However, because intrathecally administered exogenous BDNF does not improve motor function and survival in ALS patients [108] or autonomic nervous system function [109,125], it is essential to target the altered alternative splicing of the TrkB, as it is strongly related to the maintenance of NMJs done by the bidirectional synaptic and neurotrophic controls, as has already been pointed out. The gene discussed is BDNF; the disease is amyotrophic lateral sclerosis.