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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