Research Centre for the Neurosciences of Ageing, Academic Unit of Psychological and Addiction Medicine, Australian National University Medical School, Canberra, Australia.
Aust N Z J Psychiatry. 2012 Dec;46(12):1145-58. doi: 10.1177/0004867412457224. Epub 2012 Sep 18.
Direct neuronal loss or deafferentation of the putamen, a critical hub in corticostriatal circuits, may result in diverse and distinct cognitive and motoric dysfunction in neurodegenerative disease. Differential putaminal morphology, as a quantitative measure of corticostriatal integrity, may thus be evident in Huntington's disease (HD), Alzheimer's disease (AD) and frontotemporal dementia (FTD), diseases with differential clinical dysfunction.
HD (n = 17), FTD (n = 33) and AD (n = 13) patients were diagnosed according to international consensus criteria and, with healthy controls (n = 17), were scanned on the same MRI scanner. Patients underwent brief cognitive testing using the Neuropsychiatry Unit Cognitive Assessment Tool (NUCOG). Ten MRI scans from this dataset were manually segmented as a training set for the Adaboost algorithm, which automatically segmented all remaining scans for the putamen, yielding the following subset of the data: 9 left and 12 right putamen segmentations for AD; 25 left and 26 right putamina for FTD; 16 left and 15 right putamina for HD; 12 left and 12 right putamina for controls. Shape analysis was performed at each point on the surface of each structure using a multiple regression controlling for age and sex to compare radial distance across diagnostic groups.
Age, but not sex and intracranial volume (ICV), were significantly different in the segmentation subgroups by diagnosis. The AD group showed significantly poorer performance on cognitive testing than FTD. Mean putaminal volumes were HD < FTD < AD ≤ controls, controlling for age and ICV. The greatest putaminal shape deflation was evident in HD, followed by FTD, in regions corresponding to the interconnections to motoric cortex.
Differential patterns of putaminal atrophy in HD, FTD and AD, with relevance to corticostriatal circuits, suggest the putamen may be a suitable clinical biomarker in neurodegenerative disease.
壳核（皮质纹状体回路的关键枢纽）的神经元直接丢失或去传入可能导致神经退行性疾病中不同且独特的认知和运动功能障碍。因此，作为皮质纹状体完整性的定量测量，壳核形态的差异可能在亨廷顿病（HD）、阿尔茨海默病（AD）和额颞叶痴呆（FTD）中表现出来，这些疾病具有不同的临床功能障碍。
根据国际共识标准诊断 HD（n = 17）、FTD（n = 33）和 AD（n = 13）患者，并与健康对照组（n = 17）在同一 MRI 扫描仪上进行扫描。患者使用神经精神病学单位认知评估工具（NUCOG）进行简短的认知测试。该数据集的 10 个 MRI 扫描被手动分割为 Adaboost 算法的训练集，该算法自动分割所有剩余的壳核扫描，从而获得数据的以下子集：AD 有 9 个左侧和 12 个右侧壳核分割；FTD 有 25 个左侧和 26 个右侧壳核；HD 有 16 个左侧和 15 个右侧壳核；对照组有 12 个左侧和 12 个右侧壳核。使用多元回归控制年龄和性别，在每个结构的表面的每个点上进行形状分析，以比较诊断组之间的径向距离。
按诊断分组，年龄而不是性别和颅内体积（ICV）在分割亚组中差异显著。AD 组的认知测试表现明显差于 FTD 组。在控制年龄和 ICV 后，HD < FTD < AD ≤对照组。HD 中可见最大的壳核形状萎缩，其次是 FTD，对应于与运动皮层的连接区域。
HD、FTD 和 AD 中壳核萎缩的不同模式与皮质纹状体回路有关，这表明壳核可能是神经退行性疾病的合适临床生物标志物。
