Early limbic microstructural alterations in apathy and depression in de novo Parkinson's disease
Early limbic microstructural alterations in apathy and depression in de novo Parkinson's disease
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DOI：
10.1002/mds.27793
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发表时间：
2019-07-15
影响因子：
8.6
通讯作者：
Thobois, Stephane
中科院分区：
文献类型：
--
作者：
Prange, Stephane;Metereau, Elise;Thobois, Stephane
背景原发性帕金森病患者的结构改变是否是冷漠和抑郁的基础尚不清楚。本研究的目的是调查新发帕金森病患者的冷漠和抑郁是否与结构改变有关，以及结构异常与多巴胺能或多巴胺能功能障碍的关系。方法在一项多模式成像病例对照研究中，我们使用基于体素的形态测量和扩散张量成像结合基于白色物质束的空间统计学，比较了灰质的形态和微结构架构，该研究招募了14名冷漠和13名非冷漠的原发性帕金森病患者和15名年龄匹配的健康对照，并与突触前多巴胺能和多巴胺能系统的PET成像配对。结果情感淡漠的帕金森病患者双侧内侧皮质-纹状体边缘系统的微结构改变，表现为前纹状体和膝前前扣带皮质的各向异性分数降低，平均扩散率增加，并伴有多巴胺能功能障碍。此外，显微结构的改变扩展到内侧额叶皮质，膝下前扣带回皮质和胼胝体下回，内侧丘脑，和尾侧中脑，这表明中断的远程非多巴胺能投射起源于脑干，除了在胼胝体半球间连接和额纹状体联合束的显微结构的改变在病程早期。此外，在冷漠和nonapathetic患者的抑郁症状相关的微结构异常揭示了一个独特的，主要是右侧的边缘子网络，涉及边缘和额叶联合束。结论：与冷漠和抑郁相关的早期边缘系统微结构改变强调了早期非多巴胺能神经元投射和相关皮质和皮质下网络的破坏作用，这些网络是帕金森病非运动和神经精神症状的可变表达的基础。(c)2019国际帕金森和运动障碍协会
Background Whether structural alterations underpin apathy and depression in de novo parkinsonian patients is unknown. The objectives of this study were to investigate whether apathy and depression in de novo parkinsonian patients are related to structural alterations and how structural abnormalities relate to serotonergic or dopaminergic dysfunction. Methods We compared the morphological and microstructural architecture in gray matter using voxel-based morphometry and diffusion tensor imaging coupled with white matter tract-based spatial statistics in a multimodal imaging case-control study enrolling 14 apathetic and 13 nonapathetic patients with de novo Parkinson's disease and 15 age-matched healthy controls, paired with PET imaging of the presynaptic dopaminergic and serotonergic systems. Results De novo parkinsonian patients with apathy had bilateral microstructural alterations in the medial corticostriatal limbic system, exhibiting decreased fractional anisotropy and increased mean diffusivity in the anterior striatum and pregenual anterior cingulate cortex in conjunction with serotonergic dysfunction. Furthermore, microstructural alterations extended to the medial frontal cortex, the subgenual anterior cingulate cortex and subcallosal gyrus, the medial thalamus, and the caudal midbrain, suggesting disruption of long-range nondopaminergic projections originating in the brainstem, in addition to microstructural alterations in callosal interhemispheric connections and frontostriatal association tracts early in the disease course. In addition, microstructural abnormalities related to depressive symptoms in apathetic and nonapathetic patients revealed a distinct, mainly right-sided limbic subnetwork involving limbic and frontal association tracts. Conclusions Early limbic microstructural alterations specifically related to apathy and depression emphasize the role of early disruption of ascending nondopaminergic projections and related corticocortical and corticosubcortical networks which underpin the variable expression of nonmotor and neuropsychiatric symptoms in Parkinson's disease. (c) 2019 International Parkinson and Movement Disorder Society