Objective-Methods:Chronic cerebral-hypoperfusion is a key contributor to vascular cognitive impairment, with blood-brain barrier (BBB) dysfunction proposed as an early driver of white matter injury. The temporal-evolution and regional-heterogeneity of BBB-leakage remain poorly characterized in vivo. We longitudinally assessed BBB permeability in Sprague-Dawley rats subjected to bilateral-common carotid artery occlusion (2VO) versus sham controls using contrast-enhanced T1-weighted MRI 9.4T over 12-weeks. Gadolinium-leakage maps were generated and analyzed in predefined regions (cortex, hippocampus, striatum, corpus callosum). Exploratory histological observations included GFAP immunostaining, and circulating biochemical biomarkers (sTWEAK, MMP-9, GOT, cytokines) were quantified.Results:Localized BBB disruption was observed at weeks 3, 6 post-2VO and progressed heterogeneously, with pronounced leakage strictly targeted toward corpus callosum, hippocampus and striatum. Despite descriptive trends showing increased astroglial activation, systemic biochemical biomarkers did not correlate with imaging-derived central BBB-leakage. Volumetric analysis revealed subtle but significant brain atrophy (18% whole-brain reduction) preceding overt T2-signal abnormalities. In the 2VO model studied, BBB dysfunction in chronic-hypoperfusion appears to be a dynamic, region-specific process.Conclusion:Longitudinal contrast-enhanced MRI detected changes that were not mirrored by the circulating biomarkers studied, suggesting its potential utility as a surrogate endpoint in preclinical studies, which should be confirmed in larger cohorts and complementary models.
No takes yet. Share an insight, caveat, or question.
Sampedro‐Viana et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: