Alzheimer’s disease is a progressive neurodegenerative disease that causes cognitive decline and neuronal loss. While inflammation occurs as a defense mechanism in response to infection, toxins, and injury, an imbalance between pro and anti-inflammatory cascades results in severe neuroinflammation that could eventually trigger neurodegeneration. Cerebrovascular inflammation is known to exacerbate amyloid and tau pathology in AD patients. We have previously demonstrated that amyloid-beta (A𝛽) peptides, toxic proteins that accumulate in the AD brain, increases the cerebrovascular expression of an inflammatory marker, vascular cell adhesion molecule-1 (VCAM-1), which promotes the infiltration of immune cells into the brain. However, the molecular mechanisms by which A𝛽 exposure contributes to increased VCAM-1 expression and cerebrovascular inflammation remain poorly understood. Thus, we hypothesize that A𝛽 proteins promote VCAM-1 expression by altering the signaling in the Src-FAK-MAPK pathway at the BBB endothelium. Increased expression of VCAM-1 at the blood-brain barrier could potentially be used as a novel early detection marker for Alzheimer’s disease.
After attending this rapid-fire session, the attendees will be able to interpret the role of vascular cell adhesion molecule-1 (VCAM-1) in cerebrovascular inflammation during Alzheimer’s disease.
The rapid-fire session will explore alterations in the expression of various proteins and phospho-proteins in the inflammation signaling pathway following amyloid beta exposure to human cerebral microvascular endothelial cells.
The rapid-fire session explores the potential of early diagnostic markers for Alzheimer's disease.