| Résumé | Elevation of transforming growth factor-beta 1 (TGFβ1), a key extracellular matrix regulator, has been documented in the brain and cerebral vasculature of Alzheimer's disease (AD) patients. Transgenic mice overexpressing TGFβ1 in the brain (TGF mice) develop AD-like vascular structural changes, impaired vasomotricity, and compromised neurovascular coupling. We have demonstrated that cerebrovascular dysfunction in both aged and young TGF mice is normalized by the peroxisome proliferator-activated receptor-γ agonist pioglitazone. Our aims are to (a) characterize the cerebrovascular proteome of TGF mice and its perturbation by pioglitazone using label-free mass spectrometry-based quantitative proteomics, and (b) identify proteins that orchestrate pioglitazone-mediated recovery of cerebrovascular function. |
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