Eustache Pierre, Nemmi Federico, Saint-Aubert Laure, Pariente Jeremie, Péran Patrice
Inserm, imagerie cérébrale et handicaps neurologiques, UMR 825; CHU Purpan - Pavillon Baudot, Place du Dr Baylac, Toulouse, France.
Université de Toulouse, UPS, imagerie cérébrale et handicaps neurologiques, UMR 825; CHU Purpan - Pavillon Baudot, Toulouse, France.
J Alzheimers Dis. 2016;50(4):1035-50. doi: 10.3233/JAD-150353.
One objective of modern neuroimaging is to identify markers that can aid in diagnosis, monitor disease progression, and impact long-term drug analysis. In this study, physiopathological modifications in seven subcortical structures of patients with mild cognitive impairment (MCI) due to Alzheimer's disease (AD) were characterized by simultaneously measuring quantitative magnetic resonance parameters that are sensitive to complementary tissue characteristics (e.g., volume atrophy, shape changes, microstructural damage, and iron deposition). Fourteen MCI patients and fourteen matched, healthy subjects underwent 3T-magnetic resonance imaging with whole-brain, T1-weighted, T2*-weighted, and diffusion-tensor imaging scans. Volume, shape, mean R2*, mean diffusivity (MD), and mean fractional anisotropy (FA) in the thalamus, hippocampus, putamen, amygdala, caudate nucleus, pallidum, and accumbens were compared between MCI patients and healthy subjects. Comparisons were then performed using voxel-based analyses of R2*, MD, FA maps, and voxel-based morphometry to determine which subregions showed the greatest difference for each parameter. With respect to the micro- and macro-structural patterns of damage, our results suggest that different and distinct physiopathological processes are present in the prodromal phase of AD. MCI patients had significant atrophy and microstructural changes within their hippocampi and amygdalae, which are known to be affected in the prodromal stage of AD. This suggests that the amygdala is affected in the same, direct physiopathological process as the hippocampus. Conversely, atrophy alone was observed within the thalamus and putamen, which are not directly involved in AD pathogenesis. This latter result may reflect another mechanism, whereby atrophy is linked to indirect physiopathological processes.
现代神经成像的一个目标是识别有助于诊断、监测疾病进展以及影响长期药物分析的标志物。在本研究中,通过同时测量对互补组织特征(如体积萎缩、形状变化、微观结构损伤和铁沉积)敏感的定量磁共振参数,对因阿尔茨海默病(AD)导致的轻度认知障碍(MCI)患者的七个皮质下结构中的生理病理改变进行了表征。14名MCI患者和14名匹配的健康受试者接受了3T磁共振成像,包括全脑、T1加权、T2加权和扩散张量成像扫描。比较了MCI患者和健康受试者丘脑、海马体、壳核、杏仁核、尾状核、苍白球和伏隔核的体积、形状、平均R2、平均扩散率(MD)和平均分数各向异性(FA)。然后使用基于体素的R2*、MD、FA图谱分析和基于体素的形态计量学进行比较,以确定每个参数在哪些子区域显示出最大差异。关于损伤的微观和宏观结构模式,我们的结果表明,AD前驱期存在不同且独特的生理病理过程。MCI患者的海马体和杏仁核内有明显萎缩和微观结构变化,已知这些结构在AD前驱期会受到影响。这表明杏仁核与海马体受相同的直接生理病理过程影响。相反,在丘脑和壳核内仅观察到萎缩,而它们并不直接参与AD发病机制。后一结果可能反映了另一种机制,即萎缩与间接生理病理过程有关。