Research
Research Overview
Our lab investigates how traumatic brain injury (TBI), inflammation, and developmental or aging-related factors disrupt brain function, sleep–wake regulation, and neuroimmune communication. Positioned at the interface of neuroscience, immunology, and sleep and circadian biology, we use multiscale approaches—from molecular assays to whole-brain imaging and computational modeling—to reveal how injury alters immune signaling and reshapes neural circuits and behavior.
Neuroimmune Communication in Brain Injury and Infection
We investigate how the injured brain interprets, amplifies, and adapts to immune signals, and how these neuroimmune processes shape behavior, sleep–wake regulation, and recovery.
Key Questions
- How do microglia transition across reactive morphotypes after brain injury or inflammatory challenge?
- How does cytokine signaling alter sleep architecture, circadian rhythms, and homeostatic sleep pressure?
- How does inflammation propagate across the brain to produce region-specific vulnerability?
- How do sleep and arousal circuits regulate systemic immune responses following trauma or infection?
Sleep-Wake Disturbances and Brain Network Vulnerability
We examine how disruptions in sleep and arousal both reflect underlying pathology and actively exacerbate neural vulnerability following brain injury, aging, or inflammatory challenge.
Key Questions
- How do acute and chronic sleep disturbances drive neuroinflammation and impair recovery?
- Which features of sleep and circadian organization serve as early, noninvasive biomarkers of injury severity or trajectory?
- How does repetitive injury reshape sleep-generating circuits over time?
- Can you integrate sleep physiology, circadian analysis, and machine learning to identify predictive sleep signatures.
Aging, Development, Neurodegeneration, and Immune Interactions
Across the lifespan—from adolescence to aging—the brain shows distinct vulnerabilities to inflammation, injury, and neurodegeneration. We study how developmental stage and aging interact with immune signaling to shape long-term outcomes after traumatic brain injury, including effects on neural circuits, endocrine systems, and cognitive health.
Key Questions
- How do age and developmental stage alter microglial reactivity and neuroimmune responses to TBI?
- Does repetitive injury accelerate axonal degeneration, network fragmentation, or age-related cognitive decline?
- How do sleep disturbances contribute to dementia risk following injury or chronic inflammation?
- How does sustaining a TBI in adolescence influence puberty, neuroendocrine signaling, and brain maturation across the transition into adulthood?
Computational Method Development
We develop scalable computational tools and analytical frameworks to quantify injury, inflammation, and neural dysfunction with high precision. Our methods integrate cellular, circuit-level, and behavioral data to reveal how structural pathology and neuroimmune signaling shape whole-brain function.
Key Questions
- How can automated pipelines accelerate and standardize large-scale microglial morphology profiling?
- Can machine-learning models accurately predict injury burden or inflammatory state from histological or imaging features?
- How can we map degeneration and network vulnerability across the entire brain with spatial precision?
- How can computational frameworks link cellular pathology to sleep disruptions and other behavioral outcomes?