期刊
MOVEMENT DISORDERS
卷 28, 期 3, 页码 296-301出版社
WILEY
DOI: 10.1002/mds.25213
关键词
Parkinson's disease; -amyloid; dopamine; PET; MDS-UPDRS
资金
- National Institutes of Health [P01 NS015655, R01 NS070856]
- Michael J. Fox Foundation
- Department of Veterans Affairs
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
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据