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From the Memory and Aging Center (G.D.R., C.A.R., T.A.P., H.J.R., B.L.M.) and Department of Neurology (G.D.R., C.A.R., H.J.R., B.L.M.), University of California at San Francisco; Helen Wills Neuroscience Institute (A.J.F., E.C.M., S.L.B., S.C., P.P., W.J.J.), University of California at Berkeley; Lawrence Berkeley National Laboratory (A.J.F., J.P.O., S.L.B., W.J.J.), Berkeley, CA; and Departments of Psychiatry (W.E.K.) and Radiology (C.A.M.), University of Pittsburgh, PA.
Address correspondence and reprint requests to Dr. Gil Rabinovici, UCSF Memory &Aging Center, 350 Parnassus Ave., Suite 706, San Francisco, CA 94117; e-mail: grabinovici{at}memory.ucsf.edu
Background: The PET tracer 11C-labeled Pittsburgh Compound-B (11C-PIB) specifically binds fibrillar amyloid-beta (Aß) plaques and can be detected in Alzheimer disease (AD). We hypothesized that PET imaging with 11C-PIB would discriminate AD from frontotemporal lobar degeneration (FTLD), a non-Aß dementia.
Methods: Patients meeting research criteria for AD (n = 7) or FTLD (n = 12) and cognitively normal controls (n = 8) underwent PET imaging with 11C-PIB (patients and controls) and 18F-fluorodeoxyglucose (18F-FDG) (patients only). 11C-PIB whole brain and region of interest (ROI) distribution volume ratios (DVR) were calculated using Logan graphical analysis with cerebellum as a reference region. DVR images were visually rated by a blinded investigator as positive or negative for cortical 11C-PIB, and summed 18F-FDG images were rated as consistent with AD or FTLD.
Results: All patients with AD (7/7) had positive 11C-PIB scans by visual inspection, while 8/12 patients with FTLD and 7/8 controls had negative scans. Of the four PIB-positive patients with FTLD, two had 18F-FDG scans that suggested AD, and two had 18F-FDG scans suggestive of FTLD. Mean DVRs were higher in AD than in FTLD in whole brain, lateral frontal, precuneus, and lateral temporal cortex (p < 0.05), while DVRs in FTLD did not significantly differ from controls.
Conclusions: PET imaging with 11C-labeled Pittsburgh Compound-B (11C-PIB) helps discriminate Alzheimer disease (AD) from frontotemporal lobar degeneration (FTLD). Pathologic correlation is needed to determine whether patients with PIB-positive FTLD represent false positives, comorbid FTLD/AD pathology, or AD pathology mimicking an FTLD clinical syndrome.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the April 10 issue to find the title link for this article.
Supported by the U.S. Department of Energy Contract DE-AC02-05CH11231, the John Douglas French Alzheimer Foundation, the Larry S. Hillblom Foundation, NIA grant P01-AG1972403, ADRC grant P50-AG023501 and GCRC grant M01-RR00079.
Disclosures: GE Healthcare holds a license agreement with the University of Pittsburgh based on the PIB compound described in this article. Drs. Klunk and Mathis are co-inventors of PIB and, as such, have a financial interest in this license agreement. Drs. Mathis, Jagust, and Klunk have received consulting fees from GE Healthcare. The other authors report no conflicts of interest.
Received August 21, 2006. Accepted in final form December 8, 2006.
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