Imaging of amyloid burden and distribution in cerebral amyloid angiopathy
Article first published online: 7 AUG 2007
Copyright © 2007 American Neurological Association
Annals of Neurology
Volume 62, Issue 3, pages 229–234, September 2007
How to Cite
Johnson, K. A., Gregas, M., Becker, J. A., Kinnecom, C., Salat, D. H., Moran, E. K., Smith, E. E., Rosand, J., Rentz, D. M., Klunk, W. E., Mathis, C. A., Price, J. C., DeKosky, S. T., Fischman, A. J. and Greenberg, S. M. (2007), Imaging of amyloid burden and distribution in cerebral amyloid angiopathy. Ann Neurol., 62: 229–234. doi: 10.1002/ana.21164
- Issue published online: 25 SEP 2007
- Article first published online: 7 AUG 2007
- Manuscript Accepted: 18 MAY 2007
- Manuscript Revised: 30 MAR 2007
- Manuscript Received: 2 FEB 2007
- NIH (National Institute on Aging). Grant Numbers: R01-AG026484, P50 AG00513421
- National Institute of Neurological Diseases and Stroke. Grant Number: T32-NS048005
- Alzheimer Association. Grant Number: IIRG-06-26331
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.
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).
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).
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