Limited Microvascular Remodelling Occurs in the Aged Human Hippocampus in Obstructive Sleep Apnoea

Cuicui Xu1, Jessica E Owen1, Thorarinn Gislason2,3

  • 1School of Health and Biomedical Sciences, RMIT University, Bundoora, VIC 3083, Australia.

Insights

Obstructive sleep apnea (OSA) is linked to microvascular remodelling in the human hippocampus, not new vessel growth. Increased OSA severity worsens these changes, which are not affected by continuous positive airway pressure (CPAP) or age.

Area of Science:

  • Neuroscience
  • Cardiovascular Science
  • Sleep Medicine

Background:

  • Obstructive sleep apnea (OSA) causes intermittent hypoxia, leading to varied microvascular responses in different organs.
  • While mice show hippocampal angiogenesis, humans with OSA experience microvascular loss in the heart and retina.

Purpose of the Study:

  • To investigate hippocampal microvascular changes in patients with obstructive sleep apnea (OSA).
  • To determine if patient age or continuous positive airway pressure (CPAP) use influences hippocampal microvascularization in OSA.

Main Methods:

  • Quantitative analysis of immunolabelled microvessels from autopsy samples of 31 patients with confirmed OSA.
  • Comparison of microvascular parameters between low and high OSA severity groups, considering age and CPAP use.

Main Results:

  • Higher OSA severity correlated with increased mean microvessel diameter and length in the fimbria and CA4, indicating microvascular remodelling.
  • No significant difference in mean vessel counts was observed, suggesting an absence of angiogenesis.
  • Microvascular remodelling in the fimbria was associated with increased age, but CPAP treatment did not alter these patterns.

Conclusions:

  • No evidence of angiogenesis in the human hippocampus in OSA or with aging.
  • Increased OSA severity is associated with microvascular remodelling in specific hippocampal regions (fimbria and CA4).
  • CPAP use does not appear to influence OSA-related microvascular remodelling in the hippocampus.
  • Limited microvascular adaptability may contribute to hippocampal vulnerability in severe OSA.