We are excited about this developing project and will update this page as we have new results to tell you about.
Cerebral amyloid angiopathy is known to cause cerebrovascular fragility, but the specific molecular mechanisms that produce this outcome are not yet fully understood. We discovered in previous work that intense late-complement activation on arterioles appears to contribute to lytic degeneration of vascular smooth muscle and this likely is a major contributor to hemorrhage and loss of vascular reactivity and autoregulation.
In this new project, we are looking at three-dimensional imaging of the cerebrovascular network to better understand the structural changes occuring in cerebral microvessel affected by CAA and we are working to identify new molecular pathways which may help explain these changes. We are approaching these goals using our modification of the CLARITY technique to obtain high-resolution 3D confocal microscopy in human brain tissue and using RNAseq to identify regulated pathways in patients with CAA.