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Abstract #3589

Cerebral Amyloid Angiopathy Patients Exhibit Cortical Gray Matter Atrophy but Not Hypoperfusion

Randall B Stafford 1,2 , Cheryl R McCreary 2,3 , Anna Charlton 1 , Angela Zwiers 1 , X Rachel Wang 1,2 , Ikreet Cheema 2,4 , Saima Batool 1,2 , Zahinoor Ismail 1,5 , Bradley G Goodyear 2,3 , Richard Frayne 2,3 , and Eric E Smith 1,3

1 Clinical Neurosciences, University of Calgary, Calgary, AB, Canada, 2 Seaman Family MR Research Centre & Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada, 3 Radiology, University of Calgary, Calgary, AB, Canada, 4 Neuroscience, University of Calgary, Calgary, AB, Canada, 5 Mathison Centre for Mental Health Research & Education, Hotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada

Cerebral amyloid angiopathy (CAA) is caused by vascular beta-amyloid deposition, which can lead to several clinical conditions including hemorrhage, microinfarcts, and compromised vascular reactivity. Our hypothesis is that patients with CAA exhibit reduced cortical gray matter volume and hypoperfusion in the occipital lobes, which are often affected by CAA. We used a multi-modal MR protocol that included a high-resolution T1 anatomical acquisition, a T2-FLAIR acquisition, and a resting pseudo-continuous ASL acquisition. Our results did not show any difference in perfusion between participants with CAA and health age-matched controls, however we did find reduced cortical gray matter volume in CAA.

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