Gomperts S N, Rentz D M, Moran E, Becker J A, Locascio J J, Klunk W E, Mathis C A, Elmaleh D R, Shoup T, Fischman A J, Hyman B T, Growdon J H, Johnson K A
Massachusetts General Hospital, Boston, MA 02114, USA.
Neurology. 2008 Sep 16;71(12):903-10. doi: 10.1212/01.wnl.0000326146.60732.d6.
Extrapyramidal motor symptoms precede dementia in Parkinson disease (PDD) by many years, whereas dementia occurs early in dementia with Lewy bodies (DLB). Despite this clinical distinction, the neuropsychological and neuropathologic features of these conditions overlap. In addition to widespread distribution of Lewy bodies, both diseases have variable burdens of neuritic plaques and neurofibrillary tangles characteristic of Alzheimer disease (AD).
To determine whether amyloid deposition, as assessed by PET imaging with the beta-amyloid-binding compound Pittsburgh Compound B (PiB), can distinguish DLB from PDD, and to assess whether regional patterns of amyloid deposition correlate with specific motor or cognitive features.
Eight DLB, 7 PDD, 11 Parkinson disease (PD), 15 AD, and 37 normal control (NC) subjects underwent PiB-PET imaging and neuropsychological assessment. Amyloid burden was quantified using the PiB distribution volume ratio.
Cortical amyloid burden was higher in the DLB group than in the PDD group, comparable to the AD group. Amyloid deposition in the PDD group was low, comparable to the PD and NC groups. Relative to global cortical retention, occipital PiB retention was lower in the AD group than in the other groups. For the DLB, PDD, and PD groups, amyloid deposition in the parietal (lateral and precuneus)/posterior cingulate region was related to visuospatial impairment. Striatal PiB retention in the DLB and PDD groups was associated with less impaired motor function.
Global cortical amyloid burden is high in dementia with Lewy bodies (DLB) but low in Parkinson disease dementia. These data suggest that beta-amyloid may contribute selectively to the cognitive impairment of DLB and may contribute to the timing of dementia relative to the motor signs of parkinsonism.
帕金森病痴呆(PDD)中锥体外系运动症状比痴呆早出现许多年,而路易体痴呆(DLB)中痴呆出现较早。尽管有这种临床差异,但这些疾病的神经心理学和神经病理学特征存在重叠。除了路易体广泛分布外,这两种疾病都有阿尔茨海默病(AD)特征性的神经炎性斑块和神经原纤维缠结的不同负担。
通过使用β-淀粉样蛋白结合化合物匹兹堡化合物B(PiB)的PET成像评估淀粉样蛋白沉积,确定能否区分DLB和PDD,并评估淀粉样蛋白沉积的区域模式是否与特定运动或认知特征相关。
8名DLB患者、7名PDD患者、11名帕金森病(PD)患者、15名AD患者和37名正常对照(NC)受试者接受了PiB-PET成像和神经心理学评估。使用PiB分布体积比量化淀粉样蛋白负担。
DLB组的皮质淀粉样蛋白负担高于PDD组,与AD组相当。PDD组的淀粉样蛋白沉积较低,与PD组和NC组相当。相对于整体皮质滞留,AD组枕叶PiB滞留低于其他组。对于DLB、PDD和PD组,顶叶(外侧和楔前叶)/后扣带回区域的淀粉样蛋白沉积与视觉空间损害有关。DLB组和PDD组纹状体PiB滞留与运动功能损害较轻相关。
路易体痴呆(DLB)中整体皮质淀粉样蛋白负担高,但帕金森病痴呆中低。这些数据表明β-淀粉样蛋白可能选择性地导致DLB的认知损害,并可能与相对于帕金森病运动体征的痴呆发生时间有关。