Center for Neurosciences, The Feinstein Institute for Medical Research, Manhasset, NY, USA.
Department of Neurology, Northwell Health, Manhasset, NY, USA.
Cereb Cortex. 2018 Dec 1;28(12):4121-4135. doi: 10.1093/cercor/bhx267.
Little is known of the structural and functional properties of abnormal brain networks associated with neurological disorders. We used a social network approach to characterize the properties of the Parkinson's disease (PD) metabolic topography in 4 independent patient samples and in an experimental non-human primate model. The PD network exhibited distinct features. Dense, mutually facilitating functional connections linked the putamen, globus pallidus, and thalamus to form a metabolically active core. The periphery was formed by weaker connections linking less active cortical regions. Notably, the network contained a separate module defined by interconnected, metabolically active nodes in the cerebellum, pons, frontal cortex, and limbic regions. Exaggeration of the small-world property was a consistent feature of disease networks in parkinsonian humans and in the non-human primate model; this abnormality was only partly corrected by dopaminergic treatment. The findings point to disease-related alterations in network structure and function as the basis for faulty information processing in this disorder.
目前对于与神经紊乱相关的异常大脑网络的结构和功能特性知之甚少。我们使用社会网络方法来描述帕金森病(PD)代谢拓扑在 4 个独立患者样本和实验性非人类灵长类动物模型中的特征。PD 网络表现出独特的特征。密集的、相互促进的功能连接将壳核、苍白球和丘脑连接起来,形成一个代谢活跃的核心。外围由连接不活跃皮质区域的较弱连接形成。值得注意的是,网络包含一个由小脑、脑桥、额叶皮层和边缘区域中相互连接的代谢活跃节点定义的单独模块。疾病网络中小世界特性的夸大是帕金森病患者和非人类灵长类动物模型中一致的特征;这种异常仅部分通过多巴胺治疗得到纠正。这些发现表明,网络结构和功能的疾病相关改变是该疾病中信息处理错误的基础。