While studying neuroscience, I developed a strong interest in Alzheimer’s disease and the mechanisms underlying neurodegeneration. To further pursue this interest, I actively participated in the Korea University Student Neuroscience Society, where I deepened my understanding of neuroscience and neurodegenerative disorders through academic seminars, journal discussions, and literature reviews.

As I explored the field, I became particularly fascinated by the growing recognition that microglia-mediated neuroinflammation plays a critical role alongside amyloid-β and tau pathology in driving Alzheimer’s disease progression. Rather than viewing Alzheimer’s disease solely through the lens of protein aggregation, I became interested in how the dynamic responses of microglia shape disease progression.

My research interests lie at the intersection of neuroimmunology, systems biology, and functional genomics, with a particular focus on the remarkable plasticity of microglia and how their functional states are shaped by diverse pathological stimuli. Rather than simply characterizing how distinct microglial phenotypes contribute to Alzheimer’s disease, I seek to understand the mechanisms that govern stimulus-dependent microglial state transitions and determine their cellular fates within disease-associated microenvironments.

My current research integrates temporal recording technologies with single-cell transcriptomics, epigenomics, and functional genomics to uncover the dynamic regulatory principles underlying microglial state transitions. My long-term goal is to define the mechanisms that drive pathological microglial fate decisions and to develop strategies for redirecting these trajectories toward homeostatic or neuroprotective states.

Ultimately, I aspire to establish mechanistic principles for microglial state reprogramming, enabling the development of disease-modifying therapies for Alzheimer’s disease and other neurodegenerative disorders.