Jiang Xueyan, Zhang Mingkai, Yan Chuyao, Daamen Marcel, Boecker Henning, Yue Feng, Jessen Frank, Hu Xiaochen, Han Ying
State Key Laboratory of Digital Medical Engineering, School of Biomedical Engineering, Hainan University, Sanya 572022, China.
German Center for Neurodegenerative Disease (DZNE), Bonn 53127, Germany.
J Neurosci. 2025 Jun 18;45(25):e2310242025. doi: 10.1523/JNEUROSCI.2310-24.2025.
This study examined how amyloid burden affects structural and functional brain network topology in subjective cognitive decline (SCD), a risk condition for Alzheimer's disease (AD). Functional and structural brain networks were analyzed in 100 individuals with SCD and 86 normal controls (NC; both sexes included) using resting-state functional MRI and diffusion tensor imaging. Topological properties of brain networks were evaluated as indicators of information exchange efficiency and network robustness. Amyloid burden in 55 SCD participants was measured using amyloid PET imaging and a frequency-based staging method, which defined global and regional amyloid burden for four anatomical stages. Compared with NC, individuals with SCD exhibited increased functional nodal efficiency and structural nodal betweenness in the left anterior and median cingulate gyri, with no differences in network-level properties. Amyloid staging revealed four cortical divisions: Stage 1, fusiform and lateral temporal gyri; Stage 2, occipital areas; Stage 3, default mode network (DMN), midline brain, and lateral frontotemporal areas; and Stage 4, the remaining cortex. The global and regional amyloid burdens of each cortical stage were positively associated with the node-level properties of a set of DMN hubs, with the left anterior and posterior cingulate gyri being congruently associated with all amyloid stages. These findings suggest that amyloid burden continuously influences network adaptations through DMN hubs, irrespective of local proximity to pathology. Increased nodal properties in cortical hubs may reflect heightened information-processing demands during early amyloid deposition in this population at risk for AD.
本研究探讨了淀粉样蛋白负荷如何影响主观认知下降（SCD）这一阿尔茨海默病（AD）风险状况下大脑结构和功能网络拓扑。使用静息态功能磁共振成像和扩散张量成像对100名SCD个体和86名正常对照者（NC；包括男女）的大脑功能和结构网络进行了分析。大脑网络的拓扑特性被评估为信息交换效率和网络稳健性的指标。使用淀粉样蛋白PET成像和基于频率的分期方法测量了55名SCD参与者的淀粉样蛋白负荷，该方法定义了四个解剖阶段的全局和区域淀粉样蛋白负荷。与NC相比，SCD个体在左侧前扣带回和中央扣带回中表现出功能节点效率增加和结构节点中介中心性增加，而网络水平特性无差异。淀粉样蛋白分期揭示了四个皮质分区：第1阶段，梭状回和颞下回；第2阶段，枕叶区域；第3阶段，默认模式网络（DMN）、中线脑区和外侧额颞叶区域；第4阶段，其余皮质。每个皮质阶段的全局和区域淀粉样蛋白负荷与一组DMN枢纽的节点水平特性呈正相关，左侧前扣带回和后扣带回与所有淀粉样蛋白阶段均一致相关。这些发现表明，淀粉样蛋白负荷通过DMN枢纽持续影响网络适应性，而与局部病变的接近程度无关。皮质枢纽中节点特性的增加可能反映了在这个有AD风险的人群中，早期淀粉样蛋白沉积期间信息处理需求的增加。
