Aging is inevitable. Understanding it is not.
Our lab is interested in a fundamental question: how do cells communicate across space to shape nervous system aging and age-related diseases? We focus on the nervous system as a central hub of organismal aging, and aim to uncover how interactions between neurons, glial cells, and peripheral tissues collectively drive functional decline and disease progression.
Aging is not merely a cell-intrinsic process, but is actively coordinated through intercellular and systemic signaling. My previous work has contributed to this emerging view by identifying novel mechanisms of cell–cell communication in aging. For example, we demonstrated that heat shock proteins (HSPs) can act as signaling molecules transmitted from aged neurons to glial cells via extracellular vesicles, thereby modulating brain aging. We also uncovered a new role for the ion channel TMC1 in delaying neuronal aging through extrasynaptic GABA signaling. These studies illustrate how molecular signals are propagated across cells and tissues to influence nervous system aging.
Building on these discoveries, the Spatial Aging Biology & Disease Lab seeks to establish a new conceptual and technological framework to study aging in a spatial and systems context. We combine cutting-edge approaches, including proximity labeling–based cell- and tissue-specific proteomics, multi-omics sequencing, and large-scale genetic screening, with classical molecular biology, biochemistry, and computational analysis. Using multiple model systems such as C. elegans, mouse models, and organoids, we aim to uncover conserved principles as well as context-specific mechanisms of nervous system aging.
Our research directions mainly focus on:
1. Neuron-glia communication in brain aging and neurodegeneration.
2. Brain-periphery interactions and their role in nervous system aging.
3. Extracellular vesicle (EV) mediated signaling across cells/tissues/individuals during aging.