Jessica L. Jenness
University of Denver
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Featured researches published by Jessica L. Jenness.
Cognitive, Affective, & Behavioral Neuroscience | 2010
Françoise S. Maheu; Mary Dozier; Amanda E. Guyer; Darcy Mandell; Elizabeth Peloso; Kaitlin Poeth; Jessica L. Jenness; Jennifer Y. F. Lau; John P. Ackerman; Daniel S. Pine; Monique Ernst
Previous research findings have linked caregiver deprivation and emotional neglect with sensitivity to threatening cues. The present preliminary study investigated whether dysfunctions of the medial temporal lobe could underlie these associations. Using fMRI, we measured medial temporal lobe responses to emotional faces (angry, fearful, happy, neutral) among 30 youths. Eleven of the youths had a history of caregiver deprivation and emotional neglect. Attention states (i.e., attention to anger, fear, or physical attributes, or passive viewing) were systematically manipulated. Relative to comparison youths, youths with a history of caregiver deprivation and emotional neglect showed significantly greater left amygdala and left anterior hippocampus activation during the processing of threatening information. To our knowledge, these findings are the first to demonstrate altered medial temporal lobe function during the processing of threat cues in youths with a history of caregiver deprivation and emotional neglect.
Journal of the American Academy of Child and Adolescent Psychiatry | 2008
Jennifer Y. F. Lau; Shmuel Lissek; Eric E. Nelson; Yoon S. Lee; Roxann Roberson-Nay; Kaitlin Poeth; Jessica L. Jenness; Monique Ernst; Christian Grillon; Daniel S. Pine
OBJECTIVE Considerable research examines fear conditioning in adult anxiety disorders but few studies examine youths. Adult data suggest that anxiety disorders involve elevated fear but intact differential conditioning. We used a novel paradigm to assess fear conditioning in pediatric anxiety patients. METHOD Sixteen individuals with anxiety disorders and 38 healthy comparisons viewed two photographs of actresses displaying neutral expressions. One picture served as the conditioned stimulus (CS), paired with a fearful expression and a shrieking scream (CS+), whereas the other picture served as a CS unpaired with the aversive outcome (CS-). Conditioning was indexed by self-reported fear. Subjects participated in two visits involving conditioning and extinction trials. RESULTS Both groups developed greater fear of the CS+ relative to CS-. Higher fear levels collapsed across each CS characterized anxious relative to healthy subjects, but no significant interaction between group and stimulus type emerged. Fear levels at visit 1 predicted avoidance of visit 2. Fear levels to both CS types showed stability even after extinction. CONCLUSIONS Consistent with adult data, pediatric anxiety involves higher fear levels following conditioning but not greater differential conditioning. Extending these methods to neuroimaging studies may elucidate neural correlates of fear conditioning. Implications for exposure therapies are discussed.
Translational Psychiatry | 2011
Benjamin L. Hankin; Esther Nederhof; Caroline W. Oppenheimer; Jessica L. Jenness; Jami F. Young; John R. Z. Abela; Andrew Smolen; Johan Ormel; Albertine J. Oldehinkel
Positive affect has been implicated in the phenomenological experience of various psychiatric disorders, vulnerability to develop psychopathology and overall socio-emotional functioning. However, developmental influences that may contribute to positive affect have been understudied. Here, we studied youths’ 5-HTTLPR genotype and rearing environment (degree of positive and supportive parenting) to investigate the differential susceptibility hypothesis (DSH) that youth carrying short alleles of 5-HTTLPR would be more influenced and responsive to supportive and unsupportive parenting, and would exhibit higher and lower positive affect, respectively. Three independent studies tested this gene–environment interaction (GxE) in children and adolescents (age range 9–15 years; total N=1874). In study 1 (N=307; 54% girls), positive/supportive parenting was assessed via parent report, in study 2 (N=197; 58% girls) via coded observations of parent–child interactions in the laboratory and in study 3 (N=1370; 53% girls) via self report. Results from all the three studies showed that youth homozygous for the functional short allele of 5-HTTLPR were more responsive to parenting as environmental context in a ‘for better and worse’ manner. Specifically, the genetically susceptible youth (that is, S’S’ group) who experienced unsupportive, non-positive parenting exhibited low levels of positive affect, whereas higher levels of positive affect were reported by genetically susceptible youth under supportive and positive parenting conditions. These GxE findings are consistent with the DSH and may inform etiological models and interventions in developmental psychopathology focused on positive emotion, parenting and genetic susceptibility.
Journal of Clinical Psychology | 2009
Benjamin L. Hankin; Caroline W. Oppenheimer; Jessica L. Jenness; Andreas Barrocas; Benjamin G. Shapero; Jessica Goldband
Cognitive theories of depression have been shown to be potent predictors of future increases in depressive symptoms and disorder in children, adolescents, and adults. This article focuses on potential developmental origins of the main cognitive vulnerabilities, including dysfunctional attitudes, negative cognitive style, and rumination. We selectively review processes and factors that have been hypothesized to contribute to the emergence and stabilization of these cognitive risk factors. This review focuses on genetic factors, temperament, parents and peers as salient interpersonal influences, and stressful life events. We end with suggestions for future theory development and research. In particular, we emphasize the need for additional conceptual and empirical work integrating these disparate processes together into a coherent, developmental psychopathological model, and we highlight the coexistence of both stability and change in the development of cognitive vulnerabilities to depression across the lifespan.
Journal of Abnormal Psychology | 2015
Benjamin L. Hankin; Jami F. Young; John R. Z. Abela; Andrew Smolen; Jessica L. Jenness; Lauren D. Gulley; Jessica R. Technow; Andrea Barrocas Gottlieb; Joseph R. Cohen; Caroline W. Oppenheimer
Depression is a debilitating mental illness with clear developmental patterns from childhood through late adolescence. Here, we present data from the Gene Environment Mood (GEM) study, which used an accelerated longitudinal cohort design with youth (N = 665) starting in 3rd, 6th, and 9th grades, and a caretaker, who were recruited from the general community, and were then assessed repeatedly through semistructured diagnostic interviews every 6 months over 3 years (7 waves of data) to establish and then predict trajectories of depression from age 8 to 18. First, we demonstrated that overall prevalence rates of depression over time, by age, gender, and pubertal status, in the GEM study closely match those trajectories previously obtained in past developmental epidemiological research. Second, we tested whether a genetic vulnerability-stress model involving 5-HTTLPR and chronic peer stress was moderated by developmental factors. Results showed that older aged adolescents with SS/SL genotype, who experienced higher peer chronic stress over 3 years, were the most likely to be diagnosed with a depressive episode over time. Girls experiencing greater peer chronic stress were the most likely to develop depression. This study used repeated assessments of diagnostic interviewing in a moderately large sample of youth over 3 years to show that depression rates increase in middle to late adolescence, or postpubertally, and that the gender difference in depression emerges earlier in adolescence (age 12.5), or postpubertally. Additionally, genetically susceptible older adolescents who experience chronic peer stress were the most likely to become depressed over time.
International Journal of Behavioral Development | 2012
Jennifer Y. F. Lau; Amanda E. Guyer; Erin B. Tone; Jessica L. Jenness; Jessica M. Parrish; Daniel S. Pine; Eric E. Nelson
Peer rejection powerfully predicts adolescent anxiety. While cognitive differences influence anxious responses to social feedback, little is known about neural contributions. Twelve anxious and twelve age-, gender- and IQ-matched, psychiatrically healthy adolescents received “not interested” and “interested” feedback from unknown peers during a chat room task administered in a neuroimaging scanner. No group differences emerged in subjective ratings to peer feedback, but all participants reported more negative emotion at being rejected (than accepted) by peers to whom they had assigned high-desirability ratings. Further highlighting the salience of such feedback, all adolescents, independently of anxiety levels, manifested elevated responses in the amygdala-hippocampal complex bilaterally, during the anticipation of feedback. However, anxious adolescents differed from healthy adolescents in their patterns of persistent amygdala-hippocampal activation following rejection. These data carry interesting implications for using neuroimaging data to inform psychotherapeutic approaches to social anxiety.
Journal of Clinical Child and Adolescent Psychology | 2011
Benjamin L. Hankin; Jessica L. Jenness; John R. Z. Abela; Andrew Smolen
5-HTTLPR, episodic stressors, depressive and anxious symptoms were assessed prospectively (child and parent report) every 3 months over 1 year (5 waves of data) among community youth ages 9 to 15 (n = 220). Lagged hierarchical linear modeling analyses showed 5-HTTLPR interacted with idiographic stressors (increases relative to the childs own average level over time), but not nomothetic stressors (higher stress exposure relative to the sample), to predict prospective elevations in depressive, but not anxious, symptoms. Youth with copies of the S or LG alleles of 5-HTTLPR, who experienced more stressors relative to their typical level, exhibited prospective increases in depressive symptoms over time. These findings suggest that 5-HTTLPR confers susceptibility to depression via stress reactivity.
Frontiers in Psychiatry | 2011
Benjamin L. Hankin; Andrea L. Barrocas; Jessica L. Jenness; Caroline W. Oppenheimer; Lisa S. Badanes; John R. Z. Abela; Jami F. Young; Andrew Smolen
This study provides the first genetic association examination of borderline personality disorder (BPD) traits in children and adolescents (ages 9–15) using two independent samples of youth recruited from the general community. We tested the a priori hypothesis that the serotonin transporter promoter gene (5-HTTLPR) would relate specifically to BPD traits in youth. This association was hypothesized based on prior genetic association research with BPD adults and theory positing that emotion dysregulation may be a core risk process contributing to BPD. Youth provided DNA via buccal cells. Both youth and a parent completed self-report measures assessing youths BPD traits and depressive symptoms. Results from both Study 1 (N = 242) and an independent replication sample of Study 2 (N = 144) showed that carriers of the short allele of 5-HTTLPR exhibited the highest levels of BPD traits. This relation was observed even after controlling for the substantial co-occurrence between BPD traits and depressive symptoms. This specific association between 5-HTTLPR and BPD traits among youth supports previous genetic associations with adults diagnosed with BPD and provides preliminary support for a developmental extension of etiological risk for BPD among youth.
Depression and Anxiety | 2011
Jessica L. Jenness; Benjamin L. Hankin; John R. Z. Abela; Jami F. Young; Andrew Smolen
Background: Previous research, predominantly with adults, has shown that the serotonin transporter gene (5‐HTTLPR) interacts with stress (G × E) to predict depressive symptoms; however, few G × E studies have been conducted with youth using rigorous methods, particularly a prospective design and contextual interview to assess stress. This study examined the interaction between 5‐HTTLPR and stress, both chronic and episodic, to predict longitudinal change in depressive symptoms among children and adolescents. Methods: A general community sample of youth (N = 200; 57% girls; mean age: 12.09 years old) was genotyped for 5‐HTTLPR (rs 25531) at baseline. They were interviewed via contextual stress procedures to ascertain chronic family stress and episodic stressors and completed depressive symptoms questionnaires at baseline and 6 months later. Results: A significant G × E showed that chronic family stress predicted prospective increases in depressive symptoms over 6 months among youth possessing the high‐risk S allele. This G × E was not found for episodic stressors occurring in the last 6 months. There was no moderation by sex or pubertal status. Conclusions: These findings advance knowledge on G × E effects in depression among youth. This is the first study to show that chronic family stress, but not episodic stressors, when ascertained by rigorous stress interview, interacts with 5‐HTTLPR to prospectively predict depressive symptoms among children and adolescents. Depression and Anxiety, 2011.
Addictive Behaviors | 2010
Monique Ernst; David A. Luckenbaugh; Eric T. Moolchan; Veronica Temple; Jessica L. Jenness; Katherine E. Korelitz; Edythe D. London; Alane S. Kimes
This 4-year longitudinal study examined whether performance on a decision-making task and an emotion-processing task predicted the initiation of tobacco, marijuana, or alcohol use among 77 adolescents. Of the participants, 64% met criteria for an externalizing behavioral disorder; 33% did not initiate substance use; 13% used one of the three substances under investigation, 18% used two, and 36% used all three. Initiation of substance use was associated with enhanced recognition of angry emotion, but not with risky decision-making. In conclusion, adolescents who initiate drug use present vulnerability in the form of bias towards negative emotion but not toward decisions that involve risk.