2023 Travel Award Recipients
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Julia Aepfelbacher, BS | University of Pittsburgh, School of Medicine | CANlab
Name: Julia Aepfelbacher, BS
University: University of Pittsburgh, School of Medicine
Department: Psychiatry and Psychology
Program or Lab: CANlab
Mentor or PI: Dr. Rebecca Price
Poster: Experiences of Awe Mediate Ketamine’s Antidepressant Effects: A Randomized Controlled Trial in Treatment-Resistant Depression
Authors: Julia Aepfelbacher, Benjamin Panny, Rebecca B. Price
Ketamine, an NMDA-receptor antagonist, provides rapid and short-lived anti-depressant effects. Although much research has focused on neural and molecular mechanisms of action, it’s critical to also consider psychological mechanisms that may contribute to therapeutic efficacy, including ketamine’s psychedelic properties, to inform development of novel approaches that prolong and/or heighten its effects.
116 participants with depression, n=77 who received a ketamine infusion (0.5mg/kg over 40 minutes) and n=39 matched controls who received saline placebo, completed a validated measure of awe (the AWE-scale) at 40 minutes post-infusion. Mean AWE-scores (total and sub-domains) were tested as potential mediators of clinical depression outcomes, measured by % improvement in Montgomery-Asberg Depression Rating Scale (MADRS) at five time points post-infusion (24 hour, 5 days, 12 days, 21 days, 30 days). For comparison, general dissociative side effects (Clinician-Administered Dissociative Symptoms Scale; CADSS scores) were tested in parallel mediational models.
Total AWE-score and its sub-domains differed significantly across treatment groups at 40 minutes (p <0.0001). At 24 hours and day 5 post-infusion, total AWE-scores significantly mediated the relationship between ketamine and MADRS (a*b mediation effect: p=0.0028,
p=0.0154, respectively). From day 12 forward there was no longer a main effect of group on MADRS, but the mediating effect of AWE-score remained (p=0.0027, p=0.0018, p=0.0052, respectively). By contrast, CADSS scores did not mediate outcomes at any timepoint.
Ketamine infusion strongly induced heightened feelings of awe. These experiences significantly mediated depression outcomes, while general dissociative side effects did not. The specific awe-inspiring properties of ketamine may contribute to its anti-depressant effects.
My interest in stories and the lived experiences of those around me is fundamental to my interest in research. After graduating high school, I spent a year living in Nepal teaching English. During my time there, it became clear that compromised health was a running narrative throughout the lives of the children I taught and the friends I had made. They were deprived of adequate health care due to their position on a skewed bell curve of wealth and social status. These lessons followed me to university and inspired me to join the Individual Studies Program, where I created my major, Health and Social Inequality and was exposed to a wide array of disciplines from medical anthropology to economics and history. These forays into diverse disciplines motivated me to pursue research opportunities in the fields of clinical and epidemiological research. During my undergraduate career, I worked on projects addressing racial inequality in long-term stroke outcomes and motivated by this experience, I designed a capstone project that sought to understand the relationship between gender inequality and infant mortality rates. Informed by my interdisciplinary major, I explored infant mortality from a societal to cellular perspective including investigating social and political barriers to adequate perinatal care and the role of discrimination and stress in pregnancy physiology After graduating college, I completed a post-baccalaureate fellowship at the NIH where I managed two clinical trials in the field of HIV/AIDS. Engagement with research in a clinical setting taught me the value of listening to personal stories as a tool to help guide interventions and address problems at their root. For how can patients be expected to manage a complex life-long disease without first addressing the role of pill burden, financial insecurities, and
stigma? Inspired by the stories of our patients, I spearheaded a questionnaire sub-study about fertility desires and reproductive milestones within our maturing cohort of those who had been living with HIV since birth. As a result of the study findings, our clinic began to educate our patients about safe family planning options and alleviate misconception around fertility. When I came to the University of Pittsburgh for medical school, I knew I wanted to take my interest in patient stories and experiences to a deeper level by engaging with qualitative research. I was fortunate to find a project where I could combine this research goal with my passion for reproductive justice and women’s health. I am working with Dr. Judy Chang on a qualitative project seeking providers’ and advocates’ perspectives on reproductive justice and intimate partner violence. It was while conducting interviews with providers that I first became exposed to the field of Psychiatry. I have always been drawn to mental health and wellbeing outcomes in my patients and I am impressed with the field’s dedication to practicing societal to cellular medicine. The clinicians I spoke to effectively integrated their patient’s biomedical stories—MRI results, psychiatric evaluations—with their psychosocial complements—housing, trauma, and discrimination. Additionally, my experiences in the wards during the COVID-19 pandemic has highlighted our on-going mental health crisis and the immense need for novel therapies to address complex psychiatric conditions. It is these experiences that motivate me to pursue a career in Psychiatry and research dedicated to patient experiences in the context of groundbreaking and novel therapies for depression and suicidality.
Alexandra Alario, B.S., A.B.D. | University of Iowa | Interdisciplinary Graduate Program in Neuroscience
Name: Alexandra Alario, B.S., A.B.D.
University: University of Iowa
Department: Department of Psychiatry
Program or Lab: Interdisciplinary Graduate Program in Neuroscience
Mentor or PI: Nicholas Trapp, M.D., and Mark Niciu, M.D., Ph.D.
Poster: The potentiating effects of frontal transcranial magnetic stimulation on cortical excitability measured with visual evoked potentials
AA Alario1,2,3, EWH Tsang1, BD Pace1, NT Trapp1,2, MJ Niciu1,2 1 University of Iowa Hospitals and Clinics, Department of Psychiatry 2 Iowa Neuroscience Institute 3 The University of Iowa Interdisciplinary Graduate Program in Neuroscience
Repetitive transcranial magnetic stimulation (rTMS) is an effective intervention for treatment resistant depression (TRD) and is proposed to exert its antidepressant effects by enhancing cortical excitability. Previously reported assessments of cortical excitability use motor evoked potentials, which is not an ideal measurement due to confounding spinal cord excitability. To date, few studies have directly measured cortical excitability outside of the motor cortex. Quantifying changes in visual evoked potentials (VEPs) during electroencephalography (EEG) recordings can effectively gauge changes in cortical excitability. Thus, we have collected VEPs in 16 subjects before and after a clinically indicated treatment course of rTMS for depression. Here, we test the hypothesis that a treatment course of rTMS will enhance cortical excitability, specifically illustrated by increased VEP amplitude. Because we believe that enhanced cortical excitability is one of the primary mechanisms of rTMS’s antidepressant effects, we also hypothesize that the degree of change in cortical excitability will be correlated with improvements in depression during the treatment course. Our preliminary analyses support these hypotheses. Moving forward, future work may be able to optimize cortical excitability-inducing parameters, allowing for augmented treatment outcomes and a personalized medicine approach to treating depression.
My professional ambition is to aid in the discovery of predictors of antidepressant treatment response. Depression can be a severe and debilitating psychiatric disorder, especially when patients must undergo multiple treatment trials to find relief from their depressive symptoms. Unfortunately, a significant portion of patients will not see a benefit from first line treatments and will need more intensive interventions, such as esketamine and repetitive transcranial magnetic stimulation (rTMS). Although these secondary interventions can be effective at treating depressive symptoms, there is no method to predict treatment outcome. This means that patients and providers do not have an evidence-based method of selecting an effective treatment beyond clinical impressions and patient preference. This can result in severe financial and emotional distress to patients who must invest in uncertain outcomes, which may prolong depressive symptoms. I believe that predictive biomarkers of treatment response are a critical aspect of reducing the amount of failed treatment trials by identifying optimal treatment types on an individual basis. Biomarkers for treatment response have the power to stop the cycle of suffering by adding to a personalized medicine approach to antidepressant treatments. I am strongly motivated to reduce the burden and struggle among this severely ill population in my privileged position as a researcher on a psychiatric team.
Before identifying biomarkers of treatment response, I believe that we first need to understand how these interventional treatments for depression modulate key aspects of the disorder, such as cortical excitability and cardiovascular activity. From there, my goal is to understand how these aspects can be used as predictive biomarkers of treatment response. This understanding will inform clinical practice by introducing new measures to consider when prescribing interventions for the treatment of depression, allowing for patient-specific treatment plans.
It is unclear exactly how esketamine or rTMS exert their antidepressant effects, partially due to the elusive nature of the pathophysiology of depression. Prior work has demonstrated that esketamine and rTMS can modulate the strength of cortical activity and the autonomic nervous system activity but there is a lack of direct association with treatment outcome. Thus, my work seeks to add to the mechanistic understanding of depression treatments and the underlying condition. By discovering associations between clinical improvement and treatment-induced changes in cortical excitability and cardiovascular measures, we will add new insights to the causes and effects of depression.
Clinically, this work may also provide data-driven guidance on subtypes of patients best suited for specific treatment courses. For example, this work may identify a subgroup of patients with depression with low baseline cortical excitability who may be best suited for treatments that modulate cortical activity. Similarly, there may be a subgroup of patients with higher rates of cardiovascular comorbidities who may benefit from a treatment course known to modulate the autonomic nervous system. I strive to inform clinical practice in a patient-dependent manner and support depressed individuals with my work.
Kendall Coden, BS | Stanford University | Parker and Garner Labs
Name: Kendall Coden, BS
University: Stanford University
Department: Comparative Medicine
Program or Lab: Parker and Garner Labs
Mentor or PI: Dr. Karen Parker; Dr. Joseph Garner
Poster: Could Stereotypies be Caused by Oxidative Stress?
Kendall M. Coden, Jerome T. Geronimo, Beatriz E. Stix-Burnell, Karen J. Parker, Joseph P. Garner
Stereotypies (abnormal, repetitive, and seemingly goal-less behaviors) are central to several human neurodevelopmental and neuropsychiatric disorders (e.g., autism; schizophrenia). Stereotypies are also characteristic of captive animals raised in barren conditions. Within clinical populations, stereotypies are associated with knowledge-action dissociation and distressing affective states. We and others have shown that spontaneous stereotypies in animals are a model of human stereotypies, including evidence of homologous cortico-striatal pathophysiology. However, the neurodevelopmental etiology of these deficits remains unclear for stereotypies. Conversely, in compulsive behavior, which involves adjacent cortico-striatal loops, there is growing evidence for an etiological role of the ability of the brain to buffer against radical oxygen species (i.e., oxidative stress), including effective antioxidant therapies. To our knowledge, no studies have directly examined the relationship between stereotypies and oxidative stress. Understanding this relationship may shed light on new intervention strategies. Here, we used C57Bl/6 mice to assess the relationship between oxidative stress and stereotypies. We hypothesized that measures of oxidative stress, particularly glutathione (measured via level of total glutathione) and total antioxidant capacity, would positively predict the severity of stereotypies. To test this, we unobtrusively recorded home-cage behavior from male mice and quantified stereotypies using an established mouse ethogram. We analyzed for bioavailability of glutathione and total antioxidant capacity, via blood and urine respectively, using commercially available kits. Data from this study support our hypothesis that the etiology of stereotypies involves oxidative stress. Accordingly, antioxidant therapies (e.g., N-Acetyl- Cystine) may serve as an intervention for disorders characterized by stereotypies and repetitive behaviors more broadly.
Despite being cited as one of the most debilitating aspects of neurodevelopmental and neuropsychiatric conditions, we currently lack targeted therapeutics for abnormal repetitive behaviors (ARBs). As such, my long-term career goal is to be a principal investigator and run a translational neuroscience laboratory focused on elucidating neural mechanisms and neurobiological underpinnings of ARBs with the ultimate goal of identifying novel, targeted therapeutics for these behaviors.
My interest in the brain and behavior took root in high school while volunteering with children diagnosed with autism spectrum disorder. Perplexed by the behavioral diversity of these children, I frequently found myself theorizing about the neural mechanisms responsible for regulating behavior. Driven by my ever-growing list of questions about the brain, during my sophomore year at the University of Michigan I joined Dr. Terry Robinson’s behavioral neuroscience laboratory where I used rodent models to investigate neurobiological and behavioral implications of chronic drug use. While conducting my senior thesis, which confirmed the presence of behavioral cross-sensitization between intravenously administered cocaine and d-Amphetamine in rats, I became hooked on the scientific process and the ability to deepen our understanding of the neurological basis of behavior.
My undergraduate research experiences focused primarily on observed behaviors. Therefore, motivated to understand behavior on a neural circuit level, I accepted a Postbaccalaureate Intramural Research Training Award and joined the laboratory of Dr. Andrew Holmes at the National Institutes of Health. There, under the primary supervision of a postdoctoral fellow, I used a multi-method approach (fiber photometry, optogenetic manipulation, and viral-mediated neuroanatomical tracing) to investigate how cortico-limbic-striatal circuits regulate punishment- insensitive reward-seeking behavior. My contributions at NIH resulted in co-authorship on a paper published in Biological Psychiatry (Halladay et al., 2020) and two additional co-authored manuscripts which are currently in preparation.
En route to my long-term goal, I am currently pursuing a master’s degree in Laboratory Animal Science at Stanford University. I am working with Drs. Karen Parker and Joseph Garner to investigate the neurobiology underlying stereotyped behaviors in a murine model. From previous studies by Dr. Garner, we know that compulsive behaviors, a type of ARB, are caused by oxidative damage in the prefrontal cortico-striatal loops. We also know that stereotypy, another form of ARB, is caused by dysfunction of the premotor cortico-striatal loops. Based on this, I hypothesized that stereotypy may be related to oxidative damage in the premotor cortico-striatal loops. To investigate this, I observed and coded home-cage stereotypy in mice. I then measured levels of oxidative damage in the brain and assessed the correlation between these biological measures and the severity of stereotypy. Preliminary data support my hypothesis that stereotypy is related to oxidative damage and highlight therapeutic potential of antioxidants in treating or preventing ARBs.
A highlight of my research career thus far has been learning from and collaborating with other scientists. Neuroscience is a highly interdisciplinary field, and therefore, multidisciplinary collaborations are necessary for producing new, innovative studies. Therefore, I actively seek out opportunities to be in community and in conversation with other scientists. Holding a strong interest in affective neuroscience, the opportunity to attend the Wisconsin Symposium on Emotion will provide me with the opportunity to meet other scientists holding shared interests in affect and behavior. In turn, this will help me grow my scientific network and enable development of innovative studies that expand our understanding of the brain and emotion
Stephanie N. DeCross, MA | Harvard University | Clinical Science, Stress & Development Lab
Name: Stephanie N. DeCross, MA
University: Harvard University
Program or Lab: Clinical Science, Stress & Development Lab
Mentor or PI: Katie A. McLaughlin, PhD
Poster: Neural alterations in threat reversal learning as mechanisms linking childhood trauma and transdiagnostic psychopathology in youth
Authors: Stephanie N. DeCross, MA, Sahana Kribakaran, MA, Paola Odriozola, PhD, Margaret A. Sheridan, PhD, Nim Tottenham, PhD, Dylan G. Gee, PhD, Katie A. McLaughlin, PhD
Threat reversal learning is a potential mechanism linking childhood trauma (CT) to psychopathology. Threat reversal learning describes the ability to flexibly update associations of stimuli with threat and safety and is vastly understudied, particularly in developmental populations. This study aims to characterize how CT may alter the neural underpinnings of threat reversal learning in youth in ways relevant to mental health.
100 participants aged 9-19, half with exposure to CT, underwent a Pavlovian threat reversal learning task during an fMRI scan. First, one previously-neutral stimulus was paired with an aversive stimulus and thereby predicted threat (CS+); one was not and predicted safety (CS-). Then, contingencies were reversed, such that the old safety cue became the new threat cue (New CS+) and vice versa. Whole-brain contrasts, regions-of-interest analyses, and nonparametric mediation models were used to examine patterns of neural activation and whether they mediated the association between CT and psychopathology.
Youth with CT displayed reduced activation in right amygdala, hippocampus, parahippocampal gyrus (PHG), and ventromedial prefrontal cortex (vmPFC) during New CS+>New CS-, reflecting blunted discrimination between cues with reversed contingencies in canonical threat- related regions. Critically, blunted discrimination in hippocampus and PHG mediated the link between CT and transdiagnostic anxiety; blunted discrimination in right amygdala mediated the association between CT and panic; and blunted discrimination in vmPFC mediated the association between CT and PTSD.
Alterations in threat reversal learning may reflect decreased ability to flexibly update threat- safety associations and may be a key mechanism underlying the link between CT and transdiagnostic psychopathology.
Despite the prevalence of mental health difficulties, even our most effective treatments are not universally effective, reflecting our incomplete understanding of mental health disorders. Better understanding the mechanisms underlying psychopathology and clarifying how treatment operates over these mechanisms would enable intervention optimization and innovation. As a clinical psychology PhD candidate with an interdisciplinary focus, I am passionate about translational research that integrates across environmental experience, neurobiological mechanisms, psychological constructs and behavior, and clinical intervention. I am fascinated by how humans learn to detect, interpret, and respond to threat, and believe threat learning processes (e.g., threat conditioning, reversal, extinction, generalization) are compelling targets for translational research. Not only is learning a primary mechanism by which the environment shapes us to produce differential outcomes, but the threat learning processes thought to underlie the etiology of transdiagnostic, threat-based disorders (e.g., anxiety, stress-related disorders, and beyond) are the same processes implicated in effective treatment of these disorders. As I train as an affective neuroscientist, clinical psychologist, and clinician delivering psychotherapy, my experiences continually build unique insight towards bridging these connections. My research is grounded in critical thinking and synthesis across disciplines. Through my independent research with Paul J. Whalen, PhD as an undergraduate at Dartmouth College, I became captivated by how basic neural mechanisms enable humans to process and learn about threat, and how this gives rise to observable behaviors and emotions. Fascinated by the clinical implications of affective research and driven to both work directly with clinical populations and perform neuroimaging analyses myself, post-graduation I pursued a position as a clinical research coordinator at Massachusetts General Hospital/Athinoula A. Martinos Center for Biomedical Imaging in the Emotion and Social Neuroscience Lab with Daphne J. Holt, MD, PhD, working with populations with and at risk for psychosis. I played critical roles collecting, analyzing, and presenting data from several projects, including an investigation of neural correlates of threat generalization, and published a first-author manuscript on amygdala connectivity and persecutory ideation in emerging adults. Here, I developed a curiosity in developmental trajectories underlying serious mental illness. In graduate school, working with Katie A. McLaughlin at Harvard University, I am incorporating a developmental lens and investigating the effects of childhood trauma—a common environmental experience and robust risk indicator for psychopathology—during adolescence, a vulnerable period of neuroplasticity. Supported in part by the NSF Graduate Research Fellowship, my dissertation investigates how childhood trauma shapes threat learning process across development in demographically-representative samples and confers risk for transdiagnostic psychopathology. My overarching program of research additionally incorporates questions extending towards understanding how these processes underlie threat-based disorders and can be leveraged to optimize clinical interventions. In my work, I integrate interdisciplinary, multimodal methods (e.g., fMRI, psychophysiology, behavioral tasks, self-report) and advanced statistical techniques (e.g., mixed effects modeling, nonlinear modeling, machine learning). I bring a novel twist to studying threat learning by examining learning as a dynamic process over time. For example, I have demonstrated patterns of neural activation and connectivity consistent with poorer discrimination between threat and safety cues over time in youth exposed to childhood trauma during Pavlovian threat conditioning. These changes in activation and connectivity longitudinally mediated distinct profiles of psychopathology two years later. Building upon this, emerging findings suggest that upon reversal of threat/safety contingencies, trauma-exposed children additionally display blunted discrimination in brain regions that process contextual threat, and these alterations are associated with transdiagnostic threat-based psychopathology. An impaired ability to differentiate threat from safety implies that trauma-exposed youth may be more likely to generalize fear responses to other, similar cues, a hypothesis I will test with data collected in my own intensive study that measured psychophysiological responses to threat generalization, clinical symptoms, and more (e.g., behavioral pattern separation, intolerance of uncertainty) in adolescents exposed to interpersonal violence. Through such work, I hope to elucidate common pathways to psychopathology to inform clinical intervention.
Julia Evanski, BS | Wayne State University | Trauma History Investigation of Neurodevelopment in Kids (THINK) Lab
Name: Julia Evanski, BS
University: Wayne State University
Department: Department of Psychiatry and Behavioral Neurosciences
Program or Lab: Trauma History Investigation of Neurodevelopment in Kids (THINK) Lab
Mentor or PI: Dr. Hilary Marusak
Poster: Brewing Trouble: Exploring the effects of prenatal caffeine exposure on frontolimbic white matter microstructure in adolescents
Authors: Julia M. Evanski, Clara G. Zundel, Hilary A. Marusak
Caffeine, the most widely used stimulant in the world, is also frequently consumed by pregnant individuals. However, research has shown that prenatal caffeine exposure can negatively impact offspring neurodevelopment by inhibiting fetal growth, increasing the risk of premature birth, and increasing risk of externalizing problems during childhood. Furthermore, it may alter brain structure, including the development of frontolimbic pathways associated with cognitive and emotion-related functioning. In this study, we investigated the relationship between prenatal caffeine exposure and integrity of frontolimbic white matter pathways during childhood (M±SD age=9.91±0.62 years; 47.8% female) using data from the Adolescent Brain Cognitive Development Study (n=11,869). Prenatal caffeine exposure was measured via retrospective report from caregivers, and fractional anisotropy (FA) was estimated for ten frontolimbic white matter tracts (five/hemisphere). In this sample, 63.3% of caregivers reported caffeine use during pregnancy. Results indicated that prenatal caffeine exposure was associated with lower FA in the right and left fornix (β=-0.00121, CI =[-0.00238, -0.0005], p = 0.041; β=-0.0013, CI =[-0.00242, -0.0001], p = 0.024), respectively as well as in the right cingulum bundle (β=-0.002, CI =[- 0.0039, -0.0001], p = 0.039). These findings suggest that prenatal caffeine exposure can lead to microstructural alterations in the fornix and cingulum bundle a decade later, which may contribute to neurobehavioral problems reported in offspring. Thus, it is recommended that individuals limit caffeine consumption during pregnancy.
My primary career goal is to become the principal investigator of an independent research lab focused on characterizing how early-life adversity can lead to stress-related disorders, such as anxiety, depression, and posttraumatic stress disorder (PTSD), as well as to develop novel interventions that can aid in the prevention and treatment of these disorders. From a young age, I have demonstrated a passion, curiosity, and concerted interest in neuroscience. During high school, I enrolled in several STEM-based Advanced Placement and honors classes and took on leadership roles in numerous student-led clubs and organizations. During my undergraduate studies, I joined the Lyman Briggs Residential College at Michigan State University (MSU), I was a member of the Honors College, I earned a bachelor’s degree in both Neuroscience and Human Biology. In addition to my academic studies, I was immersed in research as an undergraduate research assistant in Dr. Jan Brascamp’s Visual Neuroscience Lab at MSU, starting in my first year. This three-year, in- depth experience introduced me to all stages of research, from study design and conception to data collection and analysis. I also led an individual project, which focused on understanding basics of the visual system, including attention and perception of afterimages (e.g., visual ambiguity). Unfortunately, my project did not culminate in a presentation because data collection was suspended, and conferences were cancelled as a result of the pandemic. Nevertheless, this research experience and coursework reaffirmed my career path and that I have the necessary skills and motivation to thrive as a neuroscience researcher. Furthermore, my undergraduate research focused on visual systems, specifically visual ambiguity. While, this research fascinated me, I knew that it was a steppingstone for me to delve deeper into human psychiatric disorder research.
After graduation, I was hired as a full-time research assistant in Dr. Hilary Marusak’s THINK Lab at Wayne State University (WSU) in 2021. My goals were to further extend the breadth and scope of my research training and to gain experience in new areas to me: the endocannabinoid (eCB) system and neuroimaging. A few months after joining the lab I developed my own research project, focused on understanding the impact of prenatal cannabis exposure on neurodevelopmental outcomes in children. I presented preliminary data from this project as oral presentations at the 2022 meetings of the Society of Biological Psychiatry and the International Cannabinoid Research Society, and my first-author manuscript is currently under review, with a second first-author manuscript in preparation. I also have 2 co-authored publications and over 30 conference abstracts. These experiences have taught me time management, how to work independently as well as in a team, and how to participate in interdisciplinary translational science. I have also fostered relationships with physicians and researchers across the university, including neurologists, psychiatrists, psychologists, and exercise physiologists. I believe strongly that bringing together different disciplines and techniques provide innovative new perspectives and solutions for combatting public health problems, such as anxiety disorders.
Through these diverse research experiences, I have developed a strong interest in early-life adversity and its potential impacts on neurodevelopment and mental health. I am interested in characterizing the effects of cannabinoid exposure during sensitive periods of development (e.g., during adolescence or the prenatal period) on brain development and mental health outcomes. I am also interested in potential therapeutic effects of interventions that target the eCB system, such as exercise or cannabidiol (CBD), for improving mental health outcomes in at-risk youth. My long-term goal is to find avenues of mental health intervention in youth, that could be accessible, applicable, and therapeutic, to stress-
related disorders, or trauma-exposed youth.
John McClellan France, PhD candidate | Wayne State University | Translational Neuroscience Program / Detroit Trauma Project
Name: John McClellan France, PhD candidate
University: Wayne State University
Department: Psychiatry and Behavioral Neurosciences
Program or Lab: Translational Neuroscience Program / Detroit Trauma Project
Mentor or PI: Dr. Tanja Jovanovic
Poster: Reduced Cortical Glutamatergic Neurotransmission during Inhibitory Control with Negative Emotional Stimuli in Trauma-Exposed Youth
Authors: John McClellan France, Dalal Khatib, Shaurel A. Valbrun, William M. Davie, Sattvik Basarkod, Vaibhav A. Diwadkar, Jeffrey A. Stanley and Tanja Jovanovic
Childhood trauma may heighten negative emotional responses, which may overwhelm cognitive control. However, the neural mechanisms supporting cognitive control in negative emotional contexts remain unknown. We utilized functional magnetic resonance spectroscopy (1H fMRS) to investigate dynamic changes in cortical glutamate to assess the impact of negative emotional processing on neural mechanisms supporting cognitive control in trauma-exposed youth.
N=17 trauma-exposed youth (58% female, age=11.8±0.8yrs, trauma=3±2events) underwent 1H fMRS and completed an inhibitory control task presented with and without negative emotional stimuli, representing the “Negative Emotion” and “No Emotion” task conditions, respectfully.
Spectra were collected from the medial dorsal anterior cingulate cortex (dACC) and processed to quantify task-related changes in glutamate, or glutamate modulation. Repeated measures generalized estimating equations (GEE) were used to assess the effect of emotion condition on dACC glutamate modulation. Trauma was defined as any DSM-5 criterion A trauma assessed using the Traumatic Events Screening Inventory (TESI).
A significant main effect of emotion was found (x2= 4.18, p=0.04), such that trauma-exposed youth demonstrated significantly less glutamate during the Negative Emotion condition compared to the No Emotion condition. Self-reported trauma frequency was not associated with percent change in glutamate from baseline during the Negative Emotion task conditions (r=- 0.31, p=0.23).
We demonstrate for the first-time reduced dACC glutamate modulation in trauma-exposed youth during motor inhibitory control with the influence of negative emotional stimuli. These findings suggest dACC glutamate modulation is a potential neural mechanis gnitive
control in the context of negative emotion in trauma-exposed youth.
Most youth will have had a traumatic experience at some point during their formative years. While most individuals are not dramatically impacted by these experiences, some will develop and live with an anxiety or trauma-related disorder. Moreover, the risk for developing these disorders increases with the frequency of trauma exposure. In Detroit MI, the community that helped raise me, the rates of these experiences are high. On average, the children we work with have endorsed 3 traumatic events all before the age of 9 years old. What are the mechanisms by which experiences of childhood trauma confers increased risk for anxiety and trauma-related disorders during adolescence? How might these mechanisms inform early interventions to support vulnerable populations like trauma-exposed youth? As these traumatic experiences are all too common not only in Detroit but across the globe, I plan to spend my academic career contributing to the answer to these questions. My research experiences prior to graduate school include clinical research of trauma exposure in Detroit’s emergency departments and child development research at the local university, Wayne State University (WSU). Through these experiences, I began to conceptualize anxiety disorders as developmental disorders and that experiences of trauma may shape some developmental trajectories towards psychopathology. As a graduate student at WSU, I continue to advance this understanding with the mentorship of Dr. Tanja Jovanovic whose multifaceted research program is aimed at examining the impact of childhood trauma on sensitive periods of development like late childhood and early adolescence when anxiety disorders emerge. Concurrently, I have received further training in functional neuroimaging with the mentorship of Drs. Hilary Marusak (WSU) and Jennifer Stevens (Emory University) investigating neural correlates of negative emotional processing in trauma-exposed youth. We have found that self-reported trauma exposure frequency is associated with elevated amygdala response to potentially threatening faces (France et al, in prep), greater fear-potentiated startle during threat and safety learning (France et al, in prep), greater skin conductance when reporting trauma history (Wiltshire et al 2022), and greater risk for anxiety (France et al, 2022). Moreover, I synthesized the literature to determine that complex interactions between emotional brain regions and other brain circuits elicited during negative emotional processing may underlie variability in anxiety symptoms in trauma-exposed individuals (France and Jovanovic, 2022). Collectively, this work led to the central hypothesis for my dissertation research: elevated negative emotional reactivity resulting from trauma exposure may overwhelm cognitive control, and lead to heightened risk for anxiety during adolescence. To address the neuroplastic mechanisms supporting cognitive control in negative emotional contexts, I sought further mentorship from Dr. Jeffery Stanley (WSU), an MR physicist who specializes in functional magnetic resonance spectroscopy (fMRS) to investigate functional changes in brain biochemistry in vivo. Together, we have implemented this technique to assess childhood trauma’s impact on task-based modulation of cortical glutamate when cognitive control is required in negative emotional contexts – which had never been investigated before and will significantly add to findings from functional MRI studies of emotion regulation. In support of this project, I was awarded the WSU New Investigator Grant which has led to the preliminary findings I hope to share at the 2023 Wisconsin Symposium on Emotion. My future work in this regard will investigate cortical glutamate modulation as a novel biomarker of risk and resilience to posttraumatic stress and potential therapeutic target during sensitive periods of development. I will greatly benefit from attending the 28th annual Wisconsin Symposium on Emotion by expanding my understanding of neuroplasticity with the expert talks on leveraging glutamatergic neuroplasticity during sensitive periods (Dr. Rebecca Price) and cortical neurostimulation therapy for affective disorders (Dr. Nolan Williams), among others. I am excited for this unique opportunity to learn from leaders in the field of emotion neuroscience with research interests similar to my own. I aim to spur future mentorships and collaborations as I enter the field as an independent translational neuroscientist focusing on neurodevelopmental mechanisms underlying pediatric anxiety, in the context of childhood trauma exposure.
Naomi Gancz, MA | University of California, Los Angeles | Developmental Psychology Program
Name: Naomi Gancz, MA
University: University of California, Los Angeles
Program or Lab: Developmental Psychology
Mentor or PI: Bridget Callaghan, PhD
Poster: A Gut Feeling: Examining Electrogastrography as a Biomarker of Affective Responses
Authors: Gancz, N.N., Savoca, P.W., Callaghan, B.L.
The digestive system is not only critical for homeostasis but is also responsive to affective states. However, it is typically overlooked by psychophysiological biomarkers. We examined electrogastrography (EGG) as a novel biomarker of autonomic response to affective stimuli. EGG is an inexpensive, noninvasive, and informative method that uses skin-level electrodes to measure the electrical rhythm of the stomach. Via the autonomic nervous system, this activity is sensed and, in turn, modulated by the brain. Thus, changes in the EGG in response to a stimulus, such as psychosocial stress, can yield information both about the specific response of the stomach to the stimulus and, more broadly, about the response induced in the central and peripheral nervous system. Despite its high potential, this methodology is underutilized and under-researched. We will recruit (N=50) undergraduate students. While they are fasted, we will record their EGG, as well as electrocardiogram and electrodermal activity, before, during, and after the Montreal Imaging Stress Task. We will measure the distributions of pre- to post-stress ratios of the EGG dominant frequency and percentage of power in the normal frequency range. We will also measure the association between EGG, heart-rate variability, and electrodermal activity. The results of this study will demonstrate the utility of the EGG as an affective state biomarker that is easily implemented, especially for researchers already utilizing electrophysiology equipment.
My research examines the effects of early psychosocial experience on individuals’ ability to respond adaptively to challenges later in life. In particular, I am interested in the effects of early adversity on the development of the brain-gut-microbiome axis (BGMA) and its response to allostatic demands. To approach this question, I utilize a variety of methodologies, including electrophysiology, microbiome sequencing, and structural equation modeling. The study I propose to present at the Wisconsin Symposium on Emotion will examine whether electrogastrography (EGG), a noninvasive method that measures the electrical activity produced by the stomach during peristalsis, is an informative marker of autonomic response to affectively salient stimuli. To this end, we are examining the EGG signal of undergraduates before, during, and after completion of the Montreal Imaging Stress Task (MIST). The primary goal of this research is to optimize parameters for the use of EGG in psychosocial research, as this signal is highly artifact-prone. The secondary goal is to examine whether state anxiety or early adversity exposure explain interindividual variation in the EGG response to the MIST. EGG, which is regulated by both the sympathetic and parasympathetic branches of the nervous systems, may provide unique information on the manifestation of affective responses in the stomach and gut. Data collection for the first stage of this study is complete. The methodology and preliminary results will be presented as a poster at the Society for Affective Science Meeting in March of 2023. I will use this initial data and feedback received at this meeting in order to refine methodological parameters and minimize data loss to artifacts. Data collection for the second stage of this study, which will implement these new parameters, will begin in April of 2023. I will present these refined parameters at the Wisconsin Symposium on Emotion. Ultimately, I plan to use this methodology to examine the EGG response to a variety of stimuli in both undergraduates and community samples. By integrating these findings with my other areas of research, I will contribute to understanding of the effects of early adversity on the BGMA, which will lead to the development of treatments and interventions to improve outcomes in individuals exposed to early adversity.
Agatha Laboe, BA | Washington University School of Medicine | Center for Healthy Weight and Wellness
Name: Agatha Laboe, BA
University: Washington University School of Medicine
Program or Lab: Center for Healthy Weight and Wellness
Mentor or PI: Ellen Fitzsimmons-Craft, PhD
*In Fall 2023, I will be starting the clinical psychology PhD program at the University of Wisconsin-Madison, under the mentorship Dr. Katherine Schaumberg*
Poster: An Empirical Investigation of the Affect Regulation Theory of Compulsive Exercise
Poster Abstract Although exercise is considered a health-promoting behavior, compulsive exercise, affecting up to 80% of individuals with eating disorders (EDs), is harmful. Prominent theoretical models propose that affect regulation is the main psychological reinforcer of compulsive exercise; however, experimental studies testing these models are lacking. The current study aims to map trajectories of positive and negative affect during an acute (30-minute) bout of exercise amongst individuals with and without compulsive exercise, with future analyses to examine whether and when trajectories of affective change diverge. Participants include a pilot sample of young women (current n=28; data collection ongoing) aged 14-22 years (10 individuals with EDs; 18 healthy controls). Participants were interviewed using the Eating Disorder Examination and self-reported their reasons for exercise engagement using the Compulsive Exercise Test. Additionally, participants completed the Physical Activity Affect Scale (PAAS) before, during (every 5 minutes), and after a 30-minute exercise bout. In healthy controls, mean scores on the PAAS Positive Affect and Negative Affect subscales were 1.83 and 0.94 before exercise and 2.00 and 0.72 after exercise, respectively. In individuals with EDs, mean scores on the PAAS Positive Affect and Negative Affect subscales were 1.3 and 0.9 before exercise and 1.5 and 0.8 after exercise, respectively. Thus, with a 30-minute exercise bout, positive affect increased and negative affect decreased in both healthy controls and individuals with EDs, evidence for affective changes with exercise engagement. Increased power and additional analyses will continue to clarify effects.
As an incoming clinical psychology PhD student at the University of Wisconsin-Madison, I am interested in understanding adaptive versus maladaptive eating and exercise and ultimately, developing, improving, and disseminating treatments for eating disorders (EDs). I am curious about applying an affective neuroscience lens to the study of EDs to better understand the role that emotion processing plays in the development, maintenance, and remediation of EDs. Attending the Wisconsin Symposium on Emotion would offer me the opportunity to learn about novel research techniques in the field of affective neuroscience, which I could apply to the study of EDs throughout my graduate school career and beyond.
My interest in research was born from a desire to understand how lifestyle behaviors impact well-being. Throughout my four years at Notre Dame (ND), I worked under Dr. Cindy Bergeman,
coordinating a project that aims to advance understanding of successful adult development. Struck by how many participants described exercise as a contributor to their well-being, I used existing data to examine how duration and intensity of exercise moderate daily stress reactivity, work that culminated in a poster presentation and a first-author manuscript under review. I found that greater duration and intensity of exercise buffered stress reactivity, and also that intensity of exercise had a greater buffering effect when duration was shorter. I was left wondering if these results would hold in those with clinical EDs, and I became curious about at what point adaptive behaviors (e.g, exercise) become maladaptive, which factors predispose maladaptive relationships with exercise and/or food, and the extent to which these relationships are hereditary.
To pursue these questions, I worked for three years with Dr. Dawn Gondoli, who has conducted extensive research on disordered eating in mother-daughter dyads. I noticed that although there was much cross-sectional research suggesting maternal transmission of disordered eating, there was scant research on the impact daughters might have on their mothers. Subsequently, I tested the effects of mothers’ and daughters’ own body dissatisfaction on their own eating pathology (actor effects) and each other’s eating pathology (partner effects). This work culminated in a poster presentation and honors thesis, which won a departmental award and is published in Body Image. Findings indicated that mother and daughter body dissatisfaction significantly predicted their own eating pathology, and although no significant partner main effects occurred, a notable actor-partner interaction emerged, such that mothers’ body dissatisfaction significantly predicted higher levels of their own restrained eating only when their daughters were ages 16 and older. I speculated that perhaps mothers view older daughters’ restrictive eating as more acceptable than younger daughters’ given the pervasiveness of dieting among young adults, and as such, they may be more inclined to emulate their older daughters.
Upon graduating from ND with the highest award presented by the Department of Psychology, I pursued a postbaccalaureate research position with Dr. Denise Wilfley and Dr. Ellen Fitzsimmons-Craft at Washington University School of Medicine (WUSM) to explore my interest in innovative interventions for EDs. For the past 20 months, I have coordinated a NIMH-funded R34 clinical trial developing and testing an app for individuals discharging from acute treatment for anorexia nervosa. As director of recruitment, retention, and data collection, I have contributed to the development of the intervention, conducted interviews to ensure user-centered design, assisted with training intervention staff, and maintained a strong partnership with our industry partner. My work in this role has also resulted in rich professional experience, including three accepted conference presentations, one co-authored manuscript under review, and one first-author manuscript under review. At WUSM, I have also sought to diversify the study of EDs. Notably, I worked with the National Eating Disorders Assocation to add food insecurity (FI) screening questions to the online ED screen freely available on their website. I then spearheaded a project to examine ED risk and treatment-seeking status by food security status, which served as the starting point for a first-author manuscript that is under review.
In sum, through my work, I have approached the study of EDs from multiple angles. As I embark on my graduate school journey, I am eager to learn about innovative approaches to further advance the study of EDs. Particularly, I am excited about applying an affective neuroscience lens to the study of EDs, and I am thrilled at the prospect of attending the Wisconsin Symposium on Emotion to not only learn about cutting-edge research in the field of emotion science, but also network with scientific leaders who could help me move my research ideas forward.”
Kristen Montgomery, BS | University of Colorado Anschutz Medical Campus | Lab of Translational Psychiatry
Name: Kristen Montgomery, BS
University: University of Colorado Anschutz Medical Campus
Program or Lab: Lab of Translational Psychiatry
Mentor or PI: Tracy L. Bale, Ph.D.
Poster: DREADD-ing Stress: Using chemogenetics to bypass variability and examine sex-specific vulnerabilities to chronic CRF activation
Authors: Kristen Montgomery, Morgan Bridi, Lillian Folts, Ruth Marx-Rattner, Hannah Zierden, and Tracy Bale
Chronic lifetime adversity is one of the strongest predictors of neuropsychiatric disease. Further understanding of mechanisms underlying disease risk requires consideration of additional factors, such as biological sex, and is essential for developing novel therapeutic interventions. Current rodent stress paradigms consist of sensory, psychological, and homeostatic stressors that converge onto corticotropin-releasing factor (CRF) neurons in the paraventricular nucleus of the hypothalamus (PVN) and activate the hypothalamic-pituitary-adrenal (HPA) axis, ultimately resulting in glucocorticoid release. While these stressors effectively induce a stress response, a lack of consistency in the type and timing of exposures across research groups and the use of paradigms that are only effective in one sex present challenges for reproducibility and translational relevance. We hypothesized that chemogenetic activation of CRF neurons replicates the physiological effects of traditional stress paradigms while bypassing the limitations of those models. We utilized the Designer Receptors Exclusively Activated by Designed Drugs (DREADD) model and administered the DREADD ligand clozapine-N-oxide (CNO) daily to adult male and female mice expressing the Gq-coupled DREADD receptor hM3Dq on all CRF neurons. Following chronic CRF activation, male hM3Dq-expressing mice showed decreased body and thymus weights and dysregulated HPA activity. In contrast, female hM3Dq-expressing mice were resistant to the physiological effects of chronic CRF activation despite releasing higher levels of corticosterone in response to CNO than males but showed elevated freezing behavior. These results suggest that the detrimental effects of chronic stress differ both by sex and
brain region and may underlie differential vulnerability to stress-related neuropsychiatric disorders.
The ability of an organism to respond to environmental or homeostatic threats is essential to survival. While mounting a rapid and appropriate response acutely is adaptive, repeated and pervasive stress experience across the lifespan is one of the greatest predictors of neuropsychiatric disorder development. My interest in understanding the consequences of stress and trauma on long-term health outcomes began as an undergraduate working with Dr. Mary Meagher examining the mechanisms by which stress-mediated immune alterations accelerate disease progression in a mouse model of multiple sclerosis. Following completion of my bachelor’s degree, I worked as a research assistant with Dr. Santosh D’Mello and accidentally discovered my passion for neurodevelopmental sex differences research. My work with Dr. D’Mello investigated how triplication of the X-linked gene MECP2 imparts male-specific neuronal loss in the prefrontal cortex, hippocampus, and cerebellum.
This sex-specificity was always thought to be due to selective inactivation of the X chromosome with the triplication in females. I found, however, that females express both MeCP2 RNA and protein at equivalent levels to that of males with the triplication yet are resistant to neuronal loss and present primarily with affective dysregulation. These surprising results led me deep into the literature on sex differences in neurodevelopmental and neuropsychiatric disorders and the realization that this was what I wanted to study in graduate school. I joined Dr. Tracy Bale’s lab for my graduate work to pursue two of my major interests, stress- and trauma-related disease risk and sex differences across the lifespan. My research in the Bale Lab examined the biological mechanisms by which maternal preconception stress programs sex-specific offspring disease risk. I found that female, but not male, offspring from dams stressed prior to conception had dramatically altered hypothalamic neuron transcriptomes during the juvenile period, a critical developmental plasticity window. Dysregulation of stress circuitry maturation during this period may underlie vulnerability to stress-relevant disorders later in life and aligns with findings from human data that children born to parents who experienced significant lifetime adversity have an increased incidence of affective disorders. I also developed a novel stress model using chemogenetics to bypass the variability associated with traditional rodent stress paradigms and directly activate the corticotropin-releasing factor (CRF) system which integrates stress signals and orchestrates responses. I found that males are more vulnerable to the physiological effects of chronic CRF activation despite producing lower levels of corticosterone upon activation of the hypothalamic-pituitary-adrenal (HPA) axis. Females, on the other hand, are resistant to many of the physiological effects of chronic CRF activation but appear to have a limbic-specific vulnerability which may underlie the female-specific heightened risk for affective disorders. My current work is using our chemogenetic stress model to assess sex-specific risk to stress and trauma during the highly plastic and critical juvenile period. I ultimately plan to pursue a research career dedicated to understanding sex-specific mechanisms of vulnerability to neuropsychiatric disorders with an emphasis on sensitive developmental periods. Attending the Wisconsin Symposium on Emotion would provide me with the opportunity for collaborative scientific discussions with experts in the field and for networking with potential mentors as I explore postdoctoral training opportunities for the next stage of my career.
Reut Naim, PhD | National Institute of Mental Health (NIMH) | Neuroscience and Novel Therapeutics
Name: Reut Naim, PhD
University: National Institute of Mental Health (NIMH)
Department: Emotion and Development Branch
Program or Lab: Neuroscience and Novel Therapeutics
Mentor or PI: Melissa A. Brotman, PhD.
Poster: Linking Daily Dynamics of Irritable Mood and Sleep in Pediatric Sample: Clinical and Conceptual Implications
Authors: Reut Naim, Jennifer Meigs, Katharina Kircanski, Miryam Kiderman, Melissa A. Brotman
Background: There is an established association between sleep and emotion dysregulation and psychopathology. Insufficient sleep among youth presents across multiple mood and behavioral psychiatric diagnoses, negatively associated with impairment and adult psychopathology. While preliminary research suggests associations between insufficient sleep and irritability, this area is vastly understudies and existing data is retrospective. The purpose of the current study is to leverage a technology-based platform using ecological momentary assessments (EMA), to investigate real-time trajectories between sleep duration and irritability symptoms in pediatric youth.
Methods: A transdiagnostic sample of youth (N=125, M age=12.58, SD=2.56, 74.4% males, 68.8% White) and their parents received smartphone prompts 3x/day for seven days to report on youths’ irritability symptoms (i.e., grouchiness, frustration, anger), wake times, and bedtimes. Multilevel modeling explored bidirectional associations between sleep duration at night T with irritability the morning after (T+1), and between irritability at the evening (T-1) and sleep at night T. Age and questionnaire-based trait irritability scores were entered as covariates.
Results: Bidirectional associations were found between sleep and irritabilty. Decreased sleep predicted increased levels of morning frustration and grouchiness as reported by both informants (all ps<.049), and of morning anger as reported by the parent (b=-.26, SE=.05, p<.001). On the inverse direction, increased evening anger predicting decreased sleep (b=-.17, SE=.07, p=.019).
Conclusions: Synergetic associations between sleep and irritability were observed, highlighting the value of EMA to broaden current understanding of sleep-mood dynamics in real life. Sleep insufficiency may serve as a potential treatment target to improve daily irritability in clinical
As a clinician-researcher my drive is to address key issues associated with identifying mechanisms and establish empirically supported treatments for emotional dysregulated youth, particularly with sever irritability. Irritability is a negative valence, high arousal state, conceptualized as a low threshold for frustration and proneness to anger. It is associated with disruptive behaviors and temper outbursts. Clinically impairing irritability is among the most common psychiatric problems in youth, presenting in multiple clinical diagnoses, predicting later psychopathology and functional impairment. Despite its public health significance, the mechanisms of pediatric irritability are largely unknown and there are no empirically supported treatments. My interests on exploring mechanisms as potential treatment targets for emotional dysregulation problems evolved throughout my graduate training in Professor Yair Bar- Haim’s lab, Tel-Aviv University, while I explored maladaptive cognitive processing in the context of anxiety, stress, and trauma, and how cognitive bias modification training could implicitly prime emotion regulation in response to clinically relevant stimuli (e.g., Naim et al., 2015, AJP). In my current work in Dr. Brotman’s Neuroscience and Novel Therapeutics lab, the National Institute of Mental Health, I investigate aberrant processing of affective stimuli and response reactivity as potential mechanisms underlying pediatric irritability. I leverage a multi-modal approach that includes physiology [e.g., functional magnetic resonance imaging (fMRI) and peripheral measures], cognitive- behavioral paradigms, clinical assessment, and ecological momentary assessment (EMA). I have utilized EMA to investigate real-time irritability presentation in youth’s daily lives (Naim et al. 2021, Development and Psychopathology) and to explore daily fluctuations in positive and negative affect (Naim et al, 2022, Depression and Anxiety). Finding provided evidence to the transdiagnostic nature of irritability while emphasizing increased severity and fluctuations of symptoms among emotional dysregulated youth. Elevated frustration emerged as a core clinical component of irritability. Taking a mechanistic approach, I used physiological recording to examine the relation between cardiovascular reactivity and irritability in a context of frustration (Naim et al., 2021, IJMPR). A transdiagnostic sample of youth were measured for cardiovascular reactivity during a frustration-inducing task via a wearable device. Higher irritability was associated with increased physiological reactivity during the task and with lower recovery rate following the task. I further extended this peripheral work to a neural level to explore the neurobiology of irritability while attending to angry-face stimuli (Naim et al., 2022, Neuropsychopharmacology). I performed fMRI analyses for brain activation and amygdala functional connectivity. In a transdiagnostic sample of 351 youth, I found that youth with high irritability who also present attention bias towards angry faces had a poor amygdala connectivity with multiple brain regions (e.g. inferior frontal gyrus) implicated with regulation of attention and emotion. Taken together, these preliminary findings suggest aberrant affective processing and increased physiological reactivity for anger-inducing cues in irritability, providing the foundation to explore these as potential treatment targets. As a first step, our group conducted a clinical study of novel treatment for irritable youth applying exposure to anger-inducing stimuli (Naim et al., 2021, BMJ Open). Patients were gradually exposed and directed their attention to evocative triggers repeatedly and controllably in sessions. The goal was to increase youth’s tolerance to the negative affect and to enhance adaptive regulation. Preliminary data suggest efficacy of this intervention in reducing irritability symptoms.
This travel award would provide me with the funding to attend and present my current work on sleep and irritable mood daily dynamics. My participation will inform my goals on integrating clinical science and advanced quantitative methods to study phenotyping and mechanisms of irritability by learning from researchers and experts on the complex interaction plays between brain, genes, and environmental factors in the context of mood and emotions.
Benjamin Panny, BS | University of Pittsburgh | MS Biostatistics, Clinical Application of Neuroscience Laboratory
Name: Benjamin Panny, BS
University: University of Pittsburgh
Department: Department of Biostatistics, Department of Psychiatry
Program or Lab: MS Biostatistics, Clinical Application of Neuroscience Laboratory
Mentor or PI: Dr. Rebecca Price
Poster: Inferring reward and path learning in depressed patients with logistic regression and active inference
Background: The “two-step” task allows researchers to parse the influences of rewards and path types (high vs. low probability) on participant decisions and behaviors during task performance. The influence of ketamine and cognitive training interventions on two-step task performance in depressed patients is unknown. Additionally, how to optimally fit active inference models to this task in this population is an open question.
Methods: Task data was collected in a sample of depressed patients (n = 104) in a RCT involving a single ketamine infusion and automated self-association training. Task data was collected at between 2 to 5 visits for each participant. Multilevel logistic regression models were fit to the data to compare reward and path learning according to intervention arm. “Out of the box” active inference simulations were used to simulate plausible performance on this task.
Results: Reward-learning (“model-free planning”) and Reward x Path-learning (“model-based planning”) were present in our sample. Ketamine infusion did not affect these patterns relative to placebo infusion, nor did percent change in depression symptom scores over time. The influence of model-based planning significantly decreased over time in participants who received ketamine and automated self-association training. Active inference simulations of the task recreated standard model-based planning patterns over a variety of learning and decay rates.
Conclusion: Model-free and model-based behavior patterns are present in a sample of people with depression and our combined intervention appears to affect model-based planning over time. In
principle, active inference can computationally phenotype people’s two-step task performance.
My research interests lie in methods and models at the intersection of psychology, neuroscience, computer science, and statistics. This is expressed in my current work that goes in three directions. In the first direction, I help develop a reproducible analysis pipeline for data streams. Specifically, I engineer predictive features and build machine learning models using mobile sensing data (e.g., phone sensors, Fitbit data) to help predict cancer-related health outcomes with Dr. Carissa Low. However, this passive data type also has relevance to several other health outcomes, such as anxiety and depression severity or binge-drinking episodes. This work motivates me to attend this symposium in part to meet potential collaborators with interests in data streams (mobile sensing or otherwise) in the context of affective disorders, as well as people who are interested in open science, open-source code, and reproducible analyses.
The second direction I work in is analyzing neuroimaging data in the context of OCD. To this end, I have submitted a first-author paper with Drs. Rebecca Price and Susanne Ahmari, where we investigate using a novel negative reinforcement fMRI paradigm to explore the involvement of key brain regions, such as the mOFC, in the perpetuation of compulsive behaviors.
In the third direction I work in, I am focused on developing statistical and computational models of human behavior and decision-making. In one branch of this direction, I am developing agent-based models in collaboration with Dr. Donald Burke to understand influences of networks and health beliefs (as construed in the “Health Belief Model”) on addiction, its remission, and its “contagion”-like properties. In another branch of this direction, which I hope to present as a poster at this symposium, I am using the “two-step task” to parse the influences of rewards and path types (e.g., high vs. low probability) on decision-making. I am using statistical models, hybrid reinforcement learning, and active inference to understand depressed patients’ choices in this task. I have discovered that active inference models do not apply “out of the box” to this task, and therefore I am working on optimal probabilistic learning strategies that can help these models fit a wide variety of performance types on this task, beyond the standard “model-based” and “model-free” patterns typically found in the literature.
Ellie P. Xu, BA | University of Southern California | Cognition and Affect Regulation Lab
Name: Ellie P. Xu, BA
University: University of Southern California
Program or Lab: Clinical Science (Cognition and Affect Regulation Lab)
Mentor or PI: Dr. Jonathan P. Stange
Poster: The mind wanders to dark places: Mind-wandering predicts subsequent rumination
Authors: Ellie P. Xu, BA, Sarah L. Zapetis, BA, Jiani Li, BA, Kaley Keefe, BA, & Jonathan P. Stange, PhD
Background: Rumination has been well-established as a cognitive risk factor for major depressive disorder (MDD). Recent work has proposed that mind-wandering may facilitate rumination, and thus risk for MDD. However, it remains unclear how these processes relate. The present study uses multilevel modeling to investigate the temporal relationship between mind-wandering and rumination.
Methods: In a sample of 38 healthy volunteers and 44 individuals with remitted MDD, we utilized ecological momentary assessment of rumination and mind-wandering 3x/day for one week. Multilevel modeling investigated whether mind-wandering predicted subsequent increases in rumination, or vice versa. Individual factors (e.g., depression history) and contextual factors (e.g., intensity of negative affect; momentary impulsivity) were examined as moderators of these relationships.
Results: Mind-wandering predicted increased rumination (β=.11, p<.05), whereas rumination did not predict increased mind-wandering (β=.08, p>.32). When individuals experienced greater negative affect (β=.06, p<.04) or acted more impulsively (β=.07, p<.02) compared to usual, they showed a stronger relationship between mind- wandering and subsequent rumination. Depression history did not significantly moderate the relationship between mind-wandering and rumination, in either direction (ps>.16).
Conclusions: Our findings support that spontaneous mind-wandering may transition into rumination, particularly when individuals are experiencing greater negative affect or
acting more impulsively than usual. This suggests that, when negative affective states are present, the mind may be more likely to dwell on salient negative content.”
As a second-year Ph.D. student, I am excited to investigate what biobehavioral mechanisms underlie deficits in emotion regulation, and how such deficits contribute to the onset and persistence of affective disorders, such as depression. Ultimately, I hope my research will inform the development of personalized, just-in-time adaptive interventions to improve success with emotion regulation, particularly by advancing our ability to identify who is at risk and when they are at risk for emotion dysregulation.
After graduating from the University of Chicago, I was selected for the National Institutes of Health Postbaccalaureate Intramural Research Training Award to conduct research with Dr. Ellen Leibenluft and Dr. Julia Linke on pediatric irritability. Pediatric irritability refers to a temperament characterized by extreme anger that confers risk for negative clinical outcomes later in life, such as depression and suicidality. To date, it remains unclear how irritability relates to difficulties in regulating negative affect. At the National Institute of Mental Health (NIMH), I focused on parsing apart irritability from general deficits in emotion regulation, using a latent bi-factor approach. My poster abstract of this work was peer-reviewed and selected for publication in the supplement of Affective Science. In a second line of work at the NIMH, I focused on investigating the role of the uncinate fasciculus, a white matter tract largely implicated in emotion regulation processes, in the risk-architecture of affective disorders. I conducted two meta-analyses and found that alterations in the uncinate fasciculus could be identified in individuals with bipolar disorder (Xu et al., 2022) or depression (Xu et al., in press), but not their first-degree relatives. Altogether, my work supported that altered white matter microstructure of the uncinate fasciculus may not confer vulnerability to affective disorders, but rather could mark a consequence or “scar” of these disorders. My work at the NIMH thus advanced my interest in continuing to investigate the role of emotion dysregulation, and its neurobiological mechanisms, in affective disorders.
To support my graduate studies, I was awarded a National Science Foundation Graduate Research Fellowship to work with Dr. Jonathan Stange at the University of Southern California. Here, I aim to investigate how emotion regulation plays a role in risk and resilience in the onset, persistence, and recurrence of depression. For my master’s project, I investigated whether impulsivity interferes with successful emotion regulation, by impacting the degree to which individuals prioritize certain emotion regulation strategies over others. I found this was true at the within-person level (Xu et al., in prep), which suggests that training individuals to prioritize certain emotion regulation strategies may improve their success with emotion regulation, particularly in moments when they are acting impulsively. I am excited to have been selected to present this work as a flash talk at the 2023 Society of Affective
Science Annual Conference. In a second line of work, I examined whether mind-wandering predicts subsequent rumination, or vice versa. I found that mind-wandering predicts subsequent rumination, particularly in moments when individuals are experiencing more negative affect or acting more impulsively than usual (Xu et al., in prep). This work supports that mind-wandering may facilitate rumination and thus may contribute to risk for depression.
I look forward to the opportunity to attend the 28th Annual WSOE to learn from and discuss research ideas with leading experts in the field of emotion science. Though I am excited to network with all the presenters, I am particularly excited by the opportunity to meet Dr. Julian Thayer, who is one of the leading researchers that proposed the neurovisceral integration model. The neurovisceral integration model relates neural structures that have been implicated in cognitive, affective, and autonomic regulation to heart rate variability (HRV) and highlights the importance of examining HRV in better understanding risk for and resilience to psychopathology. Given that my graduate school research integrates both HRV and functional magnetic resonance (fMRI) imaging to understand risk for and resilience to depression, I am particularly eager to learn more about Dr. Thayer’s cutting-edge work on the neurovisceral integration model, to further inspire my own work in this area. I plan to incorporate HRV and fMRI imaging measures in my current research, to better understand how biobehavioral mechanisms contribute to emotional dysregulation. I am excited to expand my knowledge on the latest developments in emotion science and connect with scientific leaders and trainees from diverse backgrounds. The opportunity to attend WSOE is critical to building my professional network and improving my skills in scientific communication at this crucial stage early in my career.
Nicole L. Zabik, PhD | University of Nebraska Medical Center | Blackford Lab
Name: Nicole L. Zabik, Ph.D.
University: University of Nebraska Medical Center
Department: Munroe-Meyer Institute
Program or Lab: Blackford Lab
Mentor or PI: Jennifer Blackford, PhD
Poster: Anxiety predicts activation of a BNST-anxiety network during early abstinence from an alcohol use disorder
Authors: Nicole L. Zabik, Elizabeth Flook, Brandee Feola, Margaret Benningfield, Marisa Silveri, Danny Winder, Jennifer Urbano Blackford
Alcohol used disorder (AUD) is a debilitating, chronic disorder that occurs in 30% of the US population. Recovery from AUD (abstinence) is possible; however, 50% relapse within the first year. Long-term recovery is hindered by anxiety and stress that emerges during early abstinence, likely driven by neurobehavioral changes in stress system responding from alcohol use. Understanding how these neurobehavioral changes confer risk for anxiety and subsequent relapse is essential for developing successful treatments for AUD. To determine effects of abstinence on anxiety, we used a translational model of unpredictable stress to investigate an anxiety network containing the bed nucleus of the stria terminalis (BNST). Controls (HC=20) and adults with AUD in early abstinence (EA=19) underwent functional imaging to assess neural activity to unpredictable and predictable stress in a cued anticipation task. Regression analyses were performed in SPM with group (EA/HC), anxiety, and group x anxiety as predictors. We found a group x anxiety interaction during cue presentation. HC exhibited a positive relation between anxiety and BNST, insula, and prefrontal cortex activation, while EA exhibited no relation. We also found a group x anxiety interaction during unpredictable threat cues. HC participants exhibited a positive relation between anxiety and amygdala activation, while EA exhibited no relation. These data support a growing body of work highlighting the BNST as a central hub for anxiety and its dysfunction during early abstinence, as well as the need to target anxiety-related BNST networks in early alcohol abstinence.
I received my doctorate in translational neuroscience from Wayne State University, where I was mentored by Drs. Christine A. Rabinak and Mark K. Greenwald – leaders in stress and anxiety psychopathology and its effects on long-term recovery from mental health disorders. My interests in neuroscience, maladaptive behaviors in affective disorders, and translational models of behavior were explored throughout my doctoral training and led to several important contributions to the scientific community.
In my early graduate career, I led a project that determined the effect of genetic variation of endocannabinoid signaling on neurobehavioral fear responding in a translational model of PTSD (Pavlovian fear conditioning and extinction). This project supported prior work in animals and humans that a genetic variant that increases circulating endocannabinoids, therefore dampening excessive stress responding, is associated with lesser activation of fear-related brain regions. Preliminary data from this project were also presented at Society of Biological Psychiatry (2018) and American College of Neuropsychopharmacology (2020). I published a first-author manuscript of these results in the Journal of Neuroscience Research. In addition to this publication, I also led a publication in Behavioural Brain Research that characterized differences between static-image vs. immersive-reality fear conditioning in healthy adults.
Immersive reality is on the cutting-edge for functional imaging tasks to provide a more realistic environment, leading to greater behavioral and neural engagement from participants. This publication found greater activation of fear and memory-related brain regions in the immersive environment, compared to the static image environment.
Continuing my trajectory of interests, my dissertation’s goal was defining avoidance behavior, a persistent and pervasive symptom of posttraumatic stress disorder (PTSD), how it impairs natural recovery from trauma, and how it may be modulated via external cannabinoids. My dissertation determined that trauma-related avoidance behaviors (1) do not modulate an avoidance-related brain network, but (2) increase fear-related behaviors during fear extinction recall and (3) are sensitive to low-dose external cannabinoids that can dampen excessive fear. My doctoral training was supported by a NIH Ruth L. Kirschstein National Research Service Award Individual Predoctoral Fellowship (F31) grant that was awarded upon first submission.
My focus on affective disorders and how maladaptive behaviors prevent recovery from them continue to be my focus in my post-doctoral training with Dr. Jennifer Urbano Blackford. Despite the significant impact of avoidance on several forms of psychopathology (e.g., anxiety, substance use disorders), limited research defines it on a neurobehavioral level. My work with Dr. Blackford will continue to define the hindering effects of avoidance on long- term abstinence in alcohol use disorder. Importantly, this work continues to center around affect and emotion, as well as translational paradigms to probe these behaviors and experiences in humans. We are currently developing an anxiety avoidance task to probe these effects, as well as how these behaviors change over the course of recovery.
Receiving this travel award would be incredibly timely – my research interests align with the symposium’s overarching goal of investigating emotion and affect, and specifically with this year’s focus on integrating affect into treating psychiatric disorders. The symposium’s intimate environment will be ideal for providing me with up-to-date research to integrate into future projects, networking with leaders and trainees in the field, and engaging in trainee-led discussions to foster learning and development.
One of the most rewarding and unique features of the symposium is that we provide travel awards to domestic and international students to come to UW and learn with us. These scholarships go to students at all levels of their education including: undergraduates, grad students, PhD students, post-doctoral fellows, MD students and residents training in psychiatry.
This year the HealthEmotions Research Institute will support the expenses of 10 or more trainees from the US and around the world to come to Madison and participate in the symposium. This is a wonderful opportunity for students at all levels to interact with world class scientists, meet UW-Madison faculty, and forge connections with others conducting research in the broad field of affective neuroscience.
The HealthEmotions Research Institute will provide $300 for travel and 2 nights gratis hotel accommodations for 10-15 students to attend the Wisconsin Symposium on Emotion (April 19-20, 2023) and present a poster during the poster session and reception.
The 2023 travel award competition will accept applications Jan 1st through midnight on March 15, 2023. Winners will be announced March 22, 2023 and notified by email.
Undergraduates, graduates, doctorates, post-doctorates, fellows, medical students, and residents are eligible to apply for a travel award.
Please submit your application to email@example.com in the form of one PDF file that contains the following documents in this exact order:
- 2023 Wisconsin Symposium on Emotion Travel Award Application Form
- Current CV
- Abstract for the poster you will be presenting (not to exceed 250 words)
- Personal Statement of Research Interest (one page limit)
- Letter of Student Merit
Please request that your mentor email a support letter that includes a statement of student merit directly to firstname.lastname@example.org (due on March 15, 2023)
This is a competitive award. All application materials are due by midnight on March 15, 2023. Only complete applications will be considered. The entries will be judged by a selection committee of HealthEmotions Research Institute faculty members and the winners will be notified by email on March 22, 2023.