EDITORIAL article

Front. Sleep

Sec. Sleep, Behavior and Mental Health

Volume 4 - 2025 | doi: 10.3389/frsle.2025.1616848

This article is part of the Research TopicSleep and NeurodegenerationView all 6 articles

Editorial: Sleep and Neurodegeneration

Provisionally accepted
  • 1University of Warwick, Coventry, United Kingdom
  • 2GlaxoSmithKline (China), Beijing, Beijing Municipality, China

The final, formatted version of the article will be published soon.

Ischemia stroke is a major neurological disease world-wide, and is a major cause of cognitive impairment (Elendu et al., 2023). Understanding that the neurological loss in stroke induces alterations in sleep, which in turn exacerbate neurodegeneration, in this topic, Fu et al 2024, investigated hypocretin-1 as biomarkers of poor sleep quality in stroke patients. Low levels of hypocretin-1 is a predictor of tissue damage spread following stroke (Kotan et al., 2013). Could this be related to its effect on poor sleep quality or how it interplays with blood pressure and cerebral blood flow, as posited by Fu et al? and could it later determine the cognitive impairment seen in post-stroke patients? Lv et al 2024 , looked to understand the association between poor sleep quality and cognitive impairment in elderly hypertensive patients. Both hypertension and sleep disturbances are linked to vascular dementia and cognitive impairment (Elwood et al., 2011;Emdin et al., 2016), suggesting a convergent pathway. The association between poor sleep quality and cognitive impairment in hypertensive patients spanned multiple educational levels, and affected a broad array of cognitive areas. Lv et al further suggested that this relationship may be due to the deposition of brain amyloid β-protein (Aβ).Kollarik et al 2024 have shown that enhanced slow-wave activity induced by sodium oxybate (SO) lowered amyloid burden and improved cognitive performance in early stages of Alzheimer's disease. SO, a common treatment for narcolepsy, improved cognitive performance and lowered amyloid burden through increasing delta activity gain. Decreased delta power such as that associated with Alzheimer's disease, can be caused by disorders such as obstructive sleep apnoea (Monegro et al., 2019).Hong et al 2023 explored the effects of sleep apnoea on cognitive impairment and concomitant affective disorders. Whilst sleep apnoea has long been linked to the progression and severity of affective disorders(KimKo and Kim, 2019), and also with cognitive decline (MarchiAllali and Heinzer, 2024), Hong et al investigate how these comorbidities interact with one another. Interestingly, it is the interplay between obstructive sleep apnoea and anxiety that is most strongly associated with cognitive impairment.Jones et al 2023 investigated behind the environmental and contextual factors that underlie cognitive impairment in sleep deprived patients. Whilst sleep is well known to cause cognitive impairment (Keil et al., 2023), which cognitive facets short-term sleep deprivation effects is less well understood. After extracting brain vital signs from established event-related potential components, basic attention was impaired by sleep deprivation, meaning that it is possible to use such vital signs to identify situation cognitive impairment related to acute sleep deprivation.Given the infancy of how sleep and neurodegeneration bidirectionally interact, and the relevance of studies from seemingly disparate cognitive disorders, it will be interesting to see if sleep disturbances have broader effects that interact with multiple neurodegenerative disorders, whether it's interactions with each disorder are more specific, or if it is a compilation of both.

Keywords: Sleep, Sleep apnoea, cognitive impaiment, Stroke, Hypertension, amyloid burden, Affective Disorders

Received: 23 Apr 2025; Accepted: 13 May 2025.

Copyright: © 2025 Huckstepp and Gu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Robert Timothy Richard Huckstepp, University of Warwick, Coventry, United Kingdom

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