Personality traits in unaffected twins discordant for affective disorder

Vinberg, Maj; Mortensen, Erik Lykke; Kyvik, Kirsten Ohm; Kessing, Lars Vedel

doi:10.1111/j.1600-0447.2006.00909.x

Cited by 16 publications

(14 citation statements)

References 44 publications

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“…The participants were part of a larger cohort enrolled in a high-risk study (Christensen et al, 2007;Vinberg et al, 2007). Of the total cohort of 234 individuals, 100 were below 60 years of age and able to undergo a magnetic resonance (MR) scan.…”

Section: Methodsmentioning

confidence: 99%

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Familial Risk for Mood Disorder and the Personality Risk Factor, Neuroticism, Interact in Their Association with Frontolimbic Serotonin 2A Receptor Binding

Frøkjær¹,

Vinberg

Erritzoe³

et al. 2009

Neuropsychopharmacol

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Life stress is a robust risk factor for later development of mood disorders, particularly for individuals at familial risk. Likewise, scoring high on the personality trait neuroticism is associated with an increased risk for mood disorders. Neuroticism partly reflects stress vulnerability and is positively correlated to frontolimbic serotonin 2A (5-HT 2A ) receptor binding. Here, we investigate whether neuroticism interacts with familial risk in relation to frontolimbic 5-HT 2A receptor binding. Twenty-one healthy twins with a co-twin history of mood disorder and 16 healthy twins without a co-twin history of mood disorder were included. They answered self-report personality questionnaires and underwent [ 18 F]altanserin positron emission tomography. We found a significant interaction between neuroticism and familial risk in predicting the frontolimbic 5-HT 2A receptor binding (p ¼ 0.026) in an analysis adjusting for age and body mass index. Within the high-risk group only, neuroticism and frontolimbic 5-HT 2A receptor binding was positively associated (p ¼ 0.0037). In conclusion, our data indicate that familial risk and neuroticism interact in their relation to frontolimbic 5-HT 2A receptor binding. These findings point at a plausible neurobiological link between genetic and personality risk factors and vulnerability to developing mood disorders. It contributes to our understanding of why some people at high risk develop mood disorders while others do not. We speculate that an increased stress reactivity in individuals at high familial risk for mood disorders might enhance the effect of neuroticism in shaping the impact of potential environmental stress and thereby influence serotonergic neurotransmission.

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Section: Methodsmentioning

confidence: 99%

“…Participants were interviewed about stressful life events (SLE) in the year before inclusion (recent life events), as described elsewhere (Vinberg et al, 2007).…”

Section: Clinical Data Symptom Scores and Personality Assessmentmentioning

confidence: 99%

Familial Risk for Mood Disorder and the Personality Risk Factor, Neuroticism, Interact in Their Association with Frontolimbic Serotonin 2A Receptor Binding

Frøkjær¹,

Vinberg

Erritzoe³

et al. 2009

Neuropsychopharmacol

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show abstract

“…Participants and non-participants in the latter study have been described in detail elsewhere (Vinberg et al, 2007). The current study is the first report on structural MRI findings.…”

Section: Participantsmentioning

confidence: 99%

“…Life events in the last 12 months preceding the MR scan and lifetime were recorded using a Danish version (translated to Danish after permission from the author) of the questionnaires used by (Kendler et al, 1995;Vinberg et al, 2007). Participants were asked about 9 'personal' events, i.e.…”

Section: Clinical Assessmentmentioning

confidence: 99%

“…During the recruitment period (May 2003 to September 2005), 204 high-risk and 204 low-risk twins were invited to participate in the overarching high-risk study on affective disorders (Vinberg et al, 2007). Of the initial sample of 234 participants, 20 did not want to participate in a MR scan, 19 were not scanned because of physical contraindications (metal prosthesis, artificial heart valve, etc.…”

Section: Selection Proceduresmentioning

confidence: 99%

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Hippocampal volume changes in healthy subjects at risk of unipolar depression

Baaré

Vinberg

Knudsen

et al. 2010

Journal of Psychiatric Research

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a b s t r a c tUnipolar depression is moderately heritable. It is unclear whether structural brain changes associated with unipolar depression are present in healthy persons at risk of the disorder. Here we investigated whether a genetic predisposition to unipolar depression is associated with structural brain changes. A priori, hippocampal volume reductions were hypothesized. Using a high-risk study design, magnetic resonance imaging brain scans were obtained from 59 healthy high-risk subjects having a co-twin with unipolar depression, and 53 healthy low-risk subjects without a first-degree family history of major psychiatric disorder. High-risk twins had smaller hippocampal volumes than low-risk twins (p < 0.04). The finding was most pronounced in DZ twins. Groups did not differ on global brain tissue volumes or regional tissue volumes assessed in exploratory voxel-wise whole cerebrum analyses. In conclusion, hippocampal volume reduction may index a predisposition to develop depression and thus may be predictive of future onset of the disorder. Further studies are needed to elucidate the role of (shared) environmental and genetic factors.

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DNA Modification Study of Major Depressive Disorder: Beyond Locus-by-Locus Comparisons

Wang

Pal

et al. 2015

Biological Psychiatry

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Background Major depressive disorder (MDD) exhibits numerous clinical and molecular features that are consistent with putative epigenetic misregulation. Despite growing interest in epigenetic studies of psychiatric diseases, the methodologies guiding such studies have not been well defined. Methods We performed DNA modification analysis in white blood cells from monozygotic twins discordant for MDD, in brain prefrontal cortex, and germline (sperm) samples from affected individuals and control subjects (total N = 304) using 8.1K CpG island microarrays and fine mapping. In addition to the traditional locus-by-locus comparisons, we explored the potential of new analytical approaches in epigenomic studies. Results In the microarray experiment, we detected a number of nominally significant DNA modification differences in MDD and validated selected targets using bisulfite pyrosequencing. Some MDD epigenetic changes, however, overlapped across brain, blood, and sperm more often than expected by chance. We also demonstrated that stratification for disease severity and age may increase the statistical power of epimutation detection. Finally, a series of new analytical approaches, such as DNA modification networks and machine-learning algorithms using binary and quantitative depression phenotypes, provided additional insights on the epigenetic contributions to MDD. Conclusions Mapping epigenetic differences in MDD (and other psychiatric diseases) is a complex task. However, combining traditional and innovative analytical strategies may lead to identification of disease-specific etiopathogenic epimutations.

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Personality traits in unaffected twins discordant for affective disorder

Abstract: A high genetic liability to affective disorder showed an association with neuroticism, but the association interacts with other predictors of affective disorder such as female gender, minor psychopathology and recent adversity.

Cited by 16 publications

References 44 publications

Familial Risk for Mood Disorder and the Personality Risk Factor, Neuroticism, Interact in Their Association with Frontolimbic Serotonin 2A Receptor Binding

Familial Risk for Mood Disorder and the Personality Risk Factor, Neuroticism, Interact in Their Association with Frontolimbic Serotonin 2A Receptor Binding

Hippocampal volume changes in healthy subjects at risk of unipolar depression

DNA Modification Study of Major Depressive Disorder: Beyond Locus-by-Locus Comparisons

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