@MISC{Klünemann_amyloid-contributes, author = {Hans H. Klünemann}, title = {Amyloid- Contributes to Blood–Brain Barrier Leakage in Transgenic Human Amyloid Precursor Protein Mice and in Humans With Cerebral Amyloid Angiopathy}, year = {} }
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Abstract
Background and Purpose—Cerebral amyloid angiopathy (CAA) is a degenerative disorder characterized by amyloid- (A) deposition in the blood–brain barrier (BBB). CAA contributes to injuries of the neurovasculature including lobar hemorrhages, cortical microbleeds, ischemia, and superficial hemosiderosis. We postulate that CAA pathology is partially due to A compromising the BBB. Methods—We characterized 19 patients with acute stroke with “probable CAA ” for neurovascular pathology based on MRI and clinical findings. Also, we studied the effect of A on the expression of tight junction proteins and matrix metalloproteases (MMPs) in isolated rat brain microvessels. Results—Two of 19 patients with CAA had asymptomatic BBB leakage and posterior reversible encephalopathic syndrome indicating increased BBB permeability. In addition to white matter changes, diffusion abnormality suggesting