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Obstructive sleep apnea and multiple facets of a neuroinflammatory response: a narrative review.
Gnoni, Valentina; Ilic, Katarina; Drakatos, Panagis; Petrinovic, Marija M; Cash, Diana; Steier, Joerg; Morrell, Mary J; Petanjek, Zdravko; Kalanj-Bognar, Svjetlana; Rosenzweig, Ivana.
Afiliação
  • Gnoni V; Sleep and Brain Plasticity Centre, CNS, IoPPN, King's College London, UK.
  • Ilic K; Sleep Disorders Centre, Guy's and St Thomas' Hospital, GSTT NHS, London, UK.
  • Drakatos P; Sleep and Brain Plasticity Centre, CNS, IoPPN, King's College London, UK.
  • Petrinovic MM; BRAIN, Imaging Centre, CNS, King's College London, UK.
  • Cash D; Croatian Institute for Brain Research, Centre for Excellence (HIIM), University of Zagreb School of Medicine, Zagreb, Croatia.
  • Steier J; Sleep and Brain Plasticity Centre, CNS, IoPPN, King's College London, UK.
  • Morrell MJ; Sleep Disorders Centre, Guy's and St Thomas' Hospital, GSTT NHS, London, UK.
  • Petanjek Z; Faculty of Life and Sciences Medicine, King's College London, UK.
  • Kalanj-Bognar S; Department of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
  • Rosenzweig I; MRC Centre for Neurodevelopmental Disorders, King's College London, London, UK.
J Thorac Dis ; 14(2): 564-574, 2022 Feb.
Article em En | MEDLINE | ID: mdl-35280483
ABSTRACT

Background:

Obstructive sleep apnea (OSA) is a chronic, highly prevalent, multi-system and sleep disorder, which may contribute to cognitive impairment and a variety of structural and neurophysiologic changes. The focus on OSA is warranted given its recognized links with major psychiatric and neurologic disorders, including Alzheimer's disease. Some preliminary studies suggest a dual effect of the inflammatory response in OSA. Neuroinflammation may present with initial, potentially adaptive and homeostatic, and later, a more distinctly maladaptive, precipitating and perpetuating role.

Objective:

We here propose and argue in favour of the inflammatory process in the brain as a likely binding mechanism behind at least some effects that OSA may have on the brain and its function. Several OSA-triggered molecular and cellular events, that could lead to a neurodegenerative cascade, are similarly discussed.

Methods:

This perspective reviews the body of literature that investigates potential links between the inflammatory processes in the brain and the OSA. A special emphasis is placed on a potential role for neuroplastin, a novel transmembrane synaptic protein involved in the neuroplasticity and known to be differentially regulated in the OSA.

Conclusions:

The intricate interplay between neuroinflammation and other mechanistic correlates of OSA add to the evidence that neuroinflammation may be a key target for future therapeutic strategies in a number of comorbid disorders. The future studies will need to answer whether it is sleep fragmentation (SF) or intermittent hypoxia (IH) which may drive any such neuroinflammation.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2022 Tipo de documento: Article