We therefore hypothesized that a molecule that blocks the sortilin-PGRN interaction and/or decreases sortilin levels would mimic the genetic ablation of Sort1. Accordingly, these actions would be expected to increase the levels of residual PGRN in GRN mutation carriers, restore PGRN back to physiological levels, and slow or halt the progression of FTD-GRN [32]. This evidence concerns the gene SORT1 and frontotemporal dementia.