Disease relevance of N-Methylisoquinolinium

• N-methylisoquinolinium ion could be one of the candidates of endogenous or environmental factors that produce Parkinson's disease [1].
• Endogenous synthesis of N-methyl-1,2,3,4-tetrahydroisoquinoline, a precursor of N-methylisoquinolinium ion, in the brains of primates with parkinsonism after systemic administration of 1,2,3,4-tetrahydroisoquinoline [2].

High impact information on N-Methylisoquinolinium

• N-Methyl-1,2,3,4-tetrahydroisoquinoline (NMTIQ) was found to be oxidized by monoamine oxidase (MAO) into N-methylisoquinolinium ion, which was proved to inhibit enzymes related to the metabolism of catecholamines, such as tyrosine hydroxylase, aromatic-L-amino acid decarboxylase, and MAO [3].
• As a class, the N-methylisoquinolinium ions were found to be the most active MAO-A inhibitors, with N-methyl-6-methoxyisoquinolinium ion emerging as a potent (IC50 = 0.81 microM) and competitive MAO-A inhibitor [4].
• The N-methylated compound was oxidized into N-methylisoquinolinium ion by monoamine oxidase from human brain mitochondria [5].

Gene context of N-Methylisoquinolinium

• N-Methylisoquinolinium ion (N-MIQ) has been found to inhibit the biosynthesis of catecholamines; it inhibited tyrosine hydroxylase activity in striatal tissue slices [6].

Analytical, diagnostic and therapeutic context of N-Methylisoquinolinium

• Studies on the uptake of N-methylisoquinolinium ion into rat striatal slices using high-performance liquid chromatography with fluorimetric detection [7].
• A simple and sensitive procedure for the measurement of N-methylisoquinolinium ion (NMIQ+), a putative neurotoxin, was devised using high-performance liquid chromatography (HPLC) with fluorescence detection [7].

References