Graduate Student University of Minnesota, Department of Pharmaceutics Minneapolis, Minnesota
Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by the accumulation of amyloid-beta (Aβ) peptides in plasma and brain parenchyma. Approximately 80% of AD patients exhibit vascular dysfunction and cerebrovascular inflammation, detectable before the onset of cognitive decline. Therefore, investigating the interplay between Aβ exposure and cerebrovascular inflammation and how they may exacerbate each other is crucial. Our studies show that Aβ exposure increases the expression of vascular cell adhesion molecule-1 (VCAM-1), a cerebrovascular inflammatory marker. Our in-vivo and in-vitro studies have demonstrated that TNF-alpha promotes Aβ accumulation in brain endothelial cells and augments VCAM-1 expression. Our study provides new knowledge by identifying vital molecular mediators that drive cerebrovascular inflammation and cognitive decline in AD.
Learning Objectives:
Upon completion, participants will be able to describe the importance of cerebrovascular inflammation in Alzheimer's disease.
Upon completion, participants will be able to understand the role of cerebrovascular inflammation in regulating the progression of amyloid beta pathology.
Upon completion, participants will be able to understand the molecular mechanisms governing cerebrovascular inflammation in Alzheimer's disease.
