In vivo amyloid imaging in autopsy-confirmed Parkinson disease with dementia

Department of Neurology and Pediatrics, 601 Elmwood Avenue, Box 673, University of Rochester Medical Center, Rochester, NY 14642, USA.
Neurology (Impact Factor: 8.29). 01/2010; 74(1):77-84. DOI: 10.1212/WNL.0b013e3181c7da8e
Source: PubMed


To investigate the specificity of in vivo amyloid imaging with [(11)C]-Pittsburgh Compound B (PIB) in Parkinson disease dementia (PDD).
We performed detailed neuropathologic examination for 3 individuals with PDD who had PIB PET imaging within 15 months of death.
We observed elevated cortical uptake of [(11)C]-PIB on in vivo PET imaging in 2 of the 3 cases. At autopsy, all 3 individuals had abundant cortical Lewy bodies (Braak PD stage 6), and were classified as low-probability Alzheimer disease (AD) based on NIA-Reagan criteria. The 2 PIB-positive individuals had abundant diffuse Abeta plaques but only sparse neuritic plaques and intermediate neurofibrillary tangle pathology. The PIB-negative individual had rare diffuse plaques, no neuritic plaques, and low neurofibrillary tangle burden.
[(11)C]-Pittsburgh Compound B (PIB) PET is specific for fibrillar Abeta molecular pathology but not for pathologic diagnosis of comorbid Alzheimer disease in individuals with Parkinson disease dementia. The ability to specifically identify fibrillar Abeta amyloid in the setting of alpha-synucleinopathy makes [(11)C]-PIB PET a valuable tool for prospectively evaluating how the presence of Abeta amyloid influences the clinical course of dementia in patients with Lewy body disorders.

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    • "Furthermore, in cases of patients with other types of dementias, such as Parkinson's disease with dementia, and dementia with Lewy bodies, correlation of in vivo 11 C-PiB with postmortem neuropathology showed that the high 11 C-PiB retention in these patients was primarily correlated to the presence of diffuse plaques [34] [35]. Thus, in the setting of these dementias, 11 C-PiB PET has insufficient specificity for in vivo diagnosis of comorbid AD due to its inability to distinguish between diffuse and neuritic amyloid plaques [34]. In these cases in particular, MRI could provide additional value to confirm the presence of amyloid plaque. "
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    • "Cognitive reserve and the finding that amyloid appears well before cognitive symptoms may explain some of the discrepancies in the literature [27]. Also, PiB uptake appears to be nonspecific for AD, as it has been shown to be elevated in Parkinson's dementia [72] and in Lewy body disease [73]. "
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