Abstract
gene and she was diagnosed as having FAD. Significant [C-11]PiB PET uptake was observed bilaterally in frontal, parietal, and temporal lobes, as well as in the basal ganglia, but not in the cerebellum. By histopathology, Ab immunoreactive deposits were severe in all gray matter structures of cerebrum and cerebellum. Cerebral cortical Ab deposits consisted of cored, diffuse, and cotton wool plaques (CWP). 6-CN-PiB signal was strong in cored plaques, weak-to-moderate in diffuse plaques, and absent in CWPs. In the cerebellum, Ab IHC detected a heavy burden of diffuse deposits in the parenchyma and in blood vessels, while 6-CN-PiB fluorescence was detected only in the leptomeningeal and parenchymal vessels and infrequently in small compact Ab plaques. Conclusions: As progress in imaging techniques allows us to use new tracers for misfolded proteins accumulating in neurodegenerative disease, neuropathology becomes more relevant for defining the efficiency of tracers in identifying specific lesions. The relative contribution of different Ab plaque types to [C-11]PiB PET retention in vivo is currently being investigated. Funding sources: P30AG010133, P01AG025204, U19AG032438.
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