Frontiers in Neuroscience (Apr 2022)

Abnormal Functional Connectivity of Hippocampal Subdivisions in Obstructive Sleep Apnea: A Resting-State Functional Magnetic Resonance Imaging Study

  • Xiang Liu,
  • Liting Chen,
  • Wenfeng Duan,
  • Haijun Li,
  • Linghong Kong,
  • Yongqiang Shu,
  • Panmei Li,
  • Kunyao Li,
  • Wei Xie,
  • Yaping Zeng,
  • Dechang Peng

DOI
https://doi.org/10.3389/fnins.2022.850940
Journal volume & issue
Vol. 16

Abstract

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The hippocampus is involved in various cognitive function, including memory. Hippocampal structural and functional abnormalities have been observed in patients with obstructive sleep apnoea (OSA), but the functional connectivity (FC) patterns among hippocampal subdivisions in OSA patients remain unclear. The purpose of this study was to investigate the changes in FC between hippocampal subdivisions and their relationship with neurocognitive function in male patients with OSA. Resting-state fMRI were obtained from 46 male patients with untreated severe OSA and 46 male good sleepers. The hippocampus was divided into anterior, middle, and posterior parts, and the differences in FC between hippocampal subdivisions and other brain regions were determined. Correlation analysis was used to explore the relationships between abnormal FC of hippocampal subdivisions and clinical characteristics in patients with OSA. Our results revealed increased FC in the OSA group between the left anterior hippocampus and left middle temporal gyrus; between the left middle hippocampus and the left inferior frontal gyrus, right anterior central gyrus, and left anterior central gyrus; between the left posterior hippocampus and right middle frontal gyrus; between the right middle hippocampus and left inferior frontal gyrus; and between the right posterior hippocampus and left middle frontal gyrus. These FC abnormalities predominantly manifested in the sensorimotor network, fronto-parietal network, and semantic/default mode network, which are closely related to the neurocognitive impairment observed in OSA patients. This study advances our understanding of the potential pathophysiological mechanism of neurocognitive dysfunction in OSA.

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