Monoamine Oxidase

Publication Title: 
Journal of the American Academy of Child and Adolescent Psychiatry

OBJECTIVE: To comment on the article in this issue of the Journal by Professor Michael Rutter, "Environmentally Mediated Risks for Psychopathology: Research Strategies and Findings," in the context of current research findings on gene-environment interaction, epigenetics, and gene expression. METHOD: Animal and human studies are reviewed that differentiate the role of gene expression in developmental biology and psychopathology as well as studies that begin to specify the biological mechanisms involved in determining how genotype is translated into phenotype.

Author(s): 
Kramer, Douglas A.
Publication Title: 
American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics

In recent years, the role of epigenetic phenomenon, such as methylation, in mediating vulnerability to behavioral illness has become increasingly appreciated. One prominent locus at which epigenetic phenomena are thought to be in play is the monoamine oxidase A (MAOA) locus. In order to examine the role of methylation at this locus, we performed quantitative methylation analysis across the promoter region of this gene in lymphoblast lines derived from 191 subjects participating in the Iowa Adoption Studies (IAS).

Author(s): 
Philibert, Robert A.
Gunter, Tracy D.
Beach, Steven R. H.
Brody, Gene H.
Madan, Anup
Publication Title: 
Epigenetics

DNA methylation is a key epigenetic mechanism involved in the developmental regulation of gene expression. Alterations in DNA methylation are established contributors to inter-individual phenotypic variation and have been associated with disease susceptibility. The degree to which changes in loci-specific DNA methylation are under the influence of heritable and environmental factors is largely unknown.

Author(s): 
Wong, Chloe Chung Yi
Caspi, Avshalom
Williams, Benjamin
Craig, Ian W.
Houts, Renate
Ambler, Antony
Moffitt, Terrie E.
Mill, Jonathan
Publication Title: 
Journal of Child Psychology and Psychiatry, and Allied Disciplines

BACKGROUND: The capacity to control or regulate one's emotions, cognitions and behavior is central to competent functioning, with limitations in these abilities associated with developmental problems. Parenting appears to influence such self-regulation. Here the differential-susceptibility hypothesis is tested that the more putative 'plasticity alleles' adolescents carry, the more positively and negatively influenced they will be by, respectively, supportive and unsupportive parenting.

Author(s): 
Belsky, Jay
Beaver, Kevin M.
Publication Title: 
American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics

Panic disorder (PD) is a common mental disorder, ranking highest among the anxiety disorders in terms of disease burden. The pathogenesis of PD is multifactorial with significant heritability, however only a few convincing risk genes have been reported thus far. One of the most promising candidates is the gene encoding monoamine oxidase A (MAOA), due to its key role in monoaminergic neurotransmission, established validity of animal models, and the efficacy of MAO inhibitors in the treatment of PD.

Author(s): 
Reif, Andreas
Weber, Heike
Domschke, Katharina
Klauke, Benedikt
Baumann, Christian
Jacob, Christian P.
Strˆhle, Andreas
Gerlach, Alexander L.
Alpers, Georg W.
Pauli, Paul
Hamm, Alfons
Kircher, Tilo
Arolt, Volker
Wittchen, Hans-Ulrich
Binder, Elisabeth B.
Erhardt, Angelika
Deckert, J¸rgen
Publication Title: 
The British Journal of Psychiatry: The Journal of Mental Science

BACKGROUND: Antisocial personality disorder (ASPD) is characterised by elevated impulsive aggression and increased risk for criminal behaviour and incarceration. Deficient activity of the monoamine oxidase A (MAOA) gene is suggested to contribute to serotonergic system dysregulation strongly associated with impulsive aggression and antisocial criminality. AIMS: To elucidate the role of epigenetic processes in altered MAOA expression and serotonin regulation in a population of incarcerated offenders with ASPD compared with a healthy non-incarcerated control population.

Author(s): 
Checknita, D.
Maussion, G.
LabontÈ, B.
Comai, S.
Tremblay, R. E.
Vitaro, F.
Turecki, N.
Bertazzo, A.
Gobbi, G.
CÙtÈ, G.
Turecki, G.
Publication Title: 
Advances in Clinical Chemistry

Major depressive disorder (MDD) is characterized by mood, vegetative, cognitive, and even psychotic symptoms and signs that can cause substantial impairments in quality of life and functioning. Biomarkers are measurable indicators that could help diagnosing MDD or predicting treatment response. In this chapter, lipid profiles, immune/inflammation, and neurotrophic factor pathways that have long been implicated in the pathogenesis of MDD are discussed.

Author(s): 
Huang, Tiao-Lai
Lin, Chin-Chuen
Publication Title: 
Current Opinion in Psychiatry

PURPOSE OF REVIEW: The present review aims to deliver a systematic overview of current developments and trends in (epi)genetics of anxiety and to identify upcoming challenges and opportunities. RECENT FINDINGS: Genes related to peptide and hormone signaling have been suggested for anxiety-related phenotypes, e.g., the NPSR1 gene, which has been associated predominantly with panic disorder in women, and shown to interact with environmental factors and to influence psychometric, neurophysiological, and neuroimaging correlates of anxiety.

Author(s): 
Gottschalk, Michael G.
Domschke, Katharina
Publication Title: 
The Journal of Pharmacy and Pharmacology

Diethyl maleate (DEM, 600 mg kg-1 i.p.) significantly potentiated hexobarbitone hypnosis and lowered plasma hexobarbitone level on awakening. Sleeping time following intracerebroventricular (i.c.v.) injection of phenobarbitone was also prolonged by DEM treatment. When administered to DEM-treated rats, L-tryptophan (50 mg kg-1 i.p.) significantly potentiated hexobarbitone hypnosis, although alone it had no effect in control rats.

Author(s): 
Minegishi, A.
Fukumori, R.
Satoh, T.
Kitagawa, H.
Publication Title: 
Journal of the National Cancer Institute

The effects of riboflavin deficiency on the metabolism of N-nitrosodimethylamine [(DMN) CAS: 62-75-9] and other nitrosamines were examined in rats. After weanling rats were put on a riboflavin-deficient diet, the development of the deficiency was monitored by the growth rate and the erythrocyte glutathione reductase activation coefficient. In the riboflavin-deficient rats, the liver microsomal NADPH-cytochrome c reductase activity was lower but the cytochrome P450 content was higher than that of the control. The metabolism of DMN was dependent on the severity of the deficiency.

Author(s): 
Wang, T.
Miller, K. W.
Tu, Y. Y.
Yang, C. S.

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