Different learning aberrations relate to delusion-like beliefs with different contents.

The prediction error account of delusions has had success. However, its explanation of delusions with different contents has been lacking. Persecutory delusions and paranoia are the common unfounded beliefs that others have harmful intentions towards us. Other delusions include believing that one's thoughts or actions are under external control or that events in the world have specific personal meaning. We compare learning in two different cognitive tasks, probabilistic reversal learning and Kamin blocking, that have relationships to paranoid and non-paranoid delusion-like beliefs, respectively. We find that clinical high-risk status alone does not result in different behavioural results in the probabilistic reversal learning task but that an individual's level of paranoia is associated with excessive switching behaviour. During the Kamin blocking task, paranoid individuals learned inappropriately about the blocked cue. However, they also had decreased learning about the control cue, suggesting more general learning impairments. Non-paranoid delusion-like belief conviction (but not paranoia) was associated with aberrant learning about the blocked cue but intact learning about the control cue, suggesting specific impairments in learning related to cue combination. We fit task-specific computational models separately to behavioural data to explore how latent parameters vary within individuals between tasks and how they can explain symptom-specific effects. We find that paranoia is associated with low learning rates in the probabilistic reversal learning task and the blocking task. Non-paranoid delusion-like belief conviction is instead related to parameters controlling the degree and direction of similarity between cue updating during simultaneous cue presentation. These results suggest that paranoia and other delusion-like beliefs involve dissociable deficits in learning and belief updating, which, given the transdiagnostic status of paranoia, might have differential utility in predicting psychosis.

In vivo structural connectivity of the reward system along the hippocampal long axis.

Recent work has identified a critical role for the hippocampus in reward-sensitive behaviors, including motivated memory, reinforcement learning, and decision-making. Animal histology and human functional neuroimaging have shown that brain regions involved in reward processing and motivation are more interconnected with the ventral/anterior hippocampus. However, direct evidence examining gradients of structural connectivity between reward regions and the hippocampus in humans is lacking. The present study used diffusion MRI (dMRI) and probabilistic tractography to quantify the structural connectivity of the hippocampus with key reward processing regions in vivo. Using a large sample of subjects (N = 628) from the human connectome dMRI data release, we found that connectivity profiles with the hippocampus varied widely between different regions of the reward circuit. While the dopaminergic midbrain (ventral tegmental area) showed stronger connectivity with the anterior versus posterior hippocampus, the ventromedial prefrontal cortex showed stronger connectivity with the posterior hippocampus. The limbic (ventral) striatum demonstrated a more homogeneous connectivity profile along the hippocampal long axis. This is the first study to generate a probabilistic atlas of the hippocampal structural connectivity with reward-related networks, which is essential to investigating how these circuits contribute to normative adaptive behavior and maladaptive behaviors in psychiatric illness. These findings describe nuanced structural connectivity that sets the foundation to better understand how the hippocampus influences reward-guided behavior in humans.

Prenatal maternal Inflammation, childhood cognition and adolescent depressive symptoms.

BACKGROUND: Accumulating evidence indicates that higher prenatal maternal inflammation is associated with increased depression risk in adolescent and adult-aged offspring. Prenatal maternal inflammation (PNMI) may increase the likelihood for offspring to have lower cognitive performance, which, in turn, may heighten risk for depression onset. Therefore, this study explored the potential mediating role of childhood cognitive performance in the relationship between PNMI and adolescent depressive symptoms in offspring. METHODS: Participants included 696 mother-offspring dyads from the Child Health and Development Studies (CHDS) cohort. Biomarkers of maternal inflammation [interleukin (IL)-6, IL-8, IL-1 receptor antagonist (IL-1RA) and soluble TNF receptor-II (sTNF-RII)] were assayed from first (T1) and second trimester (T2) sera. Childhood (ages 9-11) cognitive performance was assessed via standardized Peabody Picture Vocabulary Test (PPVT), a measure of receptive vocabulary correlated with general intelligence. Adolescent (ages 15-17) depressive symptoms were assessed via self-report. RESULTS: There were no significant associations between T1 biomarkers and childhood PPVT or adolescent depressive symptoms. Higher T2 IL1-RA was directly associated with lower childhood PPVT (b = -0.21, SE = 0.08, t = -2.55, p = 0.01), but not with adolescent depressive symptoms. T2 IL-6 was not directly associated with childhood PPVT, but higher T2 IL-6 was directly associated at borderline significance with greater depressive symptoms in adolescence (b = 0.05, SE = 0.03, t = 1.96, p = 0.05). Lower childhood PPVT predicted significantly higher adolescent depressive symptoms (b = -0.07, SE = 0.02, t = -2.99, p < 0.01). There was a significant indirect effect of T2 IL-1RA on adolescent depressive symptoms via childhood PPVT (b = 0.03, 95 % CI = 0.002-0.03) indicating a partially mediated effect. No significant associations were found with T2 sTNF-RII nor IL-8. CONCLUSIONS: Lower childhood cognitive performance, such as that indicated by a lower PPVT score, represents a potential mechanism through which prenatal maternal inflammation contributes to adolescent depression risk in offspring.

Childhood trauma, perceived stress and anhedonia in individuals at clinical high risk for psychosis: multigroup mediation analysis.

BACKGROUND: Evidence suggests that both childhood trauma and perceived stress are risk factors for the development of psychosis, as well as negative symptoms such as anhedonia. Previous findings link increases in perceived stress to anhedonia in individuals at clinical high risk for psychosis (CHR) and depression; however, the role of childhood trauma in this relationship has not yet been explored, despite consistent evidence that it is associated with sensitisation to later stress. AIMS: To examine whether perceived stress mediates the relationship between childhood trauma and anhedonia in a group of youth at CHR as well as in controls (groups with depression and with no diagnosed mental health concerns). METHOD: The study used multigroup mediation to examine the indirect effects of childhood trauma on anhedonia via perceived stress in CHR (n = 117) and depression groups (n = 284) and non-psychiatric controls (n = 124). RESULTS: Perceived stress mediated the relationship between childhood trauma and consummatory anhedonia regardless of group status. Perceived stress mediated the relationship between childhood trauma and anticipatory anhedonia for the CHR and depression groups, but not for non-psychiatric controls. Further, groups differed in the magnitude of this relationship, with the effects trending towards stronger for those in the CHR group. CONCLUSIONS: Our findings suggest a potential transdiagnostic pathway through which childhood trauma contributes to anhedonia across severe mental illness.

The reliability and validity of the revised Green et al. paranoid thoughts scale in individuals at clinical high-risk for psychosis.

INTRODUCTION: Paranoia is a common and impairing psychosis symptom, which exists along a severity continuum that extends into the general population. Individuals at clinical high-risk for psychosis (CHR) frequently experience paranoia and this may elevate their risk for developing full psychosis. Nonetheless, limited work has examined the efficient measurement of paranoia in CHR individuals. The present study aimed to validate an often-used self-report measure, the revised green paranoid thoughts scale (RGPTS), in this critical population. METHOD: Participants were CHR individuals (n = 103), mixed clinical controls (n = 80), and healthy controls (n = 71) who completed self-report and interview measures. Confirmatory factor analysis (CFA), psychometric indices, group differences, and relations to external measures were used to evaluate the reliability and validity of the RGPTS. RESULTS: CFA replicated a two-factor structure for the RGPTS and the associated reference and persecution scales were reliable. CHR individuals scored significantly higher on both reference and persecution, relative to both healthy (ds = 1.03, 0.86) and clinical controls (ds = 0.64, 0.73). In CHR participants, correlations between reference and persecution and external measures were smaller than expected, though showed evidence of discriminant validity (e.g., interviewer-rated paranoia, r = 0.24). When examined in the full sample, correlation magnitude was larger and follow-up analyses indicated that reference related most specifically to paranoia (ß = 0.32), whereas persecution uniquely related to poor social functioning (ß = -0.29). CONCLUSION: These results demonstrate the reliability and validity of the RGPTS, though its scales related more weakly to severity in CHR individuals. The RGPTS may be useful in future work aiming to develop symptom-specific models of emerging paranoia in CHR individuals.

VTA and Anterior Hippocampus Target Dissociable Neocortical Networks for Post-Novelty Enhancements.

The detection of novelty indicates changes in the environment and the need to update existing representations. In response to novelty, interactions across the VTA-hippocampal circuit support experience-dependent plasticity in the hippocampus. While theories have broadly suggested plasticity-related changes are also instantiated in the cortex, research has also shown evidence for functional heterogeneity in cortical networks. It therefore remains unclear how the hippocampal-VTA circuit engages cortical networks, and whether novelty targets specific cortical regions or diffuse, large-scale cortical networks. To adjudicate the role of the VTA and hippocampus in cortical network plasticity, we used fMRI to compare resting-state functional coupling before and following exposure to novel scene images in human subjects of both sexes. Functional coupling between right anterior hippocampus and VTA was enhanced following novelty exposure. However, we also found evidence for a double dissociation, with anterior hippocampus and VTA showing distinct patterns of post-novelty functional coupling enhancements, targeting task-relevant regions versus large-scale networks, respectively. Further, significant correlations between these networks and the novelty-related plasticity in the anterior hippocampal-VTA functional network suggest that the central hippocampal-VTA network may facilitate the interactions with the cortex. These findings support an extended model of novelty-induced plasticity, in which novelty elicits plasticity-related changes in both local and global cortical networks.SIGNIFICANCE STATEMENT Novelty detection is critical for adaptive behavior, signaling the need to update existing representations. By engaging the bidirectional hippocampal-VTA circuit, novelty has been shown to induce plasticity-related changes in the hippocampus. However, it remains an open question how novelty targets such plasticity-related changes in cortical networks. We show that anterior hippocampus and VTA target cortical networks at different spatial scales, with respective enhancements in post-novelty functional coupling with a task-relevant cortical region and a large-scale memory network. The results presented here support an extended model of novelty-related plasticity, in which engaging the anterior hippocampal-VTA circuit through novelty exposure propagates cortical plasticity through hippocampal and VTA functional pathways at distinct scales, targeting specific or diffuse cortical networks.

The longitudinal associations of inflammatory biomarkers and depression revisited: systematic review, meta-analysis, and meta-regression.

The innate immune system is dysregulated in depression; however, less is known about the longitudinal associations of depression and inflammatory biomarkers. We investigated the prospective associations of depression and inflammatory biomarkers [interleukin-6 (IL-6), Tumor Necrosis Factor-Alpha (TNF-α), and C-reactive protein (CRP)] in community samples, both unadjusted and adjusted for covariates. The review, registered with PROSPERO, searched for published and unpublished studies via MEDLINE/PsycINFO/PsycARTICLES/EMBASE/Proquest Dissertation. Standardized Fisher transformations of the correlation/beta coefficients, both unadjusted and adjusted for covariates, were extracted from studies examining the prospective associations of depression and inflammatory biomarkers. Systematic review conducted in January, 2019 included 38 studies representing 58,256 participants, with up to 27 studies included in random-effects meta-analysis. Higher CRP/IL-6 were associated with future depressive symptoms, and higher depressive symptoms were associated with higher future CRP/IL-6 in both unadjusted and adjusted analyses - this is the first meta-analysis reporting an adjusted association of IL-6 with future depression. The adjusted prospective associations of depression with CRP/CRP with depression were substantially attenuated and small in magnitude. No significant associations were observed for TNF-α. No conclusive results were observed in studies of clinical depression. Meta-regression indicated that the association of CRP and future depression was larger in older samples and in studies not controlling for possible infection. Small, prospective associations of depression and inflammatory biomarkers are observed in both directions, particularly for IL-6; however, the strength and importance of this relationship is likely obscured by the heterogeneity in depression and profound study/methodological differences. Implications for future studies are discussed.

Concurrent and Longitudinal Associations of Sex and Race with Inflammatory Biomarkers during Adolescence.

Chronic, systemic inflammation is implicated in physical and mental health; little is known about whether sex and racial differences detected in adulthood are observed during adolescence or about normative changes occurring during adolescence. This longitudinal, United States-based study examined four biomarkers of systemic inflammation [C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and IL-8) in 315 adolescents (51% female; 58% black; baseline age = 16.49 years (SD = 1.56; range: 12.14-21.28)] at three timepoints. Notable results included: general decline in inflammatory biomarkers in older adolescents, lower levels of TNF-α/IL-8 in black adolescents, elevated CRP/IL-6 in females, and especially higher levels of IL-6 in black, female adolescents. Implications are discussed, particularly the potential health implications of elevated IL-6 in black females.

Executive dysfunction in depression in adolescence: the role of inflammation and higher body mass.

BACKGROUND: There is substantial evidence that many depressed individuals experience impaired executive functioning. Understanding the causes of executive dysfunction in depression is clinically important because cognitive impairment is a substantial contributor to functional impairment. This study investigated whether elevated levels of an inflammatory cytokine [interleukin-6 (IL-6)] and/or higher body mass index (BMI) concurrently and/or prospectively accounted for the relationship between depressive symptoms and impaired executive functioning in adolescents. METHODS: A diverse, community sample of adolescents (N = 288; mean age = 16.33; 51.4% female; 59.0% African-American) completed assessments of height and weight, IL-6, depressive symptoms, and self-report/behavioral measures of executive functioning (selective attention, switching attention) and future orientation annually over 3 years. Adolescents experiencing acute illness or medical conditions that affect inflammation were excluded from analyses. Path analysis within a structural equation modeling framework simultaneously examined the concurrent and prospective relationships between BMI, IL-6, depressive symptoms, and the measures of cognitive functioning across three timepoints. RESULTS: Across all timepoints, higher BMI was prospectively associated with higher levels of IL-6 and depressive symptoms, while higher levels of IL-6 were associated with worse performance on three behavioral and self-report measures of cognitive functioning. Higher depressive symptoms also were prospectively associated with elevated IL-6 and both higher depressive symptoms and a higher BMI predicted worse future executive functioning via increased IL-6. CONCLUSIONS: More severe depressive symptoms and increased BMI may disrupt executive functioning via elevated IL-6.

Longitudinal changes of inflammatory biomarkers moderate the relationship between recent stressful life events and prospective symptoms of depression in a diverse sample of urban adolescents.

This study investigated whether longitudinal changes in inflammatory physiology moderated the relationship between recent stressful life events and subsequent depressive symptoms in adolescence. A diverse sample of adolescents representative of an urban community (N = 129; Age at baseline = 12.5 years; 48.8% female; 55.0% African American) completed measures of stressful life events, depressive symptoms, and two annual blood draws (BD1 and BD2). Controlling for inflammatory activity at BD1, depression at BD1, demographics and the time between assessments, increases in interleukin-6 (IL-6; b = 0.878, p = .007) and C-reactive protein (CRP; b = 0.252, p = .024) from BD1 to BD2 interacted with recent stressful life events before BD1 to predict severity of depressive symptoms at BD2. Similar associations were evident for IL-6 (b = 2.074, p = .040) and CRP (b = 0.919, p = .050) when considering acute stressful life events that had occurred within the two weeks before the first blood collection. More frequent stressful life events before BD1 predicted significantly more severe depressive symptoms at BD2, but only for adolescents with moderate (50th percentile) and high (84th percentile) levels of IL-6 and CRP at BD2. In conclusion, adolescents who experienced both recent stressful life events and larger increases in inflammatory activity following these stressors were at increased risk for more severe depressive symptoms after approximately one year. The findings indicate that the interaction of stress and larger changes in inflammatory activity following these stressors are prognostic risk factors for depression severity in adolescents.

Pubertal Status and Age are Differentially Associated with Inflammatory Biomarkers in Female and Male Adolescents.

A better understanding of the maturational correlates of inflammatory activity during adolescence is needed to more appropriately study both normal and abnormal development. Inflammation is the immune system's first response to infection, injury, or psychological stress, and it has been shown to be elevated in individuals with both physical and psychological conditions. This study examined unique associations between (1) pubertal status and inflammatory biomarkers, and (2) age and inflammatory biomarkers, and whether these relationships differed by sex in a diverse sample of 155 adolescents (54.2% female, 45.8% male; Mage = 16.22) from a northeastern city in the US. A more advanced pubertal status was uniquely associated with lower levels of tumor necrosis factor alpha (TNF-α) and interleukin-8 (IL-8). Chronological age was uniquely associated with lower IL-8 levels. The association between pubertal status and C-reactive protein (CRP) levels differed by sex: more mature females had higher CRP, whereas pubertal status and CRP were not significantly associated in males. These findings highlight an important relation between pubertal development and inflammatory activity during adolescence.

Reward Sensitivity, Cognitive Response Style, and Inflammatory Response to an Acute Stressor in Adolescents.

Inflammation is gaining support as a biological mediator between stress and many negative outcomes that have heightened risk during adolescence (e.g., mood disorders). Thus, an important line of inquiry is evaluating whether risk factors for mood psychopathology also are associated with heightened inflammatory responses to stress during this developmental period. Two prominent risk factors that interact to predict mood psychopathology are reward sensitivity and perseverative cognitive response styles, which also have been associated with heightened inflammatory proteins. These factors could influence inflammation by synergistically amplifying stress reactivity. Ninety-nine late adolescents (Mage = 18.3 years, range = 15.6-21.9 years) completed measures of reward sensitivity, cognitive response style, and blood draws before and 60-min after a modified Trier Social Stress Task to determine levels of inflammation. Higher reward drive interacted with more perseverative response style ratios (rumination relative to distraction + problem-solving) to predict larger increases in interleukin-6 (a proinflammatory protein). Follow-up analyses found that reward drive interacted with all three components of the ratio to predict change in interleukin-6. Thus, these results suggest that high reward drive and perseverative cognitive response styles are associated with increased inflammatory response to social stress in adolescents, a potential physiological mechanism linking these risk factors to mood psychopathology during this developmental period.

Prenatal Maternal Stress and the Cascade of Risk to Schizophrenia Spectrum Disorders in Offspring.

PURPOSE OF REVIEW: Disruptions in fetal development (via genetic and environmental pathways) have been consistently associated with risk for schizophrenia in a variety of studies. Although multiple obstetric complications (OCs) have been linked to schizophrenia, this review will discuss emerging evidence supporting the role of prenatal maternal stress (PNMS) in the etiology of schizophrenia spectrum disorders (SSD). In addition, findings linking PNMS to intermediate phenotypes of the disorder, such as OCs and premorbid cognitive, behavioral, and motor deficits, will be reviewed. Maternal immune and endocrine dysregulation will also be explored as potential mechanisms by which PNMS confers risk for SSD. RECENT FINDINGS: PNMS has been linked to offspring SSD; however, findings are mixed due to inconsistent and retrospective assessments of PNMS and lack of specificity about SSD outcomes. PNMS is also associated with various intermediate phenotypes of SSD (e.g., prenatal infection/inflammation, decreased fetal growth, hypoxia-related OCs). Recent studies continue to elucidate the impact of PNMS while considering the moderating roles of fetal sex and stress timing, but it is still unclear which aspects of PNMS (e.g., type, timing) confer risk for SSD specifically. PNMS increases risk for SSD, but only in a small portion of fetuses exposed to PNMS. Fetal sex, genetics, and other environmental factors, as well as additional pre- and postnatal insults, likely contribute to the PNMS-SSD association. Longitudinal birth cohort studies are needed to prospectively illuminate the mechanisms that account for the variability in outcomes following PNMS.

Immunocognitive Model of Depression Secondary to Anxiety in Adolescents.

There is evidence that anxiety precedes the onset of depression and that rumination contributes to this risk pathway in adolescence. This study examined inflammatory biomarkers as mediators in a risk model of depressive symptoms secondary to anxiety symptoms among adolescents who ruminate. A sample of 140 adolescents (52% female, 54% African American, 40% Caucasian, 6% biracial, mean age at T1 = 16.5 years, SD = 1.2 years) provided blood samples on two visits (T1 and T2; mean time between T1 and T2 = 13.5 months, SD = 5.9 months). Self-report anxiety, depression, and rumination measures were given at T1 and the depression measure was given again at a third visit (T3, mean months since T1 = 26.0 months, SD = 9.0 months). Higher anxiety predicted more interleukin-6, but not more C-reactive protein, for adolescents with high levels of rumination. Moderated mediation analyses (N for analysis after removing cases with missing data and outliers = 86) indicated that interleukin-6, but not C-reactive protein, at T2 mediated the relationship between anxiety symptoms at T1 and depressive symptoms at T3, conditional on rumination. Anxiety and rumination interacted such that, as rumination increased, anxiety predicted greater inflammation and depressive symptoms. These results demonstrate that established cognitive vulnerabilities for the development of depressive symptoms secondary to anxiety symptoms in adolescence might indirectly operate though biological mechanisms such as inflammation. In addition to highlighting risk factors and potential treatment targets for depression, this study suggests a potential biological mechanism underlying the effects of psychotherapies that reduce rumination on negative affect (e.g., cognitive behavioral therapy).

Attenuated Positive Psychotic Symptoms in Relation to Cigarette Smoking in a Nonclinical Population.

INTRODUCTION: This study explored the association between cigarette smoking and attenuated positive psychotic symptoms in a young adult nonclinical sample. METHODS: Undergraduates (N = 930), aged 18-35 years (26.3% male), completed a battery of self-report measures assessing subthreshold psychotic symptoms, cigarette smoking behavior/dependence, and drug use. RESULTS: Individuals endorsing a greater number of attenuated positive psychotic symptoms were more likely to be smokers. Exploratory analyses indicated that the odds of being a smoker were two times greater for those at potential higher risk for psychosis compared with individuals at lower risk. Results were consistent after adjusting for sex and other drug use. CONCLUSIONS: In line with findings from psychotic populations, results suggest that attenuated positive psychotic symptoms, particularly those endorsed as distressing in a nonclinical, undergraduate population, are related to cigarette smoking. IMPLICATIONS: Even in nonclinical, undergraduate populations, subthreshold psychotic symptoms are related to cigarette smoking, and cigarette smokers are twice as likely to be considered at potentially higher risk for psychosis compared with noncigarette smokers. In summary, there may be a threshold whereby psychotic symptoms confer increased risk for nicotine consumption, with endorsement of a greater number of distressing subthreshold psychotic symptoms increasing the likelihood of cigarette use.

Racial discrimination is associated with distressing subthreshold positive psychotic symptoms among US urban ethnic minority young adults.

BACKGROUND: Racial discrimination is related to depression, anxiety, and severe psychological distress, and evidence drawn from studies emanating from the United Kingdom and The Netherlands suggest racial discrimination is also related to clinical psychosis and subthreshold psychotic symptoms in racial and ethnic minority (REM) populations. The present study sought to determine the association between racial discrimination experiences and attenuated positive psychotic symptoms (APPS) in a United States (US) urban, predominantly immigrant and REM young adult population. METHODS: A cohort of 650 young adults was administered a self-report inventory for psychosis risk [i.e., Prodromal Questionnaire (PQ)], and the Experiences of Discrimination Questionnaire. The PQ allowed the dimensional assessment of APPS, as well as the categorical assessment of a potentially "high risk" group (i.e., 8 or more APPS endorsed as distressing), the latter of which was based on previous validation studies using the structured interview for prodromal syndromes. The relations between self-reported racial discrimination and APPS, and racial discrimination and "high" distressing positive PQ endorsement were determined, while accounting for anxiety and depression symptoms. RESULTS: Racial discrimination was significantly associated with APPS and with significantly higher odds of endorsing eight or more distressing APPS, even after adjusting for anxiety and depression symptoms. CONCLUSION: The present study provides preliminary evidence that racial discrimination among US ethnic minorities may be associated with APPS, as well as potentially higher risk for psychosis.

Mechanisms mediating ethnoracial discrimination and suspiciousness in Asian, Black, and Hispanic United States college students.

BACKGROUND: Despite the robust relationship between ethnoracial discrimination and positive psychotic-like experiences (PLEs) like subclinical suspiciousness in adulthood, the underlying mechanisms remain underexamined. Investigating the mechanisms previously implicated in trauma and positive PLEs - including negative-self schemas, negative-other schemas, perceived stress, dissociative experiences, and external locus of control - may inform whether ethnoracial discrimination has similar or distinct effects from other social stressors. METHOD: We examined the indirect effects of experiences of discrimination (EOD) to suspicious PLEs and total positive PLEs through negative-self schemas, negative-other schemas, perceived stress, dissociative experiences, and external locus of control in Asian (nAsian = 268), Black (nBlack = 301), and Hispanic (nHispanic = 129) United States college students. RESULTS: Among Asian participants, results indicated a significant indirect effect of EOD to suspicious PLEs and EOD to positive PLEs via perceived stress, and EOD to positive PLEs via negative-self schemas. Among Hispanic participants, results indicated a significant indirect effect of EOD to suspicious PLEs and EOD to positive PLEs via dissociative experiences. No mechanisms appeared significant in Black participants nor were any significant direct effects observed across models, despite them reporting significantly greater experiences of ethnoracial discrimination. CONCLUSIONS: Our findings suggest some shared but potentially distinct mechanisms contribute to increased suspicious PLEs and positive PLEs in Asian, Black, and Hispanic college students, with results differing by group, compared to the mechanisms underlying trauma and positive PLEs, with implications for the treatment of PLEs in college students exposed to ethnoracial discrimination.

Mapping Psychosis Risk States onto the Hierarchical Taxonomy of Psychopathology Using Hierarchical Symptom Dimensions.

Clinical high risk for psychosis (CHR) is a transdiagnostic risk state. However, it is unclear how risk states such as CHR fit within broad transdiagnostic models such as the Hierarchical Taxonomy of Psychopathology (HiTOP). In this study, a hierarchical dimensional symptom structure was defined by unfolding factor analysis of self-report data from 3,460 young adults (mage=20.3). A subsample (n=436) completed clinical interviews, 85 of whom met CHR criteria. Regression models examined relationships between symptom dimensions, CHR status, and clinician-rated symptoms. CHR status was best explained by a reality distortion dimension, with contributions from internalizing dimensions. Positive and negative attenuated psychotic symptoms were best explained by multiple psychotic and nonpsychotic symptom dimensions including reality distortion, distress, fear, detachment, and mania. Attenuated psychotic symptoms are a complex presenting problem warranting comprehensive assessment. HiTOP can provide both diagnostic precision and broad transdiagnostic coverage, making it a valuable resource for use with at-risk individuals.

Factors impacting intent to seek treatment within youth at clinical high risk for psychosis.

Existing work indicates that there is unmet need for care in those at clinical high risk (CHR) for psychosis. However, research on the factors that drive treatment seeking behaviors in this population is limited. Further, it is unknown how help-seeking behavior in CHR individuals compares to those seen in mood disorders, who have a higher rate of treatment seeking behavior. Participants (n = 559) completed an assessment of their intent to seek mental health treatment, attenuated psychosis-risk symptoms, and psychiatric symptoms and diagnoses. Participants were divided into CHR (n = 91), Mood Disorders (MD) (n = 72), or Community Controls (CC) groups (n = 396), whose intent to seek treatment was compared. Associations between intent to seek treatment with past treatment, depression, anxiety, positive and negative symptoms, distress from symptoms, intelligence quotient (IQ) estimates, and insight were assessed in CHR individuals. Further, it was assessed how this differs for the MD group. The MD group reported higher intent to seek treatment than CHR individuals, which reported higher intent to seek treatment than the CC group. In those at CHR, previous treatment, greater depression and anxiety severity, and higher distress all independently predicted higher intent to seek treatment. Depression predicted intent to seek treatment in both MD and CHR individuals. Previous treatment predicted intent to seek treatment in those at CHR. Our findings suggest that depression and past treatment utilization are critical factors in increasing intent to seek treatment in those at CHR, potentially serving as important targets for engaging this population in treatment.