A fairly straightforward explanation can be offered for the loss of actin signaling and LTP in the case of the Huntington Disease models: the disease is multiply reported to reduce the concentrations and trafficking of Brain-Derived Neurotrophic Factor (BDNF) (Zuccato et al., 2001; del Toro et al., 2006), which acts on one of the “modifier” receptors (TrkB) described in Figure 5. Here, NTRK2 is linked to juvenile Huntington disease.