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Neurology. 2010 Jan 5;74(1):77-84. doi: 10.1212/WNL.0b013e3181c7da8e.

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

Author information

  • 1Department of Neurology and Pediatrics, 601 Elmwood Avenue, Box 673, University of Rochester Medical Center, Rochester, NY 14642, USA. michelle_burack@urmc.rochester.edu

Abstract

OBJECTIVE:

To investigate the specificity of in vivo amyloid imaging with [(11)C]-Pittsburgh Compound B (PIB) in Parkinson disease dementia (PDD).

METHODS:

We performed detailed neuropathologic examination for 3 individuals with PDD who had PIB PET imaging within 15 months of death.

RESULTS:

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.

CONCLUSIONS:

[(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.

PMID:
20038776
[PubMed - indexed for MEDLINE]
PMCID:
PMC2809026
Free PMC Article

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