Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression

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• 作者：Makoto Naoi ; Peter Riederer ; Wakako Maruyama
• 关键词：Monoamine oxidase ; Types A and B MAO ; Mitochondria ; Expression ; Genetic and environmental factor ; Neurodegenerative disorders ; Abnormal behavior ; Cell death ; Neuroprotection
• 刊名：Journal of Neural Transmission
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：123
• 期：2
• 页码：91-106
• 全文大小：724 KB
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• 作者单位：Makoto Naoi (1)
  Peter Riederer (2)
  Wakako Maruyama (3)
  
  1. Department of Health and Nutrition, Faculty of Psychological and Physical Science, Aichi Gakuin University, 12 Araike, Iwasaki-cho, Nisshin, Aichi, 470-0195, Japan
  2. Clinical Neurochemistry, National Parkinson’s Foundation Centre of Excellence Laboratories, Department of Psychiatry, Psychosomatics and Psychotherapy, University Hospital Würzburg, Würzburg, Germany
  3. Department of Cognitive Brain Science, National Research Center for Geriatrics and Gerontology, Obu, Aichi, Japan
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Neurology
  Pharmacology and Toxicology
  Psychiatry
  
• 出版者：Springer Wien
• ISSN：1435-1463

文摘

Monoamine oxidase types A and B (MAO-A, MAO-B) regulate the levels of monoamine neurotransmitters in the brain, and their dysfunction may be involved in the pathogenesis and influence the clinical phenotypes of neuropsychiatric disorders. Reversible MAO-A inhibitors, such as moclobemide and befloxatone, are currently employed in the treatment of emotional disorders by inhibiting the enzymatic degradation of dopamine, serotonin and norepinephrine in the central nervous system (CNS). It has been suggested that the irreversible MAO-B inhibitors selegiline and rasagiline exert a neuroprotective effect in Parkinson’s and Alzheimer’s diseases. This effect, however, is not related to their inhibition of MAO activity; in animal and cellular models, selegiline and rasagiline protect neuronal cells through their anti-apoptotic activity and induction of pro-survival genes. There is increasing evidence that MAO-A activity, but not that of MAO-B, is implicated in the pathophysiology of neurodegenerative disorders, but also in gene induction by MAO-B inhibitors; on the other hand, selegiline and rasagiline increase MAO-A mRNA, protein, and enzyme activity levels. Taken together, these results suggest that each MAO subtype exerts effects that modulate the expression and activity of the other isoenzyme. The roles of MAO-A and -B in the CNS should therefore be re-evaluated with respect to the “type-specificity” of their inhibitors, which may not be unconditional during chronic treatment. Mao-a expression, in particular, may be implicated in pathogenesis and phenotypes in neuropsychiatric disorders. MAO-A expression is modified by mao polymorphisms affecting its transcriptional efficiency, as well as by mutations and polymorphism of parkin, Sirt1, FOXO, microRNA, presenilin-1, and other regulatory proteins. In addition, childhood maltreatment has been shown to have an impact upon adolescent social behavior in children with mao-a polymorphisms of low transcriptional activity. Low MAO-A activity may increase the levels of serotonin and norepinephrine, resulting in disturbed neurotransmitter system development and behavior. This review discusses genetic and environmental factors involved in the regulation of MAO-A expression, in the contexts of neuropsychiatric function and of the regulation of neuronal survival and death. Keywords Monoamine oxidase Types A and B MAO Mitochondria Expression Genetic and environmental factor Neurodegenerative disorders Abnormal behavior Cell death Neuroprotection