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