Journal
MOVEMENT DISORDERS
Volume 28, Issue 3, Pages 296-301Publisher
WILEY
DOI: 10.1002/mds.25213
Keywords
Parkinson's disease; -amyloid; dopamine; PET; MDS-UPDRS
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Funding
- National Institutes of Health [P01 NS015655, R01 NS070856]
- Michael J. Fox Foundation
- Department of Veterans Affairs
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Although motor impairments in Parkinson's disease (PD) are attributed to nigrostriatal dopaminergic denervation, postural instability and gait difficulty (PIGD) features are less responsive to dopaminergic medications. PIGD features are a risk factor also for the development of dementia in PD (PDD). These observations suggest that nondopaminergic mechanisms may contribute to axial motor impairments. The aim was to perform a correlative PET study to examine the relationship between neocortical -amyloid deposition ([11C]-Pittsburgh Compound B), nigrostriatal dopaminergic denervation ([11C]-dihydrotetrabenazine), and PIGD feature severity in PD patients at risk for dementia. This was a cross-sectional study of 44 PD patients (11 female and 33 male; 69.5 +/- 6.6 years of age; 7.0 +/- 4.8 years motor disease duration; mean H & Y stage: 2.7 +/- 0.5) who underwent PET, motor feature severity assessment using the Movement Disorder Society revised UPDRS, and the Dementia Rating Scale (DRS). Linear regression (R2adj = 0.147; F4,39 = 2.85; P = 0.036) showed that increased PIGD feature severity was associated with increased neocortical [11C]-Pittsburgh Compound B binding ( = 0.346; t39 = 2.13; P = 0.039) while controlling for striatal [11C]-dihydrotetrabenazine binding, age, and DRS total score. Increased neocortical -amyloid deposition, even at low-range levels, is associated with higher PIGD feature severity in PD patients at risk for dementia. This finding may explain why the PIGD motor phenotype is a risk factor for the development of PDD. (c) 2012 Movement Disorder Society
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