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This section presents current neuron-targeted therapeutic strategies, organized along a conceptual axis from extracellular modulation (e.g., receptor activation and trophic signaling) to intracellular mechanisms (e.g., signal transduction, transcriptional regulation and metabolic support)

Recently, a novel pathogenetic model has been proposed which postulated that changes in the local metabolic environment (pH, salt) may play a key role in the development of AS by induction of a Th17 pro-inflammatory phenotype through activation of glycosphingolipid sensors (encoded by the GPR genes in particularly GPR65 ) and serum and glucocorticoid-regulated kinase-1 (SGK1) ( Figure 4 - 11 )

Finally, the heterologous production of GSLs in Nicotiana benthamiana leaves revealed the GSL sulfation as a bottleneck in GSL biosynthesis