A relatively recent experimental study gives interesting insights about this issue: in a murine model of PD, where a subchronic conduritol-β-epoxide exposure induced GCase inhibition, Ginns and colleagues identified an early synaptic impairment, in the form of a reduction of striatal evoked dopamine release and altered synaptic plasticity markers, including post-synaptic density size and miRNA expression levels, together with glial activation within nigrostriatal pathway and abnormal α-synuclein accumulation (39). The gene discussed is SNCA; the disease is Parkinson disease.