About

Ruth O'Hara is a faculty member in the Department of Psychiatry and Behavioral Sciences/Public Mental Health and Population Sciences at Stanford University. Her research focuses on mental health and behavioral sciences, contributing to the understanding of public mental health issues. She is involved in academic activities related to her field, supporting the interdepartmental undergraduate Program in Human Biology.

Selected publications

• Engaging stakeholders to strengthen support for community-engaged research at Stanford School of Medicine: An institutional assessment and action planning approach

  Journal of Clinical and Translational Science · 2025-01-01 · 5 citations

  articleOpen access

  Introduction: Despite the central role that patient and community engagement plays in translational science and health equity research, there remain significant institutional barriers for researchers and their community partners to engage in this work meaningfully and sustainably. The goal of this paper is to describe the process and outcomes of Engage for Equity PLUS at Stanford School of Medicine, which was aimed at understanding and addressing institutional barriers and facilitators for community-engaged research (CEnR). Methods: = 35). These data were employed for action planning to identify strategies to build institutional support for CEnR. Results: Findings revealed several key institutional barriers to CEnR, such as the need to modify organizational policies and practices to expedite and simplify CEnR administration, silos in collaboration, and the need for capacity building. Facilitators included several offices devoted to and engaging in innovative CEnR efforts. Based on these findings, action planning resulted in three priorities: 1) Addressing IRB barriers, 2) Addressing barriers in post-award policies and procedures, and 3) Increasing training in CEnR within Stanford and for community partners. Conclusions: Addressing institutional barriers is critical for Academic Medical Centers and their partners to meaningfully and sustainably engage in CEnR. The Engage for Equity PLUS process offers a roadmap for Academic Medical Centers with translational science and health equity goals.

  PublisherOA PDFDOI

• Gene dosage effects of 22q11.2 copy number variants on in-vivo measures of white matter axonal density and dispersion

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-30

  preprintOpen access

  22q11.2 deletion (22qDel) and duplication (22qDup) carriers have an increased risk of neurodevelopmental disorders and exhibit altered brain structure, including white matter microstructure. However, the underlying cellular architecture and age-related changes contributing to these white matter alterations remain poorly understood. Neurite orientation dispersion and density imaging (NODDI) was used on mixed cross-sectional and longitudinal data to examine group differences and age-related trajectories in measures of axonal density (i.e., intracellular volume fraction; ICVF), axonal orientation (orientation dispersion index; ODI) and free water diffusion (isotropic volume fraction; ISO) in 50 22qDel (n scans = 69, mean age = 21.7, age range = 7.4-51.1, 65.2% female) and 24 22qDup (n scans = 34, mean age = 23.3, age range = 8.3-49.4, 55.0% female) carriers, and 890 controls (n scans = 901, mean age = 21.9, age range = 7.8-51.1, 54.5%). The results showed widespread gene dosage effects, with higher ICVF in 22qDel and lower ICVF in 22qDup compared to controls, and region-specific effects of the 22qDel and 22qDup on ODI and ISO measures. However, 22qDel and 22qDup carriers did not exhibit an altered age-related trajectory relative to controls. Observed differences in ICVF suggest higher white matter axonal density in 22qDel and lower axonal density in 22qDup compared to controls. Conversely, differences in ODI are highly localized, indicating region-specific effects on axonal dispersion in white matter. We do not find evidence for altered developmental trajectories of axonal density or dispersion among 22q11.2 CNV carriers, suggesting stable disruptions to neurodevelopmental events before childhood.

  PublisherOA PDFDOI

• Cellular mechanisms of early brain overgrowth in autistic children: elevated levels of GPX4 and resistance to ferroptosis

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-02-01

  preprintOpen access

  Abstract Autistic individuals with disproportionate megalencephaly (ASD-DM), characterized by enlarged brains relative to body height, have higher rates of intellectual disability and face more severe cognitive challenges than autistic children with average brain sizes. The cellular and molecular mechanisms underlying this neurophenotype remain poorly understood. To investigate these mechanisms, we generated human induced pluripotent stem cells from non-autistic typically developing children and autistic children with and without disproportionate megalencephaly. We assessed these children longitudinally from ages two to twelve years using magnetic resonance imaging and comprehensive cognitive and medical evaluations. We show that neural progenitor cells (NPCs) derived from ASD-DM children exhibit increased rates of cell survival and suppressed cell death, accompanied by heightened oxidative stress and ferrous iron accumulation. Despite these stressors, ASD-DM NPCs actively suppress apoptosis and ferroptosis by regulating proteins such as caspase-3 (CASP3), poly(ADP-ribose) polymerase 1 (PARP1), and glutathione peroxidase 4 (GPX4). Cellular ferroptotic signatures are further supported by elevated expression of selenocysteine genes, including GPX4 , in the blood of ASD-DM children and their mothers, suggesting potential hereditary or environmental influences. Furthermore, we show that peripheral expression of GPX4 and other selenocysteine genes correlate with cognitive outcomes (IQ). These findings underscore the role of ferroptosis in autism, pointing to potential diagnostic biomarkers and targets for intervention.

  PublisherOA PDFDOI

• How to Review Grant Applications

  2025-01-01

  book-chapter1st authorCorresponding
  PublisherDOI

• Data science and artificial intelligence in biology, health, and healthcare

  Journal of Clinical and Translational Science · 2025-01-01

  editorialOpen access
  PublisherOA PDFDOI

• Dysregulated regulatory T cell response in immunosuppressed individuals is associated with increased inflammation in COVID-19 breakthrough infections 2587

  The Journal of Immunology · 2025-11-01

  articleOpen access

  Abstract Description Regulating the immune balance is important for launching protective immune responses, while curtailing pathologic responses. Regulatory T cells (Tregs) and immunosuppressants play key roles in this balance. This immune balance goes awry in severe COVID-19 marked by dysfunctional inflammatory responses. In immunosuppressed individuals, who are at an increased risk for severe COVID-19, the impact of immunosuppressants on Tregs and inflammatory responses in breakthrough infections remain unclear. Using single-cell RNA sequencing, mass cytometry, and plasma proteomics, we analyzed peripheral immune responses in uninfected immunocompetent individuals, uninfected heart transplant recipients, and both immunocompetent and immunosuppressed individuals with breakthrough COVID-19 infections. Unexpectedly, uninfected heart transplant recipients exhibited higher activation and pro-inflammatory states in key immune cells (CD4+ and CD8+ T cells, B cells, and CD14+ monocytes) and elevated plasma inflammatory markers (CXCL10, IFNγ, TNF, CCL3, CCL4, and MCP-1) compared to immunocompetent counterparts. This elevated inflammatory state may be partially attributed to dysregulated Treg activity and TGFβ signaling in heart transplants. We further discovered heightened peripheral immune activation and reduced Treg activation in immunosuppressed individuals with breakthrough infections, underscoring the impact of immunosuppressants on immune balance in COVID-19. Funding Sources Supported by NIH 5T32AI007290-37, F31AI179125, T32AI007502, 5T32HL129970, the Bill and Melinda Gates Foundation OPP113682, K23 HL124663, Burroughs Wellcome Investigators in the Pathogenesis of Infectious Disease 1016687, gift from the Quattrone Family, U19AI057229 – 17W1 COVID SUPP #2, Chan Zuckerberg Biohub Investigator Program, the Mercatus Center Topic Categories Immune Mechanisms of Human Disease (HUM)

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• A Stratified Precision Medicine Trial Targeting Selective Mechanisms of Alpha 2A Agonism as a Treatment for the Cognitive Biotype of Depression: The BIomarker Guided (BIG) Study for Depression

  Research Square · 2025-02-27 · 2 citations

  preprintOpen access
  PublisherOA PDFDOI

• 76.4 Innovative Pharmacological Trials Targeting Sleep Disturbances in Autism

  Journal of the American Academy of Child & Adolescent Psychiatry · 2025-10-01

  article
  PublisherDOI

• Prior vaccination prevents overactivation of innate immune responses during COVID-19 breakthrough infection

  Science Translational Medicine · 2025-01-29 · 18 citations

  articleOpen access

  At this stage in the COVID-19 pandemic, most infections are "breakthrough" infections that occur in individuals with prior severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exposure. To refine long-term vaccine strategies against emerging variants, we examined both innate and adaptive immunity in breakthrough infections. We performed single-cell transcriptomic, proteomic, and functional profiling of primary and breakthrough infections to compare immune responses from unvaccinated and vaccinated individuals during the SARS-CoV-2 Delta wave. Breakthrough infections were characterized by a less activated transcriptomic profile in monocytes and natural killer cells, with induction of pathways limiting monocyte migratory potential and natural killer cell proliferation. Furthermore, we observed a female-specific increase in transcriptomic and proteomic activation of multiple innate immune cell subsets during breakthrough infections. These insights suggest that prior SARS-CoV-2 vaccination prevents overactivation of innate immune responses during breakthrough infections with discernible sex-specific patterns and underscore the potential of harnessing vaccines in mitigating pathologic immune responses resulting from overactivation.

  PublisherOA PDFDOI

• Sleep in Autism Spectrum Disorder: From Foundations to Frontiers

  Journal of Autism and Developmental Disorders · 2025-10-23

  articleOpen accessSenior author
  PublisherOA PDFDOI