Magnetic resonance imaging evidence for presymptomatic change in thalamus and caudate in familial Alzheimer's disease.
Magnetic resonance imaging evidence for presymptomatic change in thalamus and caudate in familial Alzheimer's disease.
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DOI：
10.1093/brain/awt065
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发表时间：
2013-05
期刊：
影响因子：
--
通讯作者：
Fox NC
中科院分区：
文献类型：
--
作者：
Ryan NS;Keihaninejad S;Shakespeare TJ;Lehmann M;Crutch SJ;Malone IB;Thornton JS;Mancini L;Hyare H;Yousry T;Ridgway GR;Zhang H;Modat M;Alexander DC;Rossor MN;Ourselin S;Fox NC
对症状前家族性阿尔茨海默病的淀粉样蛋白成像研究显示，纹状体和丘脑是淀粉样蛋白沉积的最早部位。本研究的目的是调查是否有相关的体积和扩散率的变化，在这些皮质下结构的家族性阿尔茨海默病的症状前和症状阶段。由于丘脑和纹状体参与了复杂的认知和行为功能的神经网络，我们还研究了连接白色物质束的扩散特性。一组20名早老素1突变携带者进行了体积和弥散张量磁共振成像，神经心理学和临床评估; 10名有症状，10名症状前，平均5.6岁，比他们的预期发病年龄年轻; 20名健康对照受试者也进行了研究。我们对丘脑、尾状核、壳核和海马的体积和扩散率变化进行了感兴趣区域分析，并检查了感兴趣的白色物质束（穹窿、扣带回和胼胝体）的扩散行为。基于体素的形态测量学和基于束的空间统计学也被用来提供无偏的全脑分析的体积和扩散指数的组间差异，分别。我们发现，左侧丘脑和双侧尾状核的体积减少是明显的，在症状前阶段，随着双侧丘脑和左侧尾状核的各向异性分数增加。虽然没有显着的海马体积损失是明显的症状前，减少平均扩散率观察到在右侧海马和减少平均和轴向扩散率在右侧扣带。相比之下，症状性突变携带者在所有感兴趣的白色物质束中表现出增加的平均、轴向和特别是径向扩散率，降低的分数各向异性。有症状组还显示所有感兴趣的皮质下灰质区域的萎缩和平均扩散率增加，双侧壳核的各向异性分数增加。我们认为，轴突损伤可能是症状前阿尔茨海默病的早期事件，导致轴向和平均扩散率的初始下降，然后随着轴突密度的损失而增加。选择性退化的长coursing白色物质束，与相对保存的短interneurons，可能占分数各向异性的增加，是在丘脑和尾状体症状前。这可能是由于它们的密集连接，成像变化首先出现在丘脑和纹状体，然后进展到涉及脆弱的神经元网络中的其他区域。
Amyloid imaging studies of presymptomatic familial Alzheimer’s disease have revealed the striatum and thalamus to be the earliest sites of amyloid deposition. This study aimed to investigate whether there are associated volume and diffusivity changes in these subcortical structures during the presymptomatic and symptomatic stages of familial Alzheimer’s disease. As the thalamus and striatum are involved in neural networks subserving complex cognitive and behavioural functions, we also examined the diffusion characteristics in connecting white matter tracts. A cohort of 20 presenilin 1 mutation carriers underwent volumetric and diffusion tensor magnetic resonance imaging, neuropsychological and clinical assessments; 10 were symptomatic, 10 were presymptomatic and on average 5.6 years younger than their expected age at onset; 20 healthy control subjects were also studied. We conducted region of interest analyses of volume and diffusivity changes in the thalamus, caudate, putamen and hippocampus and examined diffusion behaviour in the white matter tracts of interest (fornix, cingulum and corpus callosum). Voxel-based morphometry and tract-based spatial statistics were also used to provide unbiased whole-brain analyses of group differences in volume and diffusion indices, respectively. We found that reduced volumes of the left thalamus and bilateral caudate were evident at a presymptomatic stage, together with increased fractional anisotropy of bilateral thalamus and left caudate. Although no significant hippocampal volume loss was evident presymptomatically, reduced mean diffusivity was observed in the right hippocampus and reduced mean and axial diffusivity in the right cingulum. In contrast, symptomatic mutation carriers showed increased mean, axial and in particular radial diffusivity, with reduced fractional anisotropy, in all of the white matter tracts of interest. The symptomatic group also showed atrophy and increased mean diffusivity in all of the subcortical grey matter regions of interest, with increased fractional anisotropy in bilateral putamen. We propose that axonal injury may be an early event in presymptomatic Alzheimer’s disease, causing an initial fall in axial and mean diffusivity, which then increases with loss of axonal density. The selective degeneration of long-coursing white matter tracts, with relative preservation of short interneurons, may account for the increase in fractional anisotropy that is seen in the thalamus and caudate presymptomatically. It may be owing to their dense connectivity that imaging changes are seen first in the thalamus and striatum, which then progress to involve other regions in a vulnerable neuronal network.
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影响因子：
11
作者：
Hervé, D;Molko, N;Chabriat, H
通讯作者：
Chabriat, H
影响因子：
6.1
作者：
Bohanna, India;Georgiou-Karistianis, Nellie;Egan, Gary F.
通讯作者：
Egan, Gary F.
影响因子：
168.9
作者：
Ferri, CP;Prince, M;Scazufca, M
通讯作者：
Scazufca, M
DOI：
10.1186/alzrt59
发表时间：
2011-01-06
期刊：
Alzheimer's research & therapy
影响因子：
--
作者：
Bateman RJ;Aisen PS;De Strooper B;Fox NC;Lemere CA;Ringman JM;Salloway S;Sperling RA;Windisch M;Xiong C
通讯作者：
Xiong C
影响因子：
4
作者：
Fortea, Juan;Sala-Llonch, Roser;Sanchez-Valle, Raquel
通讯作者：
Sanchez-Valle, Raquel