Open AccessAltered hippocampal volume and functional connectivity in patients with Cushing's disease
Author(s) -
Li Chuqi,
Zhang Yanyang,
Wang Wenxin,
Zhou Tao,
Yu Xinguang,
Tao Hong
Publication year - 2022
Publication title -
brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.915
H-Index - 41
ISSN - 2162-3279
DOI - 10.1002/brb3.2507
Subject(s) - hippocampal formation , hippocampus , neuroscience , resting state fmri , functional connectivity , glucocorticoid , psychology , neuropsychology , medicine , cognition
Stress‐related brain disorders can be associated with glucocorticoid disturbance and hippocampal alteration. However, it remains largely unknown how cortisol affects the structure and function of hippocampus. Cushing's disease (CD) provides a unique “hyperexpression model” to explore the effects of excessive cortisol on hippocampus as well as the relation between these effects and neuropsychological deficits. Methods We acquired high‐resolution T1‐weighted and resting‐state functional magnetic resonance imaging in 47 CD patients and 53 healthy controls. We obtained the volume and functional connectivity of the hippocampal rostral and caudal subregions in both groups. Relationships between hippocampal alterations, neuroendocrine, and neuropsychological assessments were identified. Results Relative to control subjects, the CD patients had smaller volumes of all four hippocampal subregions. Furthermore, whole brain resting‐state functional connectivity analyses with these four different hippocampal regions as seeds revealed altered hippocampal functional connectivity with high‐order networks, involving the DMN, frontoparietal, and limbic networks in CD patients. The intrinsic hippocampal functional connectivity was associated with the quality of life of the CD patients. Conclusions Our findings elucidate the cumulative effect of excess cortisol on the morphology and function of hippocampus and reinforce the need for effective interventions in stress‐related brain disease to halt potential hippocampal damage.