{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["14(2)"],"submitter":["Gnoni V"],"pubmed_abstract":["<h4>Background</h4>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.<h4>Objective</h4>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.<h4>Methods</h4>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.<h4>Conclusions</h4>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."],"journal":["Journal of thoracic disease"],"pagination":["564-574"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8902117"],"repository":["biostudies-literature"],"pubmed_title":["Obstructive sleep apnea and multiple facets of a neuroinflammatory response: a narrative review."],"pmcid":["PMC8902117"],"pubmed_authors":["Petrinovic MM","Kalanj-Bognar S","Gnoni V","Cash D","Morrell MJ","Rosenzweig I","Steier J","Drakatos P","Ilic K","Petanjek Z"],"additional_accession":[]},"is_claimable":false,"name":"Obstructive sleep apnea and multiple facets of a neuroinflammatory response: a narrative review.","description":"<h4>Background</h4>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.<h4>Objective</h4>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.<h4>Methods</h4>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.<h4>Conclusions</h4>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.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-05-29T20:50:02.755Z","creation":"2024-11-07T10:58:30Z"},"accession":"S-EPMC8902117","cross_references":{"pubmed":["35280483"],"doi":["10.21037/jtd-21-1231"]}}