Adult neurogenesis, cell cycle and drug discovery in psychiatry

Department of Psychiatry and Behavioral Neurosciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology (Impact Factor: 7.05). 02/2009; 34(1):244. DOI: 10.1038/npp.2008.164
Source: PubMed


Neuropsychopharmacology, the official publication of the American College of Neuropsychopharmacology, publishing the highest quality original research and advancing our understanding of the brain and behavior.

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Available from: Vera Chesnokova, Feb 13, 2014
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    • "Potential mechanisms underlying PPD include adaptive changes in central monoaminergic function, the interactive involvement of neurotransmitters' genetic variants and environmental stressors on the limbic-hypothalamopituitary-adrenocortical axis regulatory system (Caspi and Moffitt, 2006), and possibly, neurotransmitter-mediated effects on neurogenesis during development and adulthood (Gaspar et al., 2003; Pechnick and Chesnokova, 2009). The complex chain of action from a gene to the development of a complex behavioural disorder also includes epigenetic alterations in response to the influence of gene–gene and gene–environment interactions (Kaminsky et al., 2006). "
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    ABSTRACT: Postpartum depression (PPD) is an under diagnosed and under treated mood disorder, with negative impact on both the mother and the infant's health. The aim of this study is to examine whether genetic variations in the monoaminergic neurotransmitter system, together with environmental stressors, contribute to the development of PPD symptoms. This nested case-control study included 275 women from a population-based cohort of delivering women in Sweden. A questionnaire containing the Edinburgh Postnatal Depression Scale was collected at 6 weeks and 6 months postpartum. Three functional polymorphisms were genotyped, catechol-O-methyltransferase (COMT)-Val158Met, monoamine oxidase A (MAOA)-upstream variable number tandem repeat (uVNTR) and serotonin transporter linked polymorphic region (5HTT-LPR). Stressful life events, maternity stressors and previous psychiatric contact were considered as potential risk factors. COMT-Val158Met was significantly associated with PPD symptoms at 6 weeks, but not at 6 months postpartum. A significant gene-gene interaction effect was present between COMT-Val158Met and MAOA-uVNTR. In a gene-environment multivariate model, COMT-Val158Met, psychiatric contact and maternity stressors were significantly associated with PPD symptoms. Among those with history of psychiatric problems, the COMT-Val158Met and 5HTT-LPR risk variants were associated with PPD symptoms, whereas in the absence of previous psychiatric contact only maternity stressors were related to PPD symptoms. The interaction effect between monoaminergic genes and environmental stressors is likely to contribute to vulnerability for PPD. The different patterns of association according to history of psychiatric problems, if replicated, might be helpful in screening strategies.
    Full-text · Article · Feb 2011 · Psychiatric genetics