Latent Variables Quantifying Neighborhood Characteristics and Their Associations with Poor Mental Health

Neighborhood characteristics can have profound impacts on resident mental health, but the wide variability in methodologies used across studies makes it difficult to reach a consensus as to the implications of these impacts. The aim of this study was to simplify the assessment of neighborhood influence on mental health. We used a factor analysis approach to reduce the multi-dimensional assessment of a neighborhood using census tracts and demographic data available from the American Community Survey (ACS). Multivariate quantitative characterization of the neighborhood was derived by performing a factor analysis on the 2011–2015 ACS data. The utility of the latent variables was examined by determining the association of these factors with poor mental health measures from the 500 Cities Project 2014–2015 data (2017 release). A five-factor model provided the best fit for the data. Each factor represents a complex multi-dimensional construct. However, based on heuristics and for simplicity we refer to them as (1) Affluence, (2) Singletons in Tract, (3) African Americans in Tract, (4) Seniors in Tract, and (5) Hispanics or Latinos in Tract. African Americans in Tract (with loadings showing larger numbers of people who are black, single moms, and unemployed along with fewer people who are white) and Affluence (with loadings showing higher income, education, and home value) were strongly associated with poor mental health (R2=0.67, R2=0.83). These findings demonstrate the utility of this factor model for future research focused on the relationship between neighborhood characteristics and resident mental health

A Bayesian computational model reveals a failure to adapt interoceptive precision estimates across depression, anxiety, eating, and substance use disorders.

Recent neurocomputational theories have hypothesized that abnormalities in prior beliefs and/or the precision-weighting of afferent interoceptive signals may facilitate the transdiagnostic emergence of psychopathology. Specifically, it has been suggested that, in certain psychiatric disorders, interoceptive processing mechanisms either over-weight prior beliefs or under-weight signals from the viscera (or both), leading to a failure to accurately update beliefs about the body. However, this has not been directly tested empirically. To evaluate the potential roles of prior beliefs and interoceptive precision in this context, we fit a Bayesian computational model to behavior in a transdiagnostic patient sample during an interoceptive awareness (heartbeat tapping) task. Modelling revealed that, during an interoceptive perturbation condition (inspiratory breath-holding during heartbeat tapping), healthy individuals (N = 52) assigned greater precision to ascending cardiac signals than individuals with symptoms of anxiety (N = 15), depression (N = 69), co-morbid depression/anxiety (N = 153), substance use disorders (N = 131), and eating disorders (N = 14)-who failed to increase their precision estimates from resting levels. In contrast, we did not find strong evidence for differences in prior beliefs. These results provide the first empirical computational modeling evidence of a selective dysfunction in adaptive interoceptive processing in psychiatric conditions, and lay the groundwork for future studies examining how reduced interoceptive precision influences visceral regulation and interoceptively-guided decision-making

Functional magnetic resonance imaging data for the association between polygenic risk scores for neuroticism and reward-punishment processing.

Neuroticism as a personality trait represents a heritable risk for psychiatric disorders. The polygenic risk score for neuroticism (N-PRS) is used to study genetic vulnerability to neuroticism. The current data present the association of the genetic risk for neuroticism to neural reward-punishment processing using functional magnetic resonance imaging. N-PRS was computed based on the individuals genotype information and a genome-wide association study on the UK Biobank data. While individuals performed a monetary incentive delay task, their neural activations for upcoming incentives (reward: gain, punishment: loss) were measured in blood oxygen level dependent (BOLD) signals during the delay phase. Multivariate ANCOVAs were used to analyze BOLD signals for finding the association between N-PRS and reward-punishment processing by the incentive valence (Related research article: H. Park, K.L. Forthman, R. Kuplicki, T.A. Victor, Tulsa 1000 Investigators, H.W. Yeh, W.K. Thompson, M.P. Paulus, Polygenic risk for neuroticism modulates response to gains and losses in the amygdala and caudate: evidence from a clinical cohort. J. Affect. Disord. 293 (2021) 124-132. https://doi.org/10.1016/j.jad.2021.06.016). These data can be used as reference data for future studies examining the role of the genetic propensity for personality traits in the context of psychiatric disorders

Polygenic risk for neuroticism moderates response to gains and losses in amygdala and caudate: Evidence from a clinical cohort

BackgroundNeuroticism is a heritable trait that contributes to the vulnerability to depression. We used polygenic risk scores (PRS) to examine genetic vulnerability to neuroticism and its associations with reward/punishment processing in a clinical sample with mood, anxiety, and substance use disorders. It was hypothesized that higher PRS for neuroticism is associated with attenuated neural responses to reward/punishment.MethodFour hundred sixty-nine participants were genotyped and their PRSs for neuroticism were computed. Associations between PRS for neuroticism and anticipatory processing of monetary incentives were examined using functional magnetic resonance imaging.ResultsIndividuals with higher PRS for neuroticism showed less anticipatory activation in the left amygdala and caudate region to incentives regardless of incentive valence. Further, these individuals exhibited altered sensitivity to gain/loss processing in the right anterior insula. Higher PRSs for neuroticism were also associated with reduced processing of gains in the precuneus.LimitationsThe study population consisted of a transdiagnostic sample with dysfunctions in positive and negative valence processing. PRS for neuroticism may be correlated with current clinical symptoms due to the vulnerability to psychiatric disorders.ConclusionsGreater genetic loading for neuroticism was associated with attenuated anticipatory responsiveness in reward/punishment processing with altered sensitivity to valences. Thus, a higher genetic risk for neuroticism may limit the degree to which positive and/or negative outcomes influence the current mood state, which may contribute to the development of positive and negative affective dysfunctions in individuals with mood, anxiety, and addictive disorders