“…These CTIQs can be metabolized via N-methylation to N-methyl-TIQs and oxidation to cytotoxic MPP + -like neurotoxins. MPP methyl-4-phenylpyridinium CIQs catechol isoquinolines; NorSal norsalsolinol or 6,7-dihydroxyl-1,2,3,4-tetrahydroisoquinoline; NMNorSal N-methylnorsalsolinol or 2methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; MeDHIQ + 2-methyl-6,7-dihydroxyisoquinolinium ion; Sal salsolinol or 1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; NMSal N-methylsalsolinol or 1(R),2-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; DiMeD-HIQ + 1,2-dimethyl-6,7-dihydroxyisoquinolinium ion; ADTIQ 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; NMADTIQ N-methyl ADTIQ or 1-acetyl-2-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; MeAcDHIQ + 1-acetyl-2-methyl-6,7-dihydroxyisoquinolinium ion [Sal]) derivatives were first found in the urine and brain of PD patients who were treated by L-3,4-dihydroxyphenylalanine (L-DOPA) [11,12] and have the most significant toxicity on cell and animal models [13][14][15]. With the confirmation of synthesis and metabolism of CIQs, more attention were paid to the role of Sal derivatives in the pathogenesis of PD as promising candidates of critical endogenous neurotoxin.…”