SWHR Emerging Scholars in Women’s Health Research Award  Symposium 2026

Elle Murata is a PhD candidate in neuroscience at the University of California, Santa Barbara, where she works in the Cognitive Neuroendocrinology Lab with Dr. Emily Jacobs. Her research uses neuroimaging to examine how disruptions to the endocrine system, including hormonal contraception, endometriosis, and menopause, shape brain structure and cognitive function. Across diverse study designs and populations, her work is unified by the central premise that endocrine rhythms are fundamental organizers of brain health. She earned her BA in Neuroscience from Middlebury College and previously worked in Clinical Endocrinology at Brigham and Women’s Hospital before beginning her doctoral training.

Abstract: Neurobiological signatures of endometriosis: characterizing pain, cognition, and brain morphology

Endometriosis affects approximately 1 in 10 women, yet its impact on the brain remains poorly understood. Traditionally approached as a gynecological condition, endometriosis is increasingly recognized as a systemic disorder with broad physiological and psychological consequences. It has been classified not only as a reproductive disorder, but also as inflammatory, metabolic, and chronic pain-related in nature. Individuals with endometriosis report lower quality of life and increased risk of developing major depression and anxiety. Despite this strong evidence linking endometriosis and mental health, the neural basis of these associations remains largely unexplored. Here, we investigated the impact of endometriosis on brain health. We enrolled women with confirmed endometriosis (n = 60) and age-matched healthy controls (n = 60) who completed biofluids, questionnaires, neuropsychological testing, and multimodal MRI. Compared to controls, participants with endometriosis reported higher anxiety, depression, and pain scores and had poorer performance on select cognitive assessments. No overall group differences in global brain morphology were observed. However, within the endometriosis group, greater pain severity was significantly associated with reduced gray matter volume and greater white matter microstructure in pain-relevant regions (e.g. anterior cingulate, corticospinal tracts). These findings suggest that endometriosis is not marked by uniform alterations in brain structure, but rather that pain severity is linked to neural differences in regions critical for pain modulation. By situating endometriosis within the broader context of women’s brain health, this work bridges clinical symptoms with neurobiological mechanisms and highlights the central role of pain in shaping neural structure.

Leah Conrad graduated from Randolph-Macon College in 2023 with a BA in behavioral neuroscience and is now a PhD candidate in brain and behavior in Natalie Tronson’s lab at the University of Michigan. Using a mouse model, Leah researches how oral contraceptive exposure and neuroimmune activity interact to confer resilience against Alzheimer’s disease. Her research interests span neuroendocrinology, neuroimmunology, and reproductive biology. After finishing her PhD she plans to do a post-doctoral fellowship before pursuing an academic career. Outside of the lab, she teaches an undergraduate course titled “The Neurobiology of Alzheimer’s Disease” and she especially enjoys hanging out with her cat Junie B.

Abstract: Alzheimer’s disease and neuroimmune activity in a mouse model of oral contraceptive exposure

Women represent two-thirds of Alzheimer’s disease diagnoses (AD) which emphasizes the importance of studying sex-dependent factors underlying this discrepancy. Previous studies show that exposures to estrogen across the lifespan, including pregnancy, hormone therapy, and oral contraceptive (OC) use, are associated with decreased risk for AD. Here, we examine how OC use may act as a resilience factor to delay AD-related pathologies including neuroimmune activation and amyloid beta (Aβ) plaques. We have previously shown that after immune challenge, OC- treated mice show decreased cytokines in the dorsal hippocampus and prefrontal cortex. This suggests that OCs may increase resilience against AD via modulation of neuroimmune processes. Currently, we aim to identify interactions between OCs and neuroimmune signaling in the development of AD. We hypothesize that OC treatment would slow AD-associated behavioral changes and pathologies including aggregation of Aβ plaques and aberrant microglial activation in a mouse model of AD. Nine-week-old female APP/PS1 mice drank daily ethinyl estradiol (EE, 0.02μg) and levonorgestrel (LVNG 0.75μg) in 10% sucrose until reaching 5.5-7 months of age before undergoing cognitive behavioral testing. APP/PS1 mice showed impaired memory as compared to wild type mice on the Context Fear Conditioning (CFC) task. Additionally, plaque count increased with age in sucrose treated APP/PS1 animals but not in EE+LVNG treated 5.5-7-month-old animals. OCs may decrease AD pathology development which may be attributed to differences in microglial function and activation states. Together, this work emphasizes how hormonal states can interact with risk and resilience factors like neuroimmune dysregulation to confer resilience against long term disease states.

Sarah Broders is a second-year PhD student in the department of bioengineering at the University of California, San Diego. She earned her BS in engineering in biomedical engineering from Duke University, where she conducted research in Dr. Nenad Bursac’s laboratory as a Pratt Research Fellow and Duke Cardiovascular Research Center CURE Fellow. Her undergraduate work focused on cardiac regeneration, including the study of cardiomyocyte proliferation in engineered heart tissues and in vivo mouse models. At UC San Diego, Sarah’s doctoral research centers on understanding how biological sex influences immune responses in cardiovascular disease. As an NHLBI T32 trainee co-mentored by Dr. Brian Aguado and Dr. Farah Sheikh, she leverages the Four Core Genotypes mouse model and high-dimensional immune profiling to disentangle the effects of sex chromosomes and sex hormones during myocarditis and the foreign body response. Her work aims to identify sex-specific immune drivers of cardiac inflammation and apply this knowledge to engineer next-generation immunomodulatory biomaterials for the injured heart. Sarah is a recipient of the Fronek Family WHISDEM Fellowship for Women’s Health Research and the SWHR Emerging Scholars in Women’s Health Research Award. Through her research and mentorship, she is committed to advancing sex-inclusive cardiovascular science and improving health outcomes for women and men alike.

Abstract: Dissecting Chromosomal and Hormonal Sex Effects on Immune Responses in Myocarditis

Myocarditis is an inflammatory heart disease affecting an estimated 1.8 million people worldwide each year and remains a major cause of acute heart failure, sudden cardiac death, and progression to dilated cardiomyopathy, particularly in young adults and athletes. Although myocarditis exhibits clear sex-based disparities, with an incidence ratio of approximately 1:2–4 female to male, how sex chromosomes and sex hormones independently shape cardiac inflammation and remodeling remains poorly defined. Here, we investigate how sex chromosomes and gonadal sex independently shape immune responses during myocarditis using the Four Core Genotypes (FCG) mouse model, which decouples chromosomal sex (XX vs. XY) from gonadal sex (ovaries vs. testes). Using high-dimensional spectral flow cytometry, we profile cardiac and systemic immune populations during experimental myocarditis to define sex-dependent immune signatures. At baseline, mice with ovaries exhibit significantly higher splenic (1.65-fold CD4⁺, 1.90-fold CD8⁺) and cardiac (2.32-fold CD4⁺, 2.88-fold CD8⁺) T cell populations compared to mice with testes, independent of sex chromosome complement. This difference persists following gonadectomy at four weeks of age, suggesting a role for sex-dependent developmental hormone exposure in regulating thymic egress and peripheral lymphocyte distribution. Ongoing studies in an experimental myocarditis model are examining whether XX mice exhibit amplified T cell activation and sustained inflammatory immune profiles relative to XY mice, consistent with a potential contribution of X chromosome dosage to heightened immune responses. These analyses include 24 markers for both lymphoid and myeloid lineages, as well as resident cardiac immune populations. Together, this work aims to define how sex chromosomes and hormones interact to regulate immune behavior during myocarditis. These findings underscore the importance of incorporating both chromosomal and hormonal sex as biological variables in inflammatory heart disease and may help explain sex-dependent differences in myocarditis progression and outcomes.