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

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

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. 2024 Feb 16:15:1323878. doi: 10.3389/fneur.2024.1323878. eCollection 2024.

Authors

Yuyu Zhou^#^{1

2}, Xiaoli Han^#³, Qingshuang Mu^#⁴, Lifei Xing⁵, Yan Wu¹, Cunbao Li², Yanlong Liu⁶, Fan Wang¹

Affiliations

¹ Beijing Hui-Long-Guan Hospital, Peking University, Beijing, China.
² Medical Neurobiology Lab, Inner Mongolia Medical University, Huhhot, China.
³ Clinical Nutrition Department, Friendship Hospital of Urumqi, Urumqi, China.
⁴ Xinjiang Key Laboratory of Neurological Disorder Research, The Second Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
⁵ Department of Neurology, Sinopharm North Hospital, Baotou, China.
⁶ School of Mental Health, Wenzhou Medical University, Wenzhou, China.

^# Contributed equally.

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) (p = 0.046). This difference was also observed when compared to both the elderly with NSOL (p = 0.022), and PSOL (p < 0.001). Among middle-aged adults with PSOL, MIP-1β exhibited a protective effect on NIHSS scores (β = -0.01, t = -2.11, p = 0.039, R² = 0.13). MIP-1α demonstrated a protective effect on NIHSS scores in the elderly with NSOL (β = -0.03, t = -2.27, p = 0.027, R² = 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.

Keywords: age; inflammation; interaction; ischemic stroke; sleep onset latency.

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by the following grants: The Technology Support Project of Xinjiang (2017E0267), the 10th Inner Mongolia Autonomous Region “Prairie excellence” Project, Natural Science Foundation of Xinjiang Province (2018D01C228), Xinjiang Outstanding Youth Science Grant (2017Q007), Natural Science Foundation of China (81560229), Beijing Natural Science Foundation (7152074), the “Qingmiao” program of Beijing Municipal Hospital Management Center (QML20212003), and the Youth Scientific Research Foundation of Beijing Huilongguan Hospital (LY202106).