Our laboratory aims to understand the physiological and pathological interactions among neurons, glial cells, immune cells, and the vascular system using multimodal imaging and functional approaches.
Alzheimer’s disease and neurodegeneration
Investigate the cellular and molecular mechanisms underlying Alzheimer’s disease and other neurodegenerative disorders, with a particular focus on neuron–glia interactions, neuroinflammation, abnormal neuronal activity, and vascular dysfunction.
Brain tumor microenvironment
Investigate interactions among tumor cells, neurons, glial cells, immune cells, and the vascular system in the brain tumor microenvironment, and examine how these interactions contribute to tumor progression and functional changes in the brain.
Neuron–glia and neuroimmune interactions
Study how microglia, astrocytes, and immune signaling regulate neuronal function and disease pathology, and explore their potential as therapeutic targets for neurological disorders.
Neurovascular coupling in health and disease
Investigate the cellular and molecular mechanisms of neurovascular coupling and examine how pathological neuronal excitation and synchronization alter cerebral hemodynamics, vascular responses, and brain function at both functional and structural levels.
Multimodal imaging of brain function and pathology
Develop and apply multimodal imaging approaches to characterize neuronal activity, glial responses, vascular dynamics, and structural changes across multiple spatial and temporal scales.
A confocal microscopy image is showing that the number of parvalbumin-expressing inhibitory neurons are increased in the DG of the hippocampus after deep brain stimulation of the anterior nuclei of the thalamus in epileptic mice. BrdU positive cells (green) which are newly generated cells also increased in the DG region and some of them are colocalized with PV expressing neurons (yellow), which indicates that DBS can result in cellular changes by increasing neurogenic substances. See Bae et al. 2022. Deep brain stimulation of the anterior nuclei of the thalamus can alleviate seizure severity and induce hippocampal GABAergic neuronal changes in a pilocarpine- induced epileptic mouse brain. Cereb Cortex 32(24): 5530-5543.