Research Vision
We envision a future where prevention and treatment of neurological disorders are grounded in a deep, causal understanding of the immune–vascular–brain axis – and designed inclusively from the start. Our lab brings together foundation-scale machine learning and experimental biology to move from prediction to intervention.
Our active-learning loop starts with interpretable, uncertainty-aware models that nominate candidate regulatory circuits. We test these directly in human organoids and isogenic iPSC-derived glial and vascular cells. The experimental results then feed back into the models, helping distinguish causal biology from correlation and surfacing clinically actionable mechanisms.
Over the next decade, this platform will deliver three field-defining resources:
- A publicly validated atlas of causal regulatory programs across disease stages and ancestries;
- Portable biomarkers of immune–vascular dysregulation to enable patient stratification;
- A translational pipeline that turns noncoding variation and RNA processing events into first-in-class therapeutic targets.
We are equally committed to transforming how this science is done. Our infrastructure embeds inclusion and rigor, from prospectively defined ancestry and sex representation thresholds to GPU-accelerated, FAIR-compliant analysis pipelines that others can adopt.
Through open resources and the training of a diverse, cross-disciplinary workforce fluent in both computation and experiment, we aim to convert immune–vascular biology into precision, population-informed interventions – reducing disparities while accelerating therapies that benefit everyone.
Research Interests
Genetic ancestry in the brain
In neuroscience and genomics, individuals with recent African ancestry (AA) account for less than 5% of large-scale research cohorts for brain disorders but are 20% more likely to experience a major mental health crisis. Furthermore, divergent responses to antipsychotics between AA and European ancestry (EA) have been linked to genetic differences. Understanding these genetic and/or regulatory differences between AA and EA in the human brain, is essential to the development of effective neurotherapeutics and potentially could decrease health disparities for neurological disorders.
Schizophrenia
Caudate nucleus and schizophrenia
Most studies of gene expression in the brain of individuals with schizophrenia have focused on cortical regions. However, subcortical nuclei such as the striatum are prominently implicated in the disease, and current antipsychotic drugs target the striatum’s dense dopaminergic innervation.
Sex differences and schizophrenia
Schizophrenia is a complex neuropsychiatric disorder with sexually dimorphic features, including differential symptomatology, drug responsiveness, and male incidence rate. To date, only the prefrontal cortex has been studied in large-scale transcriptome analyses for sex differences in schizophrenia.
Neurodegeneration
Neurodegenerative disorders disproportionately impact underserved communities, yet the molecular mechanisms that drive this imbalance remain poorly understood. Our lab is expanding into neurodegeneration research to investigate how genetic ancestry shapes vulnerability to age-related cognitive decline and neuroinflammation. By integrating transcriptomic and epigenomic datasets from postmortem brain tissues and patient-derived models, we aim to identify ancestry-aware biomarkers and therapeutic targets that can inform precision medicine approaches for Alzheimer’s disease and related dementias. We welcome collaborations that help accelerate this work and amplify its impact for diverse communities.
Collaborations
Angiotensin II receptors in the human lung
Understanding the precise distribution and function of angiotensin receptors within the lung is crucial for developing effective treatments for lung diseases like COPD and IPF. Here, our goal is to provide a foundational framework by mapping the expression patterns of AGTR1 and AGTR2 across different lung cell types and identifying their involvement in specific disease states. Our findings will offer new insights into the complex role of the renin-angiotensin system in lung health and disease, paving the way for targeted therapeutic interventions.