Na Xu, Yi Xing, Aonan Li, Shuaicheng Liu, Jing Gao, Xinyu Liu, Wuxiang Xie, Ning Guo, Yue Chen, Xiaoyue Sun, Jilin Wu, Weijun Gong, Danhong Wang, Yi Tang, Hesheng Liu
Alzheimer’s disease (AD) is characterized by dysfunction of large-scale brain networks, particularly the default mode network (DMN) and working memory network (WMN), with pathology, atrophy, and disconnection in these networks closely associated with cognitive decline [1]. Disease progression has been proposed to involve cascading dysfunction across these networks [2], with posterior DMN regions affected early and prefrontal DMN and WMN regions increasingly involved over time. Given their pivotal roles, these hub regions may represent promising targets for circuit-based AD therapies.