Vascular dementia is a growing public health concern, largely driven by vascular impairments that contribute to cognitive decline. These impairments follow two main pathways: acute and chronic. Acute vascular events (e.g., ischemic stroke, hemorrhage) can trigger rapid cognitive decline, while chronic vascular cognitive impairment (VCI) reflects cumulative damage from progressive changes such as white matter hyperintensities, often without a single triggering event. Both pathways frequently coexist, as acute strokes often occur in brains already affected by small vessel disease or neurodegeneration. Although they share overlapping mechanisms, they differ in onset, progression, and neuropathology.
The optimal timing for treatment to prevent cognitive decline likely differs between these pathways. Acute vascular events may create a critical window for neuroprotection and rehabilitation, whereas chronic pathology may require sustained, long-term preventive approaches. Understanding the relative contribution of each pathway to the cognitive impairment is essential for designing effective care plans.
This project aims to (1) compare cognitive trajectories following acute vascular events versus chronic vascular burden and assess how event timing and severity shape long-term outcomes; and (2) identify early markers of cognitive vulnerability using biomarkers (e.g., NfL, GFAP, amyloid/tau ratios) and neuroimaging features to predict progression in each pathway.
Clarifying the mechanistic distinctions and biomarker profiles between these pathways will help identify critical windows for intervention and support more tailored prevention strategies across the spectrum of vascular cognitive impairment. Ultimately, this knowledge can guide to prevent or delay vascular dementia.
