Degenerative changes in the basal ganglia (BG) are thought to contribute to neurological symptoms in Wilson’s disease (WD). However, very little is known about whether and how the BG have an influence on prospective memory (PM) by interacting with the cerebral cortex. Here, we employed structural magnetic resonance imaging to systematically examine the effect of volume atrophy of BG on cortical thickness and to evaluate the relationships between cortical thickness of regions associated with BG atrophy and PM performance in WD. Cortical thickness atrophy in the left temporal pole and medial frontal gyrus are not related to degenerative changes in BG. Cortical thickness in the left superior frontal gyrus and right orbitofrontal gyrus (ORB) have stronger correlations with volume atrophy of the left accumbens, pallidum, and putamen in WD when compared with healthy controls. Furthermore, the cortical thickness of the right ORB is not only significantly correlated with PM performance but can also distinguish the severity of PM impairment in WD. Additionally, the middle cingulate cortex was related to volume atrophy of the accumbens, and its cortical thickness has a significant positive correlation with event-based PM. Together, these findings highlight that BG-orbitofrontal circuits may serve as neural biomarkers of PM and provide implications for the neural mechanisms underlying cognitive impairment in WD.

基底神经节 (BG) 的退行性变化被认为会导致威尔逊病 (WD) 的神经系统症状。然而，关于 BG 是否以及如何通过与大脑皮层相互作用对前瞻性记忆 (PM) 产生影响，我们知之甚少。在这里，我们采用结构磁共振成像系统地检查 BG 体积萎缩对皮质厚度的影响，并评估与 BG 萎缩相关区域的皮质厚度与 WD 中 PM 性能之间的关系。左侧颞极和额内侧回的皮质厚度萎缩与 BG 的退行性变化无关。左侧额上回和右侧眶额回（ORB）的皮质厚度与左侧伏隔核体积萎缩、苍白球、与健康对照相比，WD 中的壳核。此外，右侧 ORB 的皮质厚度不仅与 PM 表现显着相关，而且还可以区分 WD 中 PM 损伤的严重程度。此外，中扣带回与伏隔核体积萎缩有关，其皮质厚度与基于事件的 PM 呈显着正相关。总之，这些发现强调了 BG 眶额回路可能作为 PM 的神经生物标志物，并为 WD 认知障碍的神经机制提供启示。中扣带回与伏隔核体积萎缩有关，其皮质厚度与基于事件的PM呈显着正相关。总之，这些发现强调了 BG 眶额回路可能作为 PM 的神经生物标志物，并为 WD 认知障碍的神经机制提供启示。中扣带回与伏隔核体积萎缩有关，其皮质厚度与基于事件的PM呈显着正相关。总之，这些发现强调了 BG 眶额回路可能作为 PM 的神经生物标志物，并为 WD 认知障碍的神经机制提供启示。