SEMA3A and amyotrophic lateral sclerosis: More specifically, a pharmacological inhibition of the Npn1 receptor was shown to delay denervation and prolong lifespan in an ALS mouse model (Venkova et al., 2014), while mice engineered to express a mutated form of Sema3A protein did not display any defects in response to denervation or the neurodegenerative disease process (Moloney et al., 2017).