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Notably, the liver, a primary organ for threonines initial catabolism, demonstrated a notable increase in SDS activity, facilitating threonines conversion into propionyl-CoA across all detected organs during fasting, likely due to the inter-organ cross-talk mediated by downstream metabolites, although muscle SDS activity remained unchanged

[118] Other possible neuroprotectors for PD are MAO-B inhibitors, NMDA-receptor antagonists, and dopamine receptor agonists