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Imaging of amyloid burden and distribution in cerebral amyloid angiopathy
Author(s) -
Johnson Keith A.,
Gregas Matt,
Becker John A.,
Kinnecom Catherine,
Salat David H.,
Moran Erin K.,
Smith Erin E.,
Rosand Jonathan,
Rentz Dorene M.,
Klunk William E.,
Mathis Chester A.,
Price Julie C.,
DeKosky Steven T.,
Fischman Alan J.,
Greenberg Steven M.
Publication year - 2007
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.21164
Subject(s) - cerebral amyloid angiopathy , pittsburgh compound b , positron emission tomography , amyloid (mycology) , medicine , pathology , stroke (engine) , alzheimer's disease , nuclear medicine , dementia , disease , mechanical engineering , engineering
Objective Cerebrovascular deposition of β‐amyloid (cerebral amyloid angiopathy [CAA]) is a major cause of hemorrhagic stroke and a likely contributor to vascular cognitive impairment. We evaluated positron emission tomographic imaging with the β‐amyloid–binding compound Pittsburgh Compound B (PiB) as a potential noninvasive method for detection of CAA. We hypothesized that amyloid deposition would be observed with PiB in CAA, and based on the occipital predilection of CAA pathology and associated hemorrhages, that specific PiB retention would be disproportionately greater in occipital lobes. Methods We compared specific cortical PiB retention in 6 nondemented subjects diagnosed with probable CAA with 15 healthy control subjects and 9 patients with probable Alzheimer's disease (AD). Results All CAA and AD subjects were PiB‐positive, both by distribution volume ratio measurements and by visual inspection of positron emission tomographic images. Global cortical PiB retention was significantly increased in CAA (distribution volume ratio 1.18 ± 0.06) relative to healthy control subjects (1.04 ± 0.10; p = 0.0009), but was lower in CAA than in AD subjects (1.41 ± 0.17; p = 0.002). The occipital‐to‐global PiB ratio, however, was significantly greater in CAA than in AD subjects (0.99 ± 0.07 vs 0.86 ± 0.05; p = 0.003). Interpretation We conclude that PiB‐positron emission tomography can detect cerebrovascular β‐amyloid and may serve as a method for identifying the extent of CAA in living subjects. Ann Neurol 2007