Brain monoamine oxidase B and A in human parkinsonian dopamine deficiency disorders

Brain - Tập 140 Số 9 - Trang 2460-2474 - 2017
Junchao Tong1,2, Gausiha Rathitharan1, Jeffrey H. Meyer3, Yoshiaki Furukawa4, Lee-Cyn Ang5, Isabelle Boileau6, Mark Guttman7, Oleh Hornykiewicz8, Stephen J. Kish1
1Human Brain Laboratory, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada
2Preclinical Imaging Unit, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada
3Research Imaging Centre and Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada
4Department of Neurology, Juntendo Tokyo Koto Geriatric Medical Center, and Faculty of Medicine, University and Post Graduate University of Juntendo, Tokyo, Japan
5Division of Neuropathology, London Health Science Centre, University of Western Ontario, London, Ontario, Canada
6Addiction Imaging Research Group, Research Imaging Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada
7Centre for Movement Disorders, Markham, Ontario, Canada
8Centre for Brain Research, Medical University of Vienna, Spitalgasse 4, A-1090 Vienna, Austria

Tóm tắt

Abstract See Jellinger (doi:10.1093/awx190) for a scientific commentary on this article.  The enzyme monoamine oxidases (B and A subtypes, encoded by MAOB and MAOA, respectively) are drug targets in the treatment of Parkinson’s disease. Inhibitors of MAOB are used clinically in Parkinson’s disease for symptomatic purposes whereas the potential disease-modifying effect of monoamine oxidase inhibitors is debated. As astroglial cells express high levels of MAOB, the enzyme has been proposed as a brain imaging marker of astrogliosis, a cellular process possibly involved in Parkinson’s disease pathogenesis as elevation of MAOB in astrocytes might be harmful. Since brain monoamine oxidase status in Parkinson’s disease is uncertain, our objective was to measure, by quantitative immunoblotting in autopsied brain homogenates, protein levels of both monoamine oxidases in three different degenerative parkinsonian disorders: Parkinson’s disease (n = 11), multiple system atrophy (n = 11), and progressive supranuclear palsy (n = 16) and in matched controls (n = 16). We hypothesized that if MAOB is ‘substantially’ localized to astroglial cells, MAOB levels should be generally associated with standard astroglial protein measures (e.g. glial fibrillary acidic protein). MAOB levels were increased in degenerating putamen (+83%) and substantia nigra (+10%, non-significant) in multiple system atrophy; in caudate (+26%), putamen (+27%), frontal cortex (+31%) and substantia nigra (+23%) of progressive supranuclear palsy; and in frontal cortex (+33%), but not in substantia nigra of Parkinson’s disease, a region we previously reported no increase in astrocyte protein markers. Although the magnitude of MAOB increase was less than those of standard astrocytic markers, significant positive correlations were observed amongst the astrocyte proteins and MAOB. Despite suggestions that MAOA (versus MAOB) is primarily responsible for metabolism of dopamine in dopamine neurons, there was no loss of the enzyme in the parkinsonian substantia nigra; instead, increased nigral levels of a MAOA fragment and ‘turnover’ of the enzyme were observed in the conditions. Our findings provide support that MAOB might serve as a biochemical imaging marker, albeit not entirely specific, for astrocyte activation in human brain. The observation that MAOB protein concentration is generally increased in degenerating brain areas in multiple system atrophy (especially putamen) and in progressive supranuclear palsy, but not in the nigra in Parkinson’s disease, also distinguishes astrocyte behaviour in Parkinson’s disease from that in the two ‘Parkinson-plus’ conditions. The question remains whether suppression of either MAOB in astrocytes or MAOA in dopamine neurons might influence progression of the parkinsonian disorders.

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