2009
DOI: 10.1038/mp.2009.113
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The 2009 Nobel conference on the role of genetics in promoting suicide prevention and the mental health of the population

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Cited by 20 publications
(22 citation statements)
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“…Personality traits including neuroticism or neurodevelopmental vulnerabilities involving impaired working memory or executive functioning resulting in poor problem solving could also be involved (Baud, 2005; Brent & Melhem, 2008; Mann et al 2009). Gene variants related, for example, to the serotonergic-, noradrenergic- and dopaminergic neurotransmitter systems appear to be associated with the risk of suicidal behaviour (Brezo et al 2008; Currier & Mann, 2008; Ernst et al 2009); interaction patterns (gene–gene, gene–development, gene–environment), however, are largely unknown (Rujescu et al 2007; Brezo et al 2008, 2010; Currier & Mann, 2008; Ernst et al 2009; Roy et al 2009; Wasserman et al 2010; Fergusson et al 2011). The genetic effect probably involves a large number of single genes or alleles, similar to what has been suggested for schizophrenia and bipolar disorder (Purcell et al 2009).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Personality traits including neuroticism or neurodevelopmental vulnerabilities involving impaired working memory or executive functioning resulting in poor problem solving could also be involved (Baud, 2005; Brent & Melhem, 2008; Mann et al 2009). Gene variants related, for example, to the serotonergic-, noradrenergic- and dopaminergic neurotransmitter systems appear to be associated with the risk of suicidal behaviour (Brezo et al 2008; Currier & Mann, 2008; Ernst et al 2009); interaction patterns (gene–gene, gene–development, gene–environment), however, are largely unknown (Rujescu et al 2007; Brezo et al 2008, 2010; Currier & Mann, 2008; Ernst et al 2009; Roy et al 2009; Wasserman et al 2010; Fergusson et al 2011). The genetic effect probably involves a large number of single genes or alleles, similar to what has been suggested for schizophrenia and bipolar disorder (Purcell et al 2009).…”
Section: Discussionmentioning
confidence: 99%
“…Concerning the latter, several possible aetiological pathways for suicidal behaviour have been suggested, for instance, direct effects from psychiatric disorders, effects of early adversity, gene–environment correlation (selection into adversity), interactions between culture and genes and causal loops from genes to environment and back again (Kendler, 2010), These two overlapping approaches, as well as other strategies, are likely to require further development of technology (e.g. neuroimaging and -physiology) for more fine-grained assessment of biological mechanisms (Wasserman et al 2010). …”
Section: Discussionmentioning
confidence: 99%
“…Another study reported differences in expression of the DARPP-32 gene, which is involved in dopamine, and possibly serotonin, regulation, between schizophrenic patients who died by suicide and due to other causes [124]. However, the specificity of these findings is very low, and a lot of work remains to be done until clinical benefits can be gained [125]. The last decade has seen an increasing use of neuroimaging in schizophrenia research on structural changes in the brains of patients.…”
Section: Biomarkers Of Suicide Risk In Schizophreniamentioning
confidence: 99%
“…Other molecular genetic studies have demonstrated findings consistent with the etiopathologic pathways suggested from the neurobiological studies of suicide, as previously reviewed (Ernst et al, 2009). Genes such as 5-HTTLPR, CRHR1, and mu-opiod-type receptors or the ROR1, CD44, FOXN3, DHX15 were identified in gene expression or GWAS studies of suicides (Wasserman et al, 2010). In Schizophrenia patients, the HPA-axis gene CRHBP confers risk for suicide attempt, and interacts with another HPA-axis gene CRHR1 with apparent consequences for suicide attempt risk and nature of attempt (De Luca et al, 2010).…”
Section: Introductionmentioning
confidence: 99%