Genomewide survey of panic disorder

Crowe, Raymond R.; Goedken, Rhinda; Samuelson, Steve; Wilson, R. Reid; Nelson, Jeffrey J.; Noyes, Russell

doi:10.1002/1096-8628(20010108)105:1<105::aid-ajmg1072>3.0.co;2-p

Cited by 88 publications

(23 citation statements)

References 28 publications

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“…[3][4][5] Several genome-wide linkage studies have tried to identify genomic regions harboring quantitative trait loci (QTLs) that influence the vulnerability for anxiety disorders. All these studies [6][7][8][9][10][11][12][13][14][15] ascertained the pedigrees through probands with panic disorder, except for one study 16 that included pedigrees with at least one member having an anxiety disorder or somatoform pain. Panic disorder is the most frequently analyzed phenotype.…”

Section: Introductionmentioning

confidence: 99%

“…Panic disorder is the most frequently analyzed phenotype. [6][7][8]13,14 Two studies focused on panic disorder with comorbid medical conditions, that is renal/ bladder conditions, thyroid irregularities, mitral valve prolapse and severe headaches. 11,15 Simple phobia and social phobia have each been investigated once.…”

Section: Introductionmentioning

confidence: 99%

“…Table 1 summarizes the most promising results so far. One region on chromosome 7 and one region on chromosome 1 showed linkage in two scans 6,8,13,14 with logarithm of odds (LOD) scores from 1.71 to 2.23. A linkage signal on chromosome 14 was observed for panic disorder, simple and social phobia in a sample of 20 families with 153 individuals.…”

Section: Introductionmentioning

confidence: 99%

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Linkage on chromosome 14 in a genome-wide linkage study of a broad anxiety phenotype

et al. 2007

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Several linkage studies on anxiety have been carried out in samples ascertained through probands with panic disorder. The results indicated that using a broad anxiety phenotype instead of a DSM-IV anxiety disorder diagnosis might enhance the chance of finding a linkage signal. In the current study, a genome-wide linkage analysis was performed on anxiety measured with a self-report questionnaire whose scores are highly correlated with DSM-IV anxiety disorders. The self-report questionnaire was included in five surveys of a longitudinal study of the Netherlands Twin Register. Genotype and phenotype data were available for 1602 twins and siblings. To estimate identity by descent , additional genotype data for 564 parents and 22 siblings were used. Linkage analyses were carried out using MERLIN-regress on the average anxiety scores across time. A linkage signal (logarithm of odds score 3.4, empirical P-value 0.07) was obtained at chromosome 14 for marker D14S65 at 105 cM (90% confidence interval, 99-115 cM bounded by markers D14S1434 and D14S985). This finding replicates a linkage finding for a broad anxiety phenotype in a clinically based sample, indicating that the region might harbor a quantitative trait locus associated with the whole spectrum of general anxiety, that is from the normal to the clinical range. Moreover, genome-wide linkage and association studies on emotionality in mice obtained significant results in a syntenic region on mouse chromosome 12. Two homolog genes lie in this region -Dlk1 (delta-like 1 homolog, Drosophila) and Rtl1 (retrotransposon-like 1). Future association studies of these genes are warranted.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Linkage on chromosome 14 in a genome-wide linkage study of a broad anxiety phenotype

et al. 2007

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“…Recurrent panic attacks define panic disorder, a common and severe anxiety disorder of unknown etiology. Although several chromosomal regions and genes have been suggested to contribute to panic disorder, the phenotypic and genetic complexity of this disorder has precluded the finding of candidate genes (Knowles et al, 1998;Weissman et al, 2000;Crowe et al, 2001;Gratacos et al, 2001; Thorgeirsson et al, 2003). It has been proposed that genetic variants of several candidate genes of neurotransmitter systems, mainly catecholaminergic, may con-tribute to the susceptibility to panic disorder (Maron et al, 2005).…”

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confidence: 99%

Transgenic mice overexpressing the full-length neurotrophin receptor TrkC exhibit increased catecholaminergic neuron density in specific brain areas and increased anxiety-like behavior and panic reaction

Dierssen

Gratacòs

Sahún

et al. 2006

Neurobiology of Disease

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“…Finally, we included data from the primary PD linkage analysis published by the Iowa group. 23 Characteristics of these three samples are also listed in Table 1. We were unable to obtain data from one other primary ANX linkage scan.…”

Section: Data Sources Samples and Measuresmentioning

confidence: 99%

Meta-analyses of genome-wide linkage scans of anxiety-related phenotypes

et al. 2012

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Genetic factors underlying trait neuroticism, reflecting a tendency towards negative affective states, may overlap genetic susceptibility for anxiety disorders and help explain the extensive comorbidity amongst internalizing disorders. Genome-wide linkage (GWL) data from several studies of neuroticism and anxiety disorders have been published, providing an opportunity to test such hypotheses and identify genomic regions that harbor genes common to these phenotypes. In all, 11 independent GWL studies of either neuroticism (n ¼ 8) or anxiety disorders (n ¼ 3) were collected, which comprised of 5341 families with 15 529 individuals. The rank-based genome scan meta-analysis (GSMA) approach was used to analyze each trait separately and combined, and global correlations between results were examined. False discovery rate (FDR) analysis was performed to test for enrichment of significant effects. Using 10 cM intervals, bins nominally significant for both GSMA statistics, P SR and P OR , were found on chromosomes 9, 11, 12, and 14 for neuroticism and on chromosomes 1, 5, 15, and 16 for anxiety disorders. Genome-wide, the results for the two phenotypes were significantly correlated, and a combined analysis identified additional nominally significant bins. Although none reached genome-wide significance, an excess of significant P SR P-values were observed, with 12 bins falling under a FDR threshold of 0.50. As demonstrated by our identification of multiple, consistent signals across the genome, meta-analytically combining existing GWL data is a valuable approach to narrowing down regions relevant for anxiety-related phenotypes. This may prove useful for prioritizing emerging genome-wide association data for anxiety disorders.

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Genomewide survey of panic disorder

Cited by 88 publications

References 28 publications

Linkage on chromosome 14 in a genome-wide linkage study of a broad anxiety phenotype

Linkage on chromosome 14 in a genome-wide linkage study of a broad anxiety phenotype

Transgenic mice overexpressing the full-length neurotrophin receptor TrkC exhibit increased catecholaminergic neuron density in specific brain areas and increased anxiety-like behavior and panic reaction

Meta-analyses of genome-wide linkage scans of anxiety-related phenotypes

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