期刊
MOVEMENT DISORDERS
卷 25, 期 15, 页码 2516-2523出版社
WILEY
DOI: 10.1002/mds.23393
关键词
Parkinson's disease; Parkinson's disease with dementia; dementia with Lewy bodies; PET
资金
- NIH [NCRR UL1RR024992, NINDS P30NS0571]
- American Parkinson Disease Association (APDA) Advanced Research Center for Parkinson Disease at Washington University in St. Louis
- APDA
- Barnes-Jewish Hospital Foundation
- NIH through the Washington University Institute of Clinical and Translational Sciences
- NARSAD
- Tourette Syndrome Association
- McDonnell Foundation
- American Academy of Neurology
- Medtronic
- Michael J. Fox Foundation
- Charles and Joanne Knight Alzheimer Research Fund
- HiQ Foundation
- WA University
- Huntington's disease Society of America
- Bander Foundation for Medical Business Ethics
- Emory
- University of Rochester
Clinicopathologic studies of Parkinson disease dementia (PDD) and dementia with Lewy bodies (DLB) commonly reveal abnormal beta-amyloid deposition in addition to diffuse Lewy bodies (alpha-synuclein aggregates), but the relationship among these neuropathologic features and the development of dementia in these disorders remains uncertain. The purpose of this study was to determine whether amyloid-beta deposition detected by PET imaging with Pittsburgh Compound B (PIB) distinguishes clinical subtypes of Lewy body-associated disorders. Nine healthy controls, 8 PD with no cognitive impairment, 9 PD with mild cognitive impairment, 6 DLB, and 15 PDD patients underwent [C-11]-PIB positron emission tomography imaging, clinical examination, and cognitive testing. The binding potential (BP) of PIB for predefined regions and the mean cortical BP (MCBP) were calculated for each participant. Annual longitudinal follow-up and postmortem examinations were per formed on a subset of participants. Regional PIB BPs and the proportion of individuals with abnormally elevated MCBP were not significantly different across participant groups. Elevated PIB binding was associated with worse global cognitive impairment in participants with Lewy body disorders but was not associated with any other clinical or neuropsychological features, including earlier onset or faster rate of progression of cognitive impairment. These results suggest that the presence of fibrillar amyloid-beta does not distinguish between clinical subtypes of Lewy body-associated disorders, although larger numbers are needed to more definitively rule out this association. Amyloid-beta may modify the severity of global cognitive impairment in individuals with Lewy body-associated dementia. (C) 2010 Movement Disorder Society
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