A major starting point of our work are patients with stroke that are examined through prospective clinical studies along with healthy individuals. We apply genetic (GWAS and sequencing) and other omics techniques to identify novel targets and pathways relevant to specific mechanistically defined stroke subtypes. We use this information to explore relationships with informative intermediate (e.g. vascular, metabolic) and related phenotypes (e.g. coronary artery disease).
We have established genetic mouse models for cerebral small vessel disease (SVD) derived from the genetic discoveries (e.g. Notch3, HtrA1, Foxf2) and use these models to identify and characterize key molecular pathways (e.g. TGF-ß signaling) and cellular targets (e.g. brain pericytes) relevant to the pathogenesis of SVD.
Another area increasingly moving into the focus of our research is atherosclerosis. We in collaboration with others recently identified several risk loci for large artery stroke and are currently exploring the role of relevant genes (e.g. HDAC9, TSPAN2) in atherogenesis and vascular injury.
Contact: Martin Dichgans, MD