Increased β-Carboline 9N-Methyltransferase Activity in the Frontal Cortex in Parkinson's Disease

• Published in: Neurobiology of disease 2000-06, Vol.7 (3), p.201-211
• Main Authors: Gearhart, Debra A., Collins, Michael A., Lee, John M., Neafsey, Edward J.
• Format: Article
• Language: English
• Subjects: Aged; Aged, 80 and over; Cadaver; Female; Frontal Lobe - enzymology; Humans; Male; Methyltransferases - metabolism; Parkinson Disease - enzymology; Reference Values; Tissue Distribution
• ISSN: 0969-9961; 1095-953X
• DOI: 10.1006/nbdi.2000.0287

Enzymatic β-carboline N-methyltransferase activities generate N-methylated β-carbolinium cations that are analogs of the parkinsonian-producing neurotoxin MPP+. We measured β-carboline-2N-methyltransferase and β-carboline-9N-methyltransferase activities in the supernatant and particulate fractions from postmortem human brains. These N-methyltransferase activities were assessed in the substantia nigra, putamen, and frontal cortex from control and Parkinson's disease cases. No significant differences were measured in any brain region in particulate and supernatant fraction β-carboline 2N-methyltransferase activity or particulate fraction β-carboline 9N-methyltransferase activity. Likewise, supernatant fraction β-carboline 9N-methyltransferase activity was similar in the putamen and substantia nigra from Parkinson's disease and control cases. Unexpectedly, supernatant fraction β-carboline 9N-methyltransferase activity was increased fourfold in Parkinson's disease frontal cortex (P < 0.05), suggesting that β-carboline N-methylation may play a role in Parkinson's disease.