{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T02:02:36Z","timestamp":1771466556535,"version":"3.50.1"},"reference-count":42,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2012,10,29]],"date-time":"2012-10-29T00:00:00Z","timestamp":1351468800000},"content-version":"vor","delay-in-days":28,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective:<\/jats:title><jats:p>Deposition of the amyloid\u2010\u03b2 (A\u03b2) peptide in neuritic plaques is a requirement for the diagnosis of Alzheimer disease (AD). Although the continued development of in vivo imaging agents such as Pittsburgh compound B (PiB) is promising, the diagnosis of AD is still challenging. This can be partially attributed to our lack of a detailed understanding of the interrelationship between the various pools and species of A\u03b2 and other common indices of AD pathology. We hypothesized that recent advances in our ability to accurately measure A\u03b2 postmortem (for example, using PiB), could form the basis of a simple means to deliver an accurate AD diagnosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods:<\/jats:title><jats:p>We conducted a comprehensive analysis of the amount of A\u03b240 and A\u03b242 in increasingly insoluble fractions, oligomeric A\u03b2, and fibrillar A\u03b2 (as defined by PiB binding), as well as plaques (diffuse and neuritic), and neurofibrillary tangles in autopsy specimens from age\u2010matched, cognitively normal controls (n = 23) and AD (n = 22) cases, across multiple brain regions.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p>Both PiB binding and the amount of sodium dodecyl sulfate (SDS)\u2010soluble A\u03b2 were able to predict disease status; however, SDS\u2010soluble A\u03b2 was a better measure. Oligomeric A\u03b2 was not a predictor of disease status. PiB binding was strongly related to plaque count, although diffuse plaques were a stronger correlate than neuritic plaques.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation:<\/jats:title><jats:p>Although postmortem PiB binding was somewhat useful in distinguishing AD from control cases, SDS\u2010soluble A\u03b2 measured by standard immunoassay was substantially better. These findings have important implications for the development of imaging\u2010based biomarkers of AD. 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