Whereas we observed the compelling rescue of AD-associated deficits by fingolimod treatment (Figure 2 and Figure 3), this rescue was not accompanied by BDNF elevations or enhanced TrkB signaling, neither in hippocampus nor neocortex (compare Supplementary Figure S3), albeit fingolimod mediated amelioration in other mouse models of brain diseases was associated with increased BDNF/TrkB signaling (see e.g., [8,11]). This evidence concerns the gene NTRK2 and Alzheimer disease.