Dr. Tian’s major research interests focus on the cross-talk mechanisms within the neuro–glial–vascular unit and their roles in cognitive decline, with a particular emphasis on the overlapping pathologies between Alzheimer’s disease (AD) and vascular dementia (VaD). Recognizing that conventional single-target strategies have fallen short, Dr. Tian’s group seeks to redefine disease mechanisms from a holistic, cell–cell interaction perspective, aiming to uncover convergent repair pathways that are common to both amyloid-related neurodegeneration and chronic cerebral hypoperfusion.
The lab employs state-of-the-art technologies including multi-omics profiling (single-cell transcriptomics and spatial genomics), advanced in vivo two-photon imaging, chemogenetic and optogenetic modulation, CRISPR-based gene editing, and customized transgenic/lesion animal models that recapitulate mixed dementia phenotypes. These tools are integrated with high-resolution histopathological validation and behavioral phenotyping to dissect dynamic cellular responses across different disease stages.
Using this platform, the lab systematically explores the mechanism of neurovascular uncoupling, glial activation heterogeneity, and glia-endothelial dysfunction in driving synaptic loss and white matter injury. Concurrently, the team develops and evaluates targeted pharmacological, genetic, and cellular therapies for vascular dementia, Alzheimer’s disease, and other neurodegenerative diseases—with a strong commitment to translating mechanistic insights into first-in-class therapeutics that feature clear molecular targets, favorable blood–brain barrier permeability, and regenerative potential, ultimately addressing the urgent unmet clinical needs of an aging global population.
