LGALS1 and prion disease: Since the oxidized form of galectin-1 lacking lectin activity promotes axonal regeneration at much lower concentrations at which galectin-1 exhibits lectin activity (Inagaki et al., 2000), S-nitrosylation of galectin-1, which protects against oxidization to maintain lectin activity, may attenuate its neuroprotective action in prion disease.