SEMA3A and amyotrophic lateral sclerosis: The findings above suggested that the expression of Sema3A by terminal Schwann cells not only suppresses nerve terminal plasticity at specific neuromuscular synapses, but may also contribute to their early and selective loss in physio-pathological conditions, including aged-related sarcopenia, cachexia, muscular dystrophies, and ALS, where the fastest muscle phenotype is more severely compromised if compared with slow-twitch muscles [193, 194].