From mechanism to classification: Understanding a novel model of cerebral small vessel disease

Abstract

The studies explored cerebral small vessel disease (cSVD), emphasizing the need for precise classification to improve prevention and intervention strategies. Kang et al. introduced an intra-cisterna-magna bevacizumab injection (ICM-BI) model in mice, which induced tight junction loss, microbleeds, and amyloid deposits. However, bevacizumab’s low affinity for murine vascular endothelial growth factor raises questions about its mechanism of action, suggesting potential off-target effects. While most cSVD models mimic arteriolosclerosis (type 1) or genetic variants (types 2 and 3), the ICM-BI model represents a novel approach to studying immune-mediated cSVD (type 4). The complexity and variability of cSVD remain significant research challenges.