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BackgroundDepression is a significant problem and it is vital to understand its underlying causes and related policy implications. Neighborhood characteristics are implicated in depression but the nature of this association is unclear. Unobserved or unmeasured factors may confound the relationship. This study addresses confounding in a twin study investigating neighborhood-level effects on depression controlling for genetics, common environment, and gene×environment (G × E) interactions.MethodData on neighborhood deprivation and depression were gathered from 3155 monozygotic twin pairs and 1275 dizygotic pairs (65.7% female) between 2006 and 2013. The variance for both depression and neighborhood deprivation was decomposed into three components: additive genetic variance (A); shared environmental variance (C); and non-shared environmental variance (E). Depression was then regressed on neighborhood deprivation to test the direct association and whether that association was confounded. We also tested for a G × E interaction in which the heritability of depression was modified by the level of neighborhood deprivation.ResultsDepression and neighborhood deprivation showed evidence of significant A (21.8% and 15.9%, respectively) and C (13.9% and 32.7%, respectively) variance. Depression increased with increasing neighborhood deprivation across all twins (p = 0.009), but this regression was not significant after controlling for A and C variance common to both phenotypes (p = 0.615). The G × E model showed genetic influences on depression increasing with increasing neighborhood deprivation (p < 0.001).ConclusionsNeighborhood deprivation is an important contributor to depression via increasing the genetic risk. Modifiable pathways that link neighborhoods to depression have been proposed and should serve as targets for intervention and research. [ABSTRACT FROM AUTHOR]

BackgroundAssociations between parental depression and offspring affective and disruptive disorders are well documented. Few genetically informed studies have explored the processes underlying intergenerational associations.MethodA semi-structured interview assessing DSM-III-R psychiatric disorders was administered to twins (n=1296) from the Australian Twin Register (ATR), their spouses (n=1046) and offspring (n=2555). We used the Children of Twins (CoT) design to delineate the extent to which intergenerational associations were consistent with a causal influence or due to genetic confounds.ResultsIn between-family analyses, parental depression was associated significantly with offspring depression [hazard ratio (HR) 1.52, 95% confidence interval (CI) 1.20–1.93] and conduct disorder (CD; HR 2.27, CI 1.31–3.93). Survival analysis indicated that the intergenerational transmission of depression is consistent with a causal (environmental) inference, with a significant intergenerational association in offspring of discordant monozygotic (MZ) twin pairs (HR 1.39, CI 1.00–1.94). Logistic regression analysis suggested that the parental depression–offspring CD association was due to shared genetic liability in the parents and offspring. No intergenerational association was found when comparing the offspring of discordant MZ twins [odds ratio (OR) 1.41, CI 0.63–3.14], but offspring of discordant dizygotic (DZ) twins differed in their rates of CD (OR 2.53, CI 0.95–6.76). All findings remained after controlling for several measured covariates, including history of depression and CD in the twins' spouses.ConclusionsThe mechanisms underlying associations between parental depression and offspring psychopathology seem to differ depending on the outcome. The results are consistent with a causal environmental role of parental depression in offspring depression whereas common genetic factors account for the association of parental depression and offspring CD. [ABSTRACT FROM PUBLISHER]

Background: Several studies have identified discrete symptom dimensions in obsessive-compulsive disorder (OCD), derived from factor analyses of the individual items or symptom categories of the Yale-Brown Obsessive-Compulsive Scale Symptom Checklist (YBOCS-SC). This study aims to extend previous work on the relationship between obsessions and compulsions by specifically including mental compulsions and reassurance-seeking. Because these compulsions have traditionally been omitted from prior factor analytic studies, their association to what have been called "pure obsessions" may have been overlooked.Method: Participants (N = 201) were recruited from two multi-site randomized clinical treatment trials for OCD. The YBOCS-SC was used to assess OCD symptoms, as it includes a comprehensive list of obsessions and compulsions, arranged by content category. Each category was given a score based on whether symptoms were present and if the symptom was a primary target of clinical concern, and a factor analysis was conducted. Mental compulsions and reassurance-seeking were considered separate categories for the analysis.Results: Using an orthogonal geomin rotation of 16 YBOCS-SC categories/items, we found a five-factor solution that explained 67% of the total variance. Inspection of items that composed each factor suggests five familiar constructs, with mental compulsions and reassurance-seeking included with sexual, aggressive, and religious obsessions (unacceptable/taboo thoughts).Conclusions: This study suggests that the concept of the "pure obsessional" (e.g., patients with unacceptable/taboo thoughts yet no compulsions) may be a misnomer, as these obsessions were factorially associated with mental compulsions and reassurance-seeking in these samples. These findings may have implications for DSM-5 diagnostic criteria. [ABSTRACT FROM AUTHOR]

Most of the methods of quantifying cortical atrophy that have been proposed involve the estimation of the volume of enlarged sulci in the cerebral cortex. The authors propose that the surface area of the sulci is a more valid measure of cortical atrophy, and describe a system for measuring the surface area of the cortex, and present data in support of the method's reliability and validity. [ABSTRACT FROM AUTHOR]

Presents the amplification of SGLT1 complementary DNA and genomic DNA from members of a family affected with glucose/galactose malabsorption (GGM). Sequence analysis reveals a single missense mutation in SGLT1 which cosegregates with the GGM phenotype and results in a complete loss of Na+-dependent glucose transport in `Xenopus' oocytes.