9. Lonafarnib treatment is effective in reducing phospho-tau in iPSC-derived neurons.
  • Fig. S10. Transcriptomic analysis of hiPSC-derived neurons harboring tau mutations.
  • Fig. S11. Ubiquitinated and sumoylated tau are not altered by lonafarnib treatment.
  • Fig. S12. Model for a Rhes pathway mechanism.
  • References (61–65
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Other Supplementary Material for this manuscript includes the following:

  • Movie S1. Lonafarnib attenuates behavioral circling in rTg4510 (mp4).
  • Data file S1. Differentially expressed genes in hiPSC-derived neurons with MAPT variants (Excel file).
  • Data file S2. Quantification data for rTg4510-treated mice (excel file).