McCance Seminar Series: Rachel Bennett, PhD
Why It Matters
If tau directly disrupts cerebral microvasculature, targeting vascular pathways could offer a complementary therapeutic route to slow or prevent Alzheimer’s progression beyond amyloid- and tau-focused approaches. This shifts part of the drug-discovery focus toward restoring microvascular function and reducing neurovascular inflammation.
Summary
Dr. Rachel Bennett presented evidence that tau pathology in Alzheimer’s disease drives microvascular dysfunction, not just the reverse. In tau-overexpressing mice she observed increased vessel tortuosity, non-perfused capillaries, blood–brain barrier leakage, impaired functional hyperemia and upregulation of endothelial adhesion molecules that capture leukocytes and obstruct flow. Her team is validating these findings in human postmortem tissue using single-nucleus RNA sequencing and advanced imaging to show similar vascular and molecular signatures. The goal is to identify vascular cell targets for therapeutics to slow neurodegeneration and cognitive decline.
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