Gab Seok Kim

We are investigating the role of interferon signaling and reactive oxygen species following stroke, as well as signal transduction in cerebrovascular diseases. Current research focuses on understanding the molecular and cellular changes, such as neuroinflammation and neurodegeneration, that occur in the brain after stroke and in other neurodegenerative diseases, particularly how interferon signaling contributes to functional outcomes in stroke. To address this, we utilize in vivo animal stroke models with unique knockout, transgenic, and reporter mice and in vitro primary cell models and tools to modulate neuroinflammation. The Kim Lab's current research focuses on exploring novel mechanisms that control microglial functions, including pro-inflammatory responses, microglial phagocytosis, and reactive oxygen species (ROS) generation in aged brains, Alzheimer's disease (AD), and other diseased states. This work builds on our recent identification of novel gene expression signatures from a scRNA-seq dataset of young and aged mice following stroke. Recently, we discovered an interferon-related gene that is highly upregulated in activated microglia and other cells in aged brains after stroke. We hypothesize that this gene (or its product) has significant potential to initiate neurodegeneration and neuroinflammation by modifying microglial functions in stroke and AD. We are investigating how other interferon-related gene products regulate blood-brain barrier integrity, immune cell infiltration into the brain, and subsequent gliosis, leading to white and gray matter injury in the cortex and thalamus following stroke and in AD brains. We believe that the gene identified in our lab may contribute to the evolution of neuroinflammation in post-stroke brains, potentially expanding infarction.