Publications

Our lab members' publications are listed below.

Assistant Professor of Psychiatry and Behavioral Sciences (Child and Adolescent Psychiatry and Child Development)

Publications

  • A prospective study of social competence in survivors of pediatric brain and solid tumors. Pediatric blood & cancer Albee, M., Allende, S., Cosgrove, V., Hocking, M. C. 2022: e29670

    Abstract

    BACKGROUND/OBJECTIVES: Survivors of pediatric brain tumors are at increased risk for difficulties with social competence, including poor social information processing (SIP) and peer relationships. Improved survival rates heighten the need to better understand these challenges and if they are specific to survivors of pediatric brain tumors versus survivors of other childhood cancers.METHODS: Fifty-one survivors of pediatric brain tumors and 34 survivors of pediatric solid tumors completed evaluations of SIP and peer relationship quality within six months of completing treatment and one year later. Caregivers completed a measure of social skills. Linear mixed models evaluated differences between survivors of pediatric brain and solid tumors on SIP and social skills and how indices of SIP were associated with peer relationships over time.RESULTS: The two groups did not differ on indices of SIP or social skills over time. A three-way interaction between measures of SIP, group, and time predicted peer relationships. Survivors of pediatric solid tumors showed a positive association between baseline social skills and theory of mind and peer relationships over time, whereas survivors of pediatric brain tumors showed an inverse association between baseline social skills and theory of mind and peer relationships over time.CONCLUSION: Findings revealed unanticipated associations between baseline SIP and social skills and peer relationships over time among survivors of pediatric brain tumors. Additional research is needed to elucidate the factors most influential on peer relationships in this group to inform interventions.

    View details for DOI 10.1002/pbc.29670

    View details for PubMedID 35312152

  • Aberrant Neural Response to Social Exclusion Without Significantly Greater Distress in Youth With Bipolar Disorder: Preliminary Findings. Frontiers in psychiatry Roybal, D. J., Cosgrove, V. E., Kelley, R., Smallwood Shoukry, R., Larios, R. M., Novy, B., Chang, K. D., Garrett, A. S. 2022; 13: 687052

    Abstract

    Background: Little is known about the effects of social exclusion on youth with bipolar disorder (BD). Understanding these effects and the functional neural correlates of social exclusion in youth with BD may establish differences from healthy youth and help identify areas of intervention.Methods: We investigated brain function in 19 youth with BD and 14 age and gender matched healthy control (HC) participants while performing Cyberball, an fMRI social exclusion task. Whole brain activation, region-of-interest, and functional connectivity were compared between groups and examined with behavioral measures.Results: Compared with the HC group, youth with BD exhibited greater activation in the left fusiform gyrus (FFG) during social exclusion. Functional connectivity between the left FFG and the posterior cingulate/precuneus was significantly greater in the HC compared with the BD group. For the HC group only, age and subjective distress during Cyberball significantly predicted mean FFG activation. No significant differences in distress during social exclusion were found between groups.Conclusion: Although preliminary due to small sample size, these data suggest that youth with BD process social exclusion in a manner that focuses on basic visual information while healthy youth make use of past experiences to interpret current social encounters. This difference may account for the social cognitive issues experienced by youth with BD, which can lead to more severe anxiety and mood symptoms.

    View details for DOI 10.3389/fpsyt.2022.687052

    View details for PubMedID 35432046

  • Peripheral inflammatory biomarkers define biotypes of bipolar depression. Molecular psychiatry Lee, Y. n., Mansur, R. B., Brietzke, E. n., Kapogiannis, D. n., Delgado-Peraza, F. n., Boutilier, J. J., Chan, T. C., Carmona, N. E., Rosenblat, J. D., Lee, J. n., Maletic, V. n., Vinberg, M. n., Suppes, T. n., Goldstein, B. I., Ravindran, A. V., Taylor, V. H., Chawla, S. n., Nogueras-Ortiz, C. n., Cosgrove, V. E., Kramer, N. E., Ho, R. n., Raison, C. A., McIntyre, R. S. 2021

    Abstract

    We identified biologically relevant moderators of response to tumor necrosis factor (TNF)-α inhibitor, infliximab, among 60 individuals with bipolar depression. Data were derived from a 12-week, randomized, placebo-controlled clinical trial secondarily evaluating the efficacy of infliximab on a measure of anhedonia (i.e., Snaith-Hamilton Pleasure Scale). Three inflammatory biotypes were derived from peripheral cytokine measurements using an iterative, machine learning-based approach. Infliximab-randomized participants classified as biotype 3 exhibited lower baseline concentrations of pro- and anti-inflammatory cytokines and soluble TNF receptor-1 and reported greater pro-hedonic improvements, relative to those classified as biotype 1 or 2. Pretreatment biotypes also moderated changes in neuroinflammatory substrates relevant to infliximab's hypothesized mechanism of action. Neuronal origin-enriched extracellular vesicle (NEV) protein concentrations were reduced to two factors using principal axis factoring: phosphorylated nuclear factorκB (p-NFκB), Fas-associated death domain (p-FADD), and IκB kinase (p-IKKα/β) and TNF receptor-1 (TNFR1) comprised factor "NEV1," whereas phosphorylated insulin receptor substrate-1 (p-IRS1), p38 mitogen-activated protein kinase (p-p38), and c-Jun N-terminal kinase (p-JNK) constituted "NEV2". Among infliximab-randomized subjects classified as biotype 3, NEV1 scores were decreased at weeks 2 and 6 and increased at week 12, relative to baseline, and NEV2 scores increased over time. Decreases in NEV1 scores and increases in NEV2 scores were associated with greater reductions in anhedonic symptoms in our classification and regression tree model (r2 = 0.22, RMSE = 0.08). Our findings provide preliminary evidence supporting the hypothesis that the pro-hedonic effects of infliximab require modulation of multiple TNF-α signaling pathways, including NF-κB, IRS1, and MAPK.

    View details for DOI 10.1038/s41380-021-01051-y

    View details for PubMedID 33658605