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Publications

Journal Article Epublish

PubMed: 38434201 DOI: 10.3389/fneur.2024.1323878

The effect of the interaction of sleep onset latency and age on ischemic stroke severity via inflammatory chemokines.

Front Neurol 15:1323878

Authors: Yuyu Zhou, Xiaoli Han, Qingshuang Mu, Lifei Xing, Yan Wu, Cunbao Li, Yanlong Liu, Fan Wang

Affiliations

  • Beijing Hui-Long-Guan Hospital, Peking University, Beijing, China. Medical Neurobiology Lab, Inner Mongolia Medical University, Huhhot, China.
  • Clinical Nutrition Department, Friendship Hospital of Urumqi, Urumqi, China.
  • Xinjiang Key Laboratory of Neurological Disorder Research, The Second Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
  • Department of Neurology, Sinopharm North Hospital, Baotou, China.
  • Beijing Hui-Long-Guan Hospital, Peking University, Beijing, China.
  • Medical Neurobiology Lab, Inner Mongolia Medical University, Huhhot, China.
  • School of Mental Health, Wenzhou Medical University, Wenzhou, China.

Abstract

Objective

Prolonged sleep onset latency (PSOL) and age have been linked to ischemic stroke (IS) severity and the production of chemokines and inflammation, both of which contribute to IS development. This study aimed to explore the relationship between chemokines, inflammation, and the interplay between sleep onset latency (SOL) and age in influencing stroke severity.

Methods

A cohort of 281 participants with mild to moderate IS was enrolled. Stroke severity was assessed using the National Institutes of Health Stroke Scale (NIHSS), and SOL was recorded. Serum levels of macrophage inflammatory protein-1alpha (MIP-1α), macrophage inflammatory protein-1beta (MIP-1β), monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured.

Results

NIHSS scores of middle-aged participants with PSOL were significantly higher than those with normal sleep onset latency (NSOL) ( = 0.046). This difference was also observed when compared to both the elderly with NSOL ( = 0.022), and PSOL ( < 0.001). Among middle-aged adults with PSOL, MIP-1β exhibited a protective effect on NIHSS scores (β = -0.01,  = -2.11,  = 0.039,  = 0.13). MIP-1α demonstrated a protective effect on NIHSS scores in the elderly with NSOL (β = -0.03,  = -2.27,  = 0.027,  = 0.12).

Conclusion

This study reveals a hitherto undocumented association between PSOL and IS severity, along with the potential protective effects of MIP-1β in mitigating stroke severity, especially among middle-aged patients.

MeSH

Aged, Macrophages, Tumor Necrosis Factor-Alpha, Interleukin-6, Chemokines, Chemokine Ccl2, Sleep Latency, Ischemic Stroke