The genetics of six neurotic disorders: a twin study. J Affect Disord

Clinical Research Unit for Anxiety Disorders, University of New South Wales, St. Vincent's Hospital, Sydney, Australia.
Journal of Affective Disorders (Impact Factor: 3.38). 06/1990; 19(1):23-9. DOI: 10.1016/0165-0327(90)90005-S
Source: PubMed


Persons who had met criteria for specific anxiety or depressive neuroses during their lifetime were identified from a sample of 446 pairs of adult twins. Although there was a genetic contribution to neuroticism and to symptoms, there was no inheritance of specific disorders. This concurs with previous work in a sample from the same Australian Twin Registry and with those from a Norwegian sample. It is concluded that while there is a genetic contribution to the predisposing trait, and therefore to the intermittent appearance of symptoms, this contribution is obscured by the grouping of symptoms into diagnoses and by the help seeking which is a prerequisite to clinical diagnosis.

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    • "Several twin studies of specific anxiety disorders have been conducted [18–21]. In most studies the concordance rates were higher for MZ twins than for DZ twins. "
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    ABSTRACT: To determine the prevalence of anxiety disorders in children with Williams syndrome (WS), their sibling closest in age, and their mothers and to examine the predictors of anxiety in these groups. The prevalence of anxiety disorders was assessed and compared to that in the general population. Children with WS had a significantly higher prevalence of specific phobia, generalized anxiety disorder (GAD), and separation anxiety in comparison to children in the general population. While mothers had a higher prevalence of GAD than population controls, the excess was accounted for by mothers who had onset after the birth of their WS child. The siblings had rates similar to the general population. This pattern of findings suggests the presence of a gene in the WS region whose deletion predisposes to anxiety disorders. It is also worthwhile to investigate relations between genes deleted in WS and genes previously implicated in anxiety disorders.
    Journal of Neurodevelopmental Disorders 03/2009; 1(1):4-14. DOI:10.1007/s11689-009-9003-1 · 3.27 Impact Factor
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    • "Findings from twin research suggest that genetics play a substantial role in the familial aggregation of PD [Hettema et al., 2001; Kendler et al., 1993, 1995, 2001; Perna et al., 1997; Scherrer et al., 2000; Silove et al., 1995; Skre et al., 1993]. The specific role of genetic factors in the etiology of PD remains, however, unclear, as some twin studies report only moderate or no heritability [Andrews et al., 1990; Kendler et al., 1993, 2001; Torgersen, 1983, 1990]. "
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    ABSTRACT: To examine the familial liability of panic disorder (PD) and agoraphobia (AG) in a community sample, namely the effect of parental PD and AG on the offspring's risk to develop either or both conditions in adolescence or adulthood. A representative community sample of N=3,021 adolescents and young adults aged 14-24 years at baseline was followed up over a period of 10 years in up to four waves. Family information was assessed by either direct interviews with at least one parent or by using subjects' family history information at either wave (N=3,014). Diagnoses and selected symptoms were assessed in both, parents and subjects, by using a standardized diagnostic interview (DSM-IV M-CIDI) with its respective family history module. (1) Parental panic attacks (PA), PD, and AG were all shown to be associated with an increased risk of offspring to also develop PA, PD, and AG. (2) Associations of parental PD were present irrespective of parental AG, whereas parental AG without PD was not associated with an increased offspring risk. (3) Outcome risk was particularly elevated in offspring of parents with PD+AG. (4) Parental PD or AG was not associated with an earlier age of onset of any syndrome in the offspring. We confirmed and expanded previous results from clinical samples that comorbid PD and AG aggregate in families. AG without PD is not familial, but it might enhance the familial transmission of PD.
    Depression and Anxiety 05/2008; 25(5):422-34. DOI:10.1002/da.20425 · 4.41 Impact Factor
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    • "contribution considered to be especially important in OCD patients with early onset of the disorder (Andrews et al., 1990; Torgersen, 1990; Pauls et al., 1995; Nestadt et al., 2000). The serotonergic system is thought to be dysregulated in OCD. "
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    ABSTRACT: The 5-HT(3) receptor is unique among the serotonin receptors in that it is a ligand-gated ion channel. Dysfunction of the serotonin system is thought to contribute to the pathogenesis of obsessive-compulsive disorder (OCD). Apart from the standard treatment with serotonin reuptake inhibitors and behavioural therapy, a 5-HT(3) receptor antagonist has recently been shown to benefit some OCD patients, suggesting the 5-HT(3) receptor as a serotonergic candidate gene in the polygenic aetiology of OCD. A functional regulatory variant of the 5-HT(3A) receptor influences 5-HT(3) receptor expression, serotonin metabolites in cerebrospinal fluid, and amygdala reactivity. We therefore assessed whether this C178T variant influences the risk of developing OCD. In a family-based approach employing the transmission disequilibrium test, we analysed a unique sample of 75 children and adolescents with OCD, as well as their biological parents. We found no evidence for a preferential transmission of either allele to the patients--the estimated transmission rate for the C allele was 0.51 (95% CI 0.36-0.65). This argues against an involvement of the 5-HT(3A) receptor in the polygenic aetiology of early-onset OCD.
    Journal of Psychopharmacology 12/2007; 21(8):833-6. DOI:10.1177/0269881106073560 · 3.59 Impact Factor
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