Microglia, Not Leukocytes, in Small Vessel Disease
Refining what "neuroinflammation" means in cSVD
Neurovascular Unit
Extracellular matrix instructs vascular identity
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Laminin composition in the vascular basement membrane is not merely structural — it actively instructs endothelial identity, mural-cell programs and stroke outcome.
First author — University of Münster
My work helped define how vascular basement membrane laminins regulate functional zonation of cerebral microvessels. By integrating single-cell RNA sequencing, imaging and functional studies in genetic mouse models, I showed that vascular laminin composition is not only structural but also instructive for endothelial identity, mural-cell programs, permeability-associated pathways and stroke outcome.
The field had long described vascular heterogeneity along the arteriovenous axis. What was missing was a cause. Loss of laminin α4 shifted endothelial identity, altered mural-cell programs, increased permeability-associated pathways and worsened stroke outcome — moving the field from descriptive vascular heterogeneity to a mechanistic view in which extracellular matrix composition instructs vascular specialization and disease vulnerability.
This also builds directly on earlier work in which I helped define the molecular architecture of perivascular drainage pathways, showing that arterial, capillary, venous, pial and arachnoid compartments can be distinguished by extracellular-matrix and structural marker signatures.
Establishes the extracellular matrix as a tractable lever on barrier function and stroke outcome — not just scaffolding, but a regulator of endothelial state.
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Refining what "neuroinflammation" means in cSVD
Not loss of protein — redistribution and phosphorylation