As such, we can speculate that NAC supplementation might act particularly in these neurons in preclinical models of PD, just like this one, either by the alteration of extra-synaptic mGlu2/3 receptors (located on neuronal terminals) [113] or by inhibiting NMDA-mediated increases in intracellular calcium levels via GSH [114]. This evidence concerns the gene GRM2 and Parkinson disease.