October 2008

Biopsy Support for the Validity of Pittsburgh Compound B Positron Emission Tomography With a Twist

Author Affiliations

Copyright 2008 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2008

Arch Neurol. 2008;65(10):1281-1283. doi:10.1001/archneur.65.10.1281

Amyloid imaging with the positron emission tomography (PET) ligand Pittsburgh Compound B (PiB) has spread to many centers around the world since the presentation of its first human studies performed in Uppsala, Sweden, in 2002.1 At the time of this writing, there are at least 17 sites in North America, 9 in Japan, 8 in Europe, 3 in Korea, and 1 in Australia that have successfully used PiB PET in thousands of subjects. Amyloid imaging with PiB has become an integral part of the Alzheimer's Disease Neuroimaging Initiative in North America and equivalent studies in Japan and Australia. The relatively rapid worldwide acceptance of this new technology lies partly in the potential utility of amyloid imaging for the following: (1) early (perhaps presymptomatic) diagnosis; (2) the development of antiamyloid therapies; and (3) deepening our understanding of the pathogenesis of Alzheimer disease (AD). Another reason for the rapid dissemination of PiB imaging may have been the body of preclinical work supporting the concept that PiB retention accurately reflects the deposition of fibrillar β-amyloid (Aβ) deposits in the brain.24 That, along with the fact that the pattern of PiB retention in humans5 matched the expected pattern of amyloid deposition deduced from the study of postmortem brain tissue,68 built confidence in the validity of amyloid imaging and encouraged the proliferation of this technology. Confidence in the relationship between PiB retention and amyloid content has been further bolstered by 2 postmortem studies that correlated in vivo PiB retention to postmortem measures of amyloid deposition. The first of these focused on a case with a clinical diagnosis of dementia with Lewy bodies and extensive cerebral amyloid angiopathy.9 The second was a case that showed the typical clinical symptoms of AD and classic AD pathological findings at autopsy.10 These postmortem studies showed that the amount and location of in vivo PiB retention in these 2 cases corresponded very well to the amount and location of Aβ deposits present after death.

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