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

  • Neurology and Preclinical Neurological Studies - Review Article
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Abstract

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.

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Abbreviations

AD:

Alzheimer’s disease

BDNF:

Brain-derived neurotrophic factor

CNS:

Central nervous system

DA:

Dopamine

DISC1:

Disrupted-in-schizophrenia 1

DSP-4:

N-(2-Chloroethyl)-N-ethyl-2-bromo-benzylamine

GAPDH:

Glyceraldehyde 3-phosphate dehydrogenase

GDNF:

Glial cell line-derived neurotrophic factor

5-HT:

5-Hydroxytryptamine (serotonin)

KLF11:

Krüppel-like factor

LRRK-2:

Leucine repeat-rich kinase 2

MAO-A and MAO-B:

Type A and B monoamine oxidase

MAPK:

Mitogen-activated protein kinase

MDMA:

3,4-Methylenedioxymethamphetamine

NE:

Norepinephrine

NGF:

Nerve growth factor

NHLH2:

Nescient helix loop helix transcription factor 2

NMDA:

N-Methyl-d-aspartate

NT-3:

Neurotrophic factor-3

PD:

Parkinson’s disease

PEA:

Phenylethylamine

ROS:

Reactive oxygen species

SNP:

Single-nucleotide polymorphisms

UPS:

Ubiquitin−proteasome system

VPA:

Valproic acid (2-propylpentanoic acid)

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Acknowledgments

This work was supported by the Research Grant for Longevity Science from the Ministry of Health, Labour and Welfare, Japan, and also by “Verein zur Erforschung von Neurodegeneration, Neuroprotektion, Neuroregeneration und Therapie e. V.”, Würzburg, Germany.

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  1. Department of Health and Nutrition, Faculty of Psychological and Physical Science, Aichi Gakuin University, 12 Araike, Iwasaki-cho, Nisshin, Aichi, 470-0195, Japan

    Makoto Naoi

  2. Clinical Neurochemistry, National Parkinson’s Foundation Centre of Excellence Laboratories, Department of Psychiatry, Psychosomatics and Psychotherapy, University Hospital Würzburg, Würzburg, Germany

    Peter Riederer

  3. Department of Cognitive Brain Science, National Research Center for Geriatrics and Gerontology, Obu, Aichi, Japan

    Wakako Maruyama

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Naoi, M., Riederer, P. & Maruyama, W. Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression. J Neural Transm 123, 91–106 (2016). https://doi.org/10.1007/s00702-014-1362-4

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