. Comparison of PiB distribution on PET with beta-amyloid deposits at autopsy. Human Amyloid Imaging 2010 Meeting Abstracts. 2010 April 9;


Background: A comparison of the distribution of PiB accumulation as seen on PET with the distribution of amyloid pathology seen on autopsy is of great interest in understanding PiB binding in vivo. Very limited autopsy/PiB correlative data exists in the literature. In this report we describe the findings of PiB scans as compared to autopsy findings on 5 subjects.

Methods: Five subjects (4 male, 1 female) who underwent antemortem PiB PET scans subsequently came to autopsy. Diagnoses were of AD (CDR global = 2), naMCI (CDR global = 1.0), aMCI (CDR global = 0.5), LBD (CDR global = 0.5), and normal control (CDR global = 0.0). They expired 9, 17, 16, 32 and 24 months after their PiB scans, respectively. The quantitative distribution of PiB on PET imaging was compared in the frontal (Fr), parietal (Par), temporal (Tem), occipital (Occ) and hippocampal (Hip) regions to the distribution of diffuse plaques, cored plaques and vascular amyloid, evaluated with beta-amyloid immunohistochemistry (Novacastra, NCL-B-amyloid; clone 6F/3D) at autopsy.

Results: PiB scans showed increased PiB binding in the subjects with AD, aMCI and LBD (global PiB cerebellar ratios = 2.7, 1.7 and 1.5) but not in the naMCI or control subjects (global PiB cerebellar ratios = 1.3 and 1.4). At autopsy, the AD, aMCI and LBD subjects showed frequent numbers of diffuse and cored amyloid plaques in neocortical areas and variable amyloid angiopathty. In the naMCI and control subjects there was a conspicuous absence of amyloid deposits (diffuse and compact plaques) and amyloid angiopathy in all areas sampled.

Conclusions: These results are consistent with the expected finding that PiB accumulation occurs in subjects with AD, aMCI, and LBD although with some variability and reflects the frequency of microscopic amyloid deposits at autopsy. The findings are also consistent with the idea that subjects with naMCI are less likely to have AD-like pathological substrate, and more likely to have prodromal, non-AD dementia.

Grant support: National Institute on Aging [P50 AG16574, U01 AG06786, K23 AG030935 and R01 AG11378]; the Robert H and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program; and the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Foundation, USA.


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  1. Toronto: HAI Amyloid Imaging Conference Abstracts