Huntington's Disease Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Sorbonne Université, Paris Brain Institute (ICM), AP-HP, Inserm, CNRS, Pitié-Salpêtrière University Hospital, Paris, France.
Brain Behav. 2023 Apr;13(4):e2940. doi: 10.1002/brb3.2940. Epub 2023 Mar 14.
Whole-brain longitudinal diffusion studies are crucial to examine changes in structural connectivity in neurodegeneration. Here, we investigated the longitudinal alterations in white matter (WM) microstructure across the timecourse of Huntington's disease (HD).
We examined changes in WM microstructure from premanifest to early manifest disease, using data from two cohorts with different disease burden. The TrackOn-HD study included 67 controls, 67 premanifest, and 10 early manifest HD (baseline and 24-month data); the PADDINGTON study included 33 controls and 49 early manifest HD (baseline and 15-month data). Longitudinal changes in fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity, and radial diffusivity from baseline to last study visit were investigated for each cohort using tract-based spatial statistics. An optimized pipeline was employed to generate participant-specific templates to which diffusion tensor imaging maps were registered and change maps were calculated. We examined longitudinal differences between HD expansion-carriers and controls, and correlations with clinical scores, including the composite UHDRS (cUHDRS).
HD expansion-carriers from TrackOn-HD, with lower disease burden, showed a significant longitudinal decline in FA in the left superior longitudinal fasciculus and an increase in MD across subcortical WM tracts compared to controls, while in manifest HD participants from PADDINGTON, there were significant widespread longitudinal increases in diffusivity compared to controls. Baseline scores in clinical scales including the cUHDRS predicted WM microstructural change in HD expansion-carriers.
The present study showed significant longitudinal changes in WM microstructure across the HD timecourse. Changes were evident in larger WM areas and across more metrics as the disease advanced, suggesting a progressive alteration of WM microstructure with disease evolution.
全脑纵向扩散研究对于检查神经退行性变过程中结构连接的变化至关重要。在这里,我们研究了亨廷顿病(HD)病程中白质(WM)微观结构的纵向变化。
我们使用具有不同疾病负担的两个队列的数据,研究了 WM 微观结构从前驱期到早期发病期的变化。TrackOn-HD 研究包括 67 名对照者、67 名前驱期和 10 名早期 HD(基线和 24 个月数据);PADDINGTON 研究包括 33 名对照者和 49 名早期 HD(基线和 15 个月数据)。使用基于束的空间统计学方法,对每个队列从基线到最后一次研究访问的分数各向异性(FA)、平均扩散系数(MD)、轴向扩散系数和径向扩散系数的纵向变化进行了研究。采用优化的流水线生成参与者特异性模板,对扩散张量成像图谱进行注册,并计算变化图谱。我们研究了 HD 扩展携带者与对照组之间的纵向差异,并与临床评分(包括复合 UHDRS [cUHDRS])进行了相关性分析。
TrackOn-HD 中疾病负担较低的 HD 扩展携带者在左侧上纵束中表现出 FA 的显著纵向下降,并且与对照组相比,皮质下 WM 束中 MD 增加,而 PADDINGTON 中的显性 HD 参与者与对照组相比,弥散度有明显的广泛的纵向增加。临床量表(包括 cUHDRS)的基线评分预测了 HD 扩展携带者的 WM 微观结构变化。
本研究显示了在 HD 病程中 WM 微观结构的显著纵向变化。随着疾病的进展,在更大的 WM 区域和更多的指标中都出现了变化,这表明 WM 微观结构随着疾病的演变而发生了进行性改变。