George Arthur Buzzell

Research topics

Matched from this investigator's NIH project titles and abstracts.

• Anxiety Disorders
• Emotion and Affective Neuroscience
• Child and Adolescent Development
• Social Neuroscience
• Developmental Cognitive Neuroscience

Active NIH awards

• A developmentally-sensitive mechanism underlying the escalation of adolescent social anxiety

  5R01MH131637-04

  NIMH · FY 2025 · $654K

  Abstract Social anxiety disorder (SAD) is a chronic, impairing condition that typically emerges during adolescence and affects about 10% of the population. Treatment response rates for SAD are markedly lower than for other anxiety disorders, thus presenting an urgent need to identify novel therapeutic targets that can inform new interventions for this difficult-to-treat disorder. We propose to address this need by testing a developmentally-informed, mechanistic model of the escalation of impairing social anxiety symptoms (SA) in early-to-mid adolescence; our model centers on Fear of Negative Evaluation (FNE) and Hypervigilance for Errors in the presence of peers, with a focus on frontal brain oscillations as central to this escalation. Adolescence represents a sensitive period for the development of social cognition and cognitive control. At the psychological level, social fears and FNE exhibit normative increases across adolescence, given the increasing importance of peers during this developmental window. At the neural level, frontal brain systems underlying social cognition and cognitive control exhibit protracted development across adolescence, including development of the frontal cortex and associated 4-8 Hz “theta” oscillations causally implicated in cognitive control. Our central hypothesis is that adolescent increases in FNE, alongside development of the frontal cortex, create a maladaptive feedback loop: adolescents become Hypervigilant to Errors in social settings, further increasing FNE, and ultimately, impairing SA. Our model predicts (Aim 1) that developmental increases in FNE lead to increased concerns over performance in the presence of peers, which in turn amplifies Hypervigilance for Errors (that is, increased strength of error-related theta oscillations). We further predict (Aim 2) that increased Hypervigilance for Errors leads to more critical self- evaluations and confirmations of initial fears, which worsen FNE/SA over time. Moreover, we predict adolescents who exhibit greater synchrony in theta oscillations across medial-lateral frontal cortex are at greatest risk and will display the largest increases in FNE/SA. To test our model, we will collect an accelerated longitudinal study of 256 adolescents, spanning ages 11-15, biologically male/female, and ranging in FNE/SA. Participants will complete a modified cognitive control task in peer presence/absence (via Zoom) as EEG is recorded. With an eye toward future translational work, we will also (Aim 3) establish the ecological validity of our neural measures by testing links to micro-coded behaviors indicative of SA within a social interaction task. Given that escalation of SA occurs during puberty and within a broader social context, we will also measure, control for, and explore the possible moderating roles of puberty, as well as effects of social and demographic variables. A key strength of this proposal is that our team has a proven record in developmental psychopathology and experimental therapeutics, providing a clear path for translating findings from this project into novel, brain-based therapeutics and thereby shortening the distance “from bench to bedside.”

• A developmentally-sensitive mechanism underlying the escalation of adolescent social anxiety

  5R01MH131637-03

  NIMH · FY 2024 · $689K

  Abstract Social anxiety disorder (SAD) is a chronic, impairing condition that typically emerges during adolescence and affects about 10% of the population. Treatment response rates for SAD are markedly lower than for other anxiety disorders, thus presenting an urgent need to identify novel therapeutic targets that can inform new interventions for this difficult-to-treat disorder. We propose to address this need by testing a developmentally-informed, mechanistic model of the escalation of impairing social anxiety symptoms (SA) in early-to-mid adolescence; our model centers on Fear of Negative Evaluation (FNE) and Hypervigilance for Errors in the presence of peers, with a focus on frontal brain oscillations as central to this escalation. Adolescence represents a sensitive period for the development of social cognition and cognitive control. At the psychological level, social fears and FNE exhibit normative increases across adolescence, given the increasing importance of peers during this developmental window. At the neural level, frontal brain systems underlying social cognition and cognitive control exhibit protracted development across adolescence, including development of the frontal cortex and associated 4-8 Hz “theta” oscillations causally implicated in cognitive control. Our central hypothesis is that adolescent increases in FNE, alongside development of the frontal cortex, create a maladaptive feedback loop: adolescents become Hypervigilant to Errors in social settings, further increasing FNE, and ultimately, impairing SA. Our model predicts (Aim 1) that developmental increases in FNE lead to increased concerns over performance in the presence of peers, which in turn amplifies Hypervigilance for Errors (that is, increased strength of error-related theta oscillations). We further predict (Aim 2) that increased Hypervigilance for Errors leads to more critical self- evaluations and confirmations of initial fears, which worsen FNE/SA over time. Moreover, we predict adolescents who exhibit greater synchrony in theta oscillations across medial-lateral frontal cortex are at greatest risk and will display the largest increases in FNE/SA. To test our model, we will collect an accelerated longitudinal study of 256 adolescents, spanning ages 11-15, biologically male/female, and ranging in FNE/SA. Participants will complete a modified cognitive control task in peer presence/absence (via Zoom) as EEG is recorded. With an eye toward future translational work, we will also (Aim 3) establish the ecological validity of our neural measures by testing links to micro-coded behaviors indicative of SA within a social interaction task. Given that escalation of SA occurs during puberty and within a broader social context, we will also measure, control for, and explore the possible moderating roles of puberty, as well as effects of social and demographic variables. A key strength of this proposal is that our team has a proven record in developmental psychopathology and experimental therapeutics, providing a clear path for translating findings from this project into novel, brain-based therapeutics and thereby shortening the distance “from bench to bedside.”

• A developmentally-sensitive mechanism underlying the escalation of adolescent social anxiety

  5R01MH131637-02

  NIMH · FY 2023 · $687K

  Abstract Social anxiety disorder (SAD) is a chronic, impairing condition that typically emerges during adolescence and affects about 10% of the population. Treatment response rates for SAD are markedly lower than for other anxiety disorders, thus presenting an urgent need to identify novel therapeutic targets that can inform new interventions for this difficult-to-treat disorder. We propose to address this need by testing a developmentally-informed, mechanistic model of the escalation of impairing social anxiety symptoms (SA) in early-to-mid adolescence; our model centers on Fear of Negative Evaluation (FNE) and Hypervigilance for Errors in the presence of peers, with a focus on frontal brain oscillations as central to this escalation. Adolescence represents a sensitive period for the development of social cognition and cognitive control. At the psychological level, social fears and FNE exhibit normative increases across adolescence, given the increasing importance of peers during this developmental window. At the neural level, frontal brain systems underlying social cognition and cognitive control exhibit protracted development across adolescence, including development of the frontal cortex and associated 4-8 Hz “theta” oscillations causally implicated in cognitive control. Our central hypothesis is that adolescent increases in FNE, alongside development of the frontal cortex, create a maladaptive feedback loop: adolescents become Hypervigilant to Errors in social settings, further increasing FNE, and ultimately, impairing SA. Our model predicts (Aim 1) that developmental increases in FNE lead to increased concerns over performance in the presence of peers, which in turn amplifies Hypervigilance for Errors (that is, increased strength of error-related theta oscillations). We further predict (Aim 2) that increased Hypervigilance for Errors leads to more critical self- evaluations and confirmations of initial fears, which worsen FNE/SA over time. Moreover, we predict adolescents who exhibit greater synchrony in theta oscillations across medial-lateral frontal cortex are at greatest risk and will display the largest increases in FNE/SA. To test our model, we will collect an accelerated longitudinal study of 256 adolescents, spanning ages 11-15, biologically male/female, and ranging in FNE/SA. Participants will complete a modified cognitive control task in peer presence/absence (via Zoom) as EEG is recorded. With an eye toward future translational work, we will also (Aim 3) establish the ecological validity of our neural measures by testing links to micro-coded behaviors indicative of SA within a social interaction task. Given that escalation of SA occurs during puberty and within a broader social context, we will also measure, control for, and explore the possible moderating roles of puberty, as well as effects of social and demographic variables. A key strength of this proposal is that our team has a proven record in developmental psychopathology and experimental therapeutics, providing a clear path for translating findings from this project into novel, brain-based therapeutics and thereby shortening the distance “from bench to bedside.”

• Ecological Assessment of Cognitive Control in Individuals with Social Anxiety

  1R21MH131928-01A1

  NIMH · FY 2023 · $406K

  PROJECT SUMMARY Social anxiety disorder is an impairing condition that typically emerges during adolescence, affecting about 10% of the population. Models of social anxiety (SA) elucidate excessive self-focus and sensitivity to mistakes as factors that negatively impact quality of life. Using traditional cognitive neuroscience paradigms, prior work has identified neural measures associated with enhanced self-detection of errors (Error Monitoring), that predicts SA, as well as anxiety more generally. However, a major challenge with translational interventions developed from cognitive neuroscience paradigms is the transfer to ecologically valid settings. There is a critical need for the design and validation of novel tasks/protocols to identify and reliably measure brain-based therapeutic targets for SA within ecologically valid, “real-world” settings that are applicable to youth. In line with our long-term goal of developing brain-based interventions for adolescent SA, the purpose of this proposal is to optimize and validate a novel, ecologically-valid task that will reliably assess neural and behavioral measures associated with social anxiety. We propose a sequential, multi-study project that leverages a mixed-methods approach to optimize and validate our novel Natural Reading task and demonstrate its utility in predicting SA. By developing an ecologically-valid paradigm early in the experimental therapeutics process, we increase the probability of successful transfer of effects in future interventions that target measures captured by this novel task; in this way, our proposal is strongly aligned with the Institute’s mission to transform the understanding and treatment of mental illnesses. We propose two aims: (1) a pilot study to optimize the design of our novel Natural Reading task and (2) a second study to establish the reliability and predictive power of the Natural Reading task in relation to SA. In Study 1, 10 youths (13-17 yrs., 5 high and 5 low SA) will perform the Natural Reading task and a traditional Flanker task, both alone and while under social observation by a peer. To investigate experiential aspects of task completion, including participants' perceptions and self-assessed task performance, qualitative methods will be employed in the analysis of semi-structured interview data. Qualitative results will be leveraged to optimize design of the Natural Reading task prior to proceeding with Study 2 data collection (Aim 2). For Study 2, within a second sample of 80 youth (13-17 yrs.), participants will perform an optimized version of the Natural Reading task and a traditional Flanker task, alone and under peer observation. Neural measures of Error Monitoring, along with associated behavioral measures, will be extracted to perform quantitative analyses. Hypothesis 2A: Both tasks will exhibit acceptable levels of reliability in neural and behavioral measures. Hypothesis 2B: Within each task, measures of Error Monitoring extracted from the peer (vs. alone) condition will predict additional variance in trait SA and state anxiety levels. Hypothesis 2C: Focusing on the peer condition, measures of Error Monitoring extracted from the Natural Reading Task will predict additional variance in SA, above and beyond measures of Error Monitoring extracted from the traditional Flanker task.