
Audrey Tyrka
· Mary E. Zucker Professor of Psychiatry and Human Behavior, Professor of Psychiatry and Human Behavior, Chair of Psychiatry and Human BehaviorBrown University · Microbiology and Immunology
Active 1991–2026
About
Audrey R. Tyrka is the Mary E. Zucker Professor and Chair of the Department of Psychiatry and Human Behavior at Brown University. She received her MD and PhD in medicine and psychology through a combined program at the University of Pennsylvania in 1999. Dr. Tyrka completed her psychiatry residency at Brown and further specialized in clinical neuroscience at the Mood Disorders Research Program and Laboratory for Clinical Neuroscience at Butler Hospital. She is also Co-Director of the COBRE Center for Stress, Trauma, and Resilience (STAR). Her research is internationally recognized for its groundbreaking work on early adversity, with discoveries related to neuroendocrine, epigenetic, and biological aging processes that underlie stress-associated mental and physical health conditions. Dr. Tyrka has contributed to pharmacologic, behavioral, and neuromodulation treatments for depression and serves as an attending psychiatrist in the Butler Hospital Transcranial Magnetic Stimulation Clinic. She is a dedicated mentor and leader in research training, serving as Principal Investigator of a NIMH-funded research training program for physician scientists in psychiatry. Her research areas include anxiety disorders, behavior, childhood abuse, cortisol, depression, development, epigenetic aging, genetics, inflammatory markers, maltreatment, mitochondrial DNA, mood disorders, neurostimulation, psychoneuroendocrinology, stress, telomeres, and treatments for these conditions.
Research topics
- Psychology
- Medicine
- Biology
- Internal medicine
- Genetics
- Clinical psychology
- Computational biology
- Environmental health
- Developmental psychology
- Psychiatry
- Engineering ethics
Selected publications
Journal of Attention Disorders · 2026-03-26
articleOpen accessObjective: There is limited evidence regarding the relationship between the severity of ADHD symptoms and the level of sleep disruption in early adolescent children. This study aimed to better understand this relationship by studying early adolescents from the Adolescent Brain Cognitive Development (ABCD) Study at the 2-year follow-up visit (mean age 12.0, n = 4,414). Methods: The “Attention Problems” scale of the Child Behavior Checklist (CBCL) was used to measure the severity of ADHD symptoms for study participants. Sleep was assessed both subjectively with the Sleep Disturbance Scale for Children (SDSC) via parent report and objectively by wrist-worn accelerometer assessment of sleep duration. Results: Total sleep disturbance showed a moderate positive correlation with ADHD symptoms ( r = .41, p < .001). In contrast, there was only a very small negative correlation between accelerometer-measured sleep duration and ADHD symptoms ( r = −.05, p < .001). Multivariate linear regression with total SDSC score as the dependent variable, adjusting for demographics, medication use, and puberty stage, showed a positive association of ADHD symptoms with total SDSC score (β = .41, 95% CI [0.38–0.44]; p < .001). A longitudinal linear mixed-effects model analysis with total SDSC score as the dependent variable also showed a positive association with ADHD symptoms with total SDSC score (β = .34, 95% CI [0.32–0.35]; p < .001). In contrast, multivariate linear regression with total sleep duration (in minutes) as the dependent variable showed only a very small negative association (β = −.03, 95% CI [−0.0–0.00]; p < .05). Conclusions: Our study shows that increased severity of ADHD symptoms is associated with worse sleep disturbance as measured by subjective parent reports; however, there is a very weak relationship between ADHD symptoms and objectively measured total sleep duration. The contrasting results are consistent with prior literature, and could be due to unmeasured variables such as deep sleep percentage or non-REM EEG delta wave power that are not captured by actigraphy. Alternatively, there is the possibility of mono-informant bias, as both the CBCL and SDSC are parent-reported, and parents may perceive relationship between worse ADHD symptoms and worse sleep disturbances, though the difference is objectively negligible.
UNC Libraries · 2026-03-26
articleOpen accessAcademic Psychiatry · 2026-03-04
articleOpen accessJournal of Family Violence · 2025-02-18
articleOpen accessJournal of Clinical and Experimental Neuropsychology · 2025-09-02 · 1 citations
articleOpen accessINTRODUCTION: Adverse childhood experiences (ACEs) are theorized to amplify the effects of poor executive functioning (EF) leading to rumination. Though, few studies test this hypothesis among adolescents. Rumination is a transdiagnostic risk factor linked to mental health problems. We tested the moderating effect of ACEs (across informants) on the association between EF (measured using neutral and negative stimuli) and depressive and anger rumination. METHOD: = 14.86, SD = .50) who completed self-reports of lifetime ACEs, depressive and anger rumination, and the affective interference resolution task (a measure of EF). Additionally, a caregiver provided lifetime report of youth ACEs, and early childhood ACEs (3-5 years of age) were assessed using child protective records and caregiver interviews. RESULTS: = .046) after controlling for gender and current mental health problems; however, these effects were no longer significant when mental health problems were removed as a covariate. Furthermore, the interaction utilizing early childhood ACEs was not significant. Lastly, the interactions between ACEs and EF assessed with neutral information on depressive rumination and brooding were null. CONCLUSIONS: There is some support for the interactive relationship between EF and ACEs on rumination. However, statistical significance varies based on model specification and assessment of constructs. It is important to utilize multi-informants to assess ACEs, EF measured across valenced stimuli, and broad conceptualizations of rumination.
Cohort Profile: Brazilian High-Risk Cohort for Mental Health Conditions (BHRC)
International Journal of Epidemiology · 2025-10-14 · 1 citations
articleOpen accessJournal of Neural Transmission · 2025-06-09
reviewOpen accessPsychoneuroendocrinology · 2025-06-05 · 1 citations
articleOpen accessSenior author9. Early Life Stress Shapes How Obesity Measures Predict Epigenetic Aging and Metabolic Health
Journal of the Academy of Consultation-Liaison Psychiatry · 2025-11-01
articleSenior authorDevelopmental Psychobiology · 2024-01-28 · 5 citations
articleOpen accessSenior authorAbstract Parent–child relationship dynamics have been shown to predict socioemotional and behavioral outcomes for children, but little is known about how they may affect biological development. The aim of this study was to test if observational assessments of parent–child relationship dynamics (cohesion, enmeshment, and disengagement) were associated with three biological indices of early life adversity and downstream health risk: (1) methylation of the glucocorticoid receptor gene ( NR3C1 ), (2) telomere attrition, and (3) mitochondrial biogenesis, indexed by mitochondrial deoxyribonucleic acid (DNA) copy number (mtDNAcn), all of which were measured in children's saliva. We tested hypotheses using a sample of 254 preschool‐aged children ( M age = 51.04 months) with and without child welfare‐substantiated maltreatment (52% with documented case of moderate‐severe maltreatment) who were racially and ethnically diverse (17% Black, 40% White, 23% biracial, and 20% other races; 45% Hispanic) and from primarily low‐income backgrounds (91% qualified for public assistance). Results of path analyses revealed that: (1) higher parent–child cohesion was associated with lower levels of methylation of NR3C1 exon 1 D and longer telomeres, and (2) higher parent–child disengagement was associated with higher levels of methylation of NR3C1 exon 1 D and shorter telomeres. Results suggest that parent–child relationship dynamics may have distinct biological effects on children.
Recent grants
NIH · $905k · 2009
Childhood Maltreatment:Biomarkers of Risk and Resilience
NIH · $2.6M · 2010–2016
Childhood Maltreatment: Epigenetic Modulation of the Glucocorticoid Receptor
NIH · $389k · 2011–2014
Early Life Stress: Epigenetic Regulation of Endocrine and Immune Pathways
NIH · $2.6M · 2014–2021
NIH · $87k
Frequent coauthors
- 551 shared
Linda L. Carpenter
Butler Hospital
- 522 shared
Lawrence H. Price
- 256 shared
Noah S. Philip
Brown University
- 141 shared
Stephanie H. Parade
Bradley Hospital
- 129 shared
Teresa E. Daniels
Butler Hospital
- 100 shared
Kathryn K. Ridout
Kaiser Permanente
- 95 shared
Hung‐Teh Kao
Brown University
- 83 shared
Lawrence H. Sweet
University of Georgia
Education
- 1999
M.D., Medicine and Psychology
University of Pennsylvania
- 1999
Ph.D., Medicine and Psychology
University of Pennsylvania
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