NTRK2 and juvenile Huntington disease: But surprising generalities are present as well: excluding Fragile X, all of cases so far studied involve the RhoA pathway, and in two instances (inflammation, Huntington Disease) this reflects a problem with BDNF “transmission.” In line with our expectation that this will hold for other models in which TBS-induced actin polymerization is impaired, it was recently reported that synaptic BDNF signaling through TrkB is markedly attenuated in Ube3a KO (Angelman syndrome) mice (Cao et al., 2013).