Unexpectedly, while enhanced BDNF/TrkB signaling mechanisms have previously been described to underlie disease ameliorating fingolimod actions, e.g., in mouse models of Rett syndrome and Huntington’s disease (Deogracias et al. 2012; Di Pardo et al. 2014; Miguez et al. 2015), such BDNF/TrkB mechanisms have not been observed in AD mice (Kartalou et al. 2020). The gene discussed is BDNF; the disease is juvenile Huntington disease.