Original Articles
Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound-B
Article first published online: 21 JAN 2004
DOI: 10.1002/ana.20009
Copyright © 2003 American Neurological Association
Additional Information
How to Cite
Klunk, W. E., Engler, H., Nordberg, A., Wang, Y., Blomqvist, G., Holt, D. P., Bergström, M., Savitcheva, I., Huang, G.-F., Estrada, S., Ausén, B., Debnath, M. L., Barletta, J., Price, J. C., Sandell, J., Lopresti, B. J., Wall, A., Koivisto, P., Antoni, G., Mathis, C. A. and Långström, B. (2004), Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound-B. Annals of Neurology, 55: 306–319. doi: 10.1002/ana.20009
Publication History
- Issue published online: 20 FEB 2004
- Article first published online: 21 JAN 2004
- Manuscript Accepted: 18 NOV 2003
- Manuscript Revised: 4 NOV 2003
- Manuscript Received: 9 SEP 2003
Funded by
- Alzheimer's Association. Grant Numbers: IIRG-95-076, TLL-01-3381, NIRG-00-2335
- National Institute of Aging. Grant Numbers: AG01039, AG20226, AG18402
- Institute for the Study of Aging/American Federation for Aging Research
- Swedish Medical Research Council. Grant Number: 05817
- Stohnes Foundation
- University of Pittsburgh Alzheimer Disease Research Center Brain Bank. Grant Number: AG05133
- Abstract
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Abstract
This report describes the first human study of a novel amyloid-imaging positron emission tomography (PET) tracer, termed Pittsburgh Compound-B (PIB), in 16 patients with diagnosed mild AD and 9 controls. Compared with controls, AD patients typically showed marked retention of PIB in areas of association cortex known to contain large amounts of amyloid deposits in AD. In the AD patient group, PIB retention was increased most prominently in frontal cortex (1.94-fold, p = 0.0001). Large increases also were observed in parietal (1.71-fold, p = 0.0002), temporal (1.52-fold, p = 0.002), and occipital (1.54-fold, p = 0.002) cortex and the striatum (1.76-fold, p = 0.0001). PIB retention was equivalent in AD patients and controls in areas known to be relatively unaffected by amyloid deposition (such as subcortical white matter, pons, and cerebellum). Studies in three young (21 years) and six older healthy controls (69.5 ± 11 years) showed low PIB retention in cortical areas and no significant group differences between young and older controls. In cortical areas, PIB retention correlated inversely with cerebral glucose metabolism determined with 18F-fluorodeoxyglucose. This relationship was most robust in the parietal cortex (r = −0.72; p = 0.0001). The results suggest that PET imaging with the novel tracer, PIB, can provide quantitative information on amyloid deposits in living subjects.

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