OBJECTIVE Regional cortical thinning in dementia with Lewy bodies (DLB) and Parkinson disease dementia (PDD) may underlie some aspect of their clinical impairments; cortical atrophy likely reflects extensive Lewy body pathology with alpha-synuclein deposits, as well as associated Alzheimer's disease co-pathologies, when present. Here we investigated the topographic distribution of cortical thinning in these Lewy body diseases compared to cognitively normal PD and healthy non-PD control subjects, explored the association of regional thinning with clinical features and evaluated the impact of amyloid deposition. METHODS Twenty-one participants with dementia with Lewy bodies (DLB), 16 with Parkinson disease (PD) - associated cognitive impairment (PD-MCI and PDD), and 24 cognitively normal participants with PD underwent MRI, PiB PET, and clinical evaluation. Cortical thickness across the brain and in regions of interest (ROIs) was compared across diagnostic groups and across subgroups stratified by amyloid status, and was related to clinical and cognitive measures. RESULTS DLB and PD-impaired groups shared a similar distribution of cortical thinning that included regions characteristic of AD, as well as the fusiform, precentral, and paracentral gyri. Elevated PiB retention in DLB and PD-impaired but not in PD-normal participants was associated with more extensive and severe cortical thinning, in an overlapping topography that selectively affected the medial temporal lobe in DLB participants. In DLB, greater thinning in AD signature and fusiform regions was associated with greater cognitive impairment. CONCLUSIONS The pattern of cortical thinning is similar in DLB and PD-associated cognitive impairment, overlapping with and extending beyond AD signature regions to involve fusiform, precentral, and paracentral regions. Cortical thinning in AD signature and fusiform regions in these diseases reflects cognitive impairment and is markedly accentuated by amyloid co-pathology. Further work will be required to determine whether the distinct topography of cortical thinning in DLB and PD-associated cognitive impairment might have value as a diagnostic and/ or outcome biomarker in clinical trials.

中文翻译：

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路易氏体疾病中的皮质变薄的地形。

目的路易体（DLB）和帕金森病痴呆（PDD）痴呆患者的局部皮质变薄可能是其临床损害的某些方面。皮质萎缩可能反映了广泛的路易体病理，伴有α-突触核蛋白沉积，以及相关的阿尔茨海默氏病共病（如果存在）。在这里，我们调查了这些路易体疾病与认知正常的PD和健康的非PD对照受试者相比的皮质变薄的地形分布，探讨了区域变薄与临床特征的关系，并评估了淀粉样蛋白沉积的影响。方法21名路易体痴呆患者（DLB），16名帕金森病（PD）相关认知障碍（PD-MCI和PDD）和24名认知正常PD受试者接受了MRI，PiB PET，和临床评估。在跨诊断层和按淀粉样蛋白状态分层的亚组中，比较了大脑和感兴趣区域（ROI）的皮质厚度，这与临床和认知指标有关。结果DLB和PD受损组的皮质变薄分布相似，其中包括AD的特征性区域，以及梭状，中央前和中央下回。在DLB和PD受损的参与者中，PiB保留升高但在PD正常参与者中却没有，这与更广泛和严重的皮质变薄有关，这是一种重叠的地形，选择性地影响了DLB参与者的内侧颞叶。在DLB中，AD签名和梭形区域变薄的程度与更大的认知障碍有关。结论在DLB和PD相关的认知障碍中，皮层变薄的模式相似，与AD签名区域重叠并延伸到AD签名区域之外，涉及梭形，中央前和中央旁区域。在这些疾病中，AD标记和梭形区域的皮层变薄反映出认知障碍，并且淀粉样蛋白共病显着加剧了皮层变薄。需要进一步的工作来确定在DLB和PD相关的认知障碍中皮层变薄的独特形貌在临床试验中是否具有作为诊断和/或结果生物标志物的价值。在这些疾病中，AD标记和梭形区域的皮层变薄反映出认知障碍，并且淀粉样蛋白共病显着加剧了皮层变薄。需要进一步的工作来确定在DLB和PD相关的认知障碍中皮层变薄的独特形貌在临床试验中是否具有作为诊断和/或结果生物标志物的价值。在这些疾病中，AD标记和梭形区域的皮层变薄反映出认知障碍，并且淀粉样蛋白共病显着加剧了皮层变薄。需要进一步的工作来确定在DLB和PD相关的认知障碍中皮层变薄的独特形貌在临床试验中是否具有作为诊断和/或结果生物标志物的价值。