Growing up with multiple neurological conditions and limited access to treatment, I became determined to pursue neuroscience—not only to better understand myself but also to develop patient-first, accessible solutions. While earning a B.S. in Neuroscience from UCLA, I recognized the need for further research training to develop viable neurological therapeutics. This led me to pursue a PhD in Clinical Neuroscience at the University of Cambridge, where I investigate Interleukin-6 signalling in Traumatic Brain Injury (TBI) and Post-Traumatic Epilepsy (PTE) to explore IL6’s therapeutic potential.

I plan to continue with a postdoctoral fellowship to translate my doctoral research into a therapy. My ultimate goal is to launch a startup that addresses health disparities, particularly in TBI, where no established cure exists.

The Hong Kong Laureate Forum offers an unparalleled opportunity to engage with Shaw Laureates and distinguished scientists, connect with like-minded peers in the global scientific community, and gain insightful feedback while showcasing my research on an international stage. Engaging with experts will provide perspectives that refine my approach to bridging neuroscience and entrepreneurship. Presenting at the Forum will be a pivotal step in my journey toward creating a neuroscience-focused startup that empowers individuals with the treatments I once lacked.

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Traumatic Brain Injury (TBI) is a leading cause of death and disability worldwide, with no established cure. Neuroinflammation drives secondary injury (additional brain damage caused by processes downstream of the initial injury), worsening recovery and increasing the risk of long-term complications like post-traumatic epilepsy (PTE). IL-6, a key inflammatory mediator post-TBI, is linked to poorer outcomes and is potentially modifiable with existing medications. An imbalance between its pathways may exacerbate neuroinflammation and hinder recovery, yet their temporal dynamics and cellular mechanisms remain poorly understood—an area my PhD investigates.
My latest work has indicated not only that IL-6 is implicated in PTE development but also that it may serve as a biomarker for predicting its onset. Emerging evidence, including our own, suggests IL-6 inhibitors like tocilizumab could be repurposed to prevent PTE. This summer, I will conduct a fellowship at USAMRICD, testing tocilizumab in an animal model. This study aims to establish the direction of the association between IL-6 and PTE discovered in the observational work undertaken during the first part of my PhD. We hypothesize that blocking IL-6 signalling in the acute phase of TBI may reduce epilepsy risk and improve recovery post-TBI, advancing IL-6 as a viable therapeutic target.