In this context, and given the concrete clinical significance of DA deficit in the manifestation of PD symptoms [33] and the successful application of the amino acid DA precursor levodopa (l-DOPA) to increase striatal DA levels as a gold standard therapeutic intervention to alleviate motor symptoms in PD patients [34, 35], it is salient that DA has been shown on a mechanistic level to inhibit various modes of NLRP3 inflammasome activation. This evidence concerns the gene NLRP3 and Parkinson disease.