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Long non-coding RNAs and accelerated aging in bipolar disorder

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dc.contributor.coauthorEkinci, S.
dc.contributor.coauthorArat Çelik, H.E.
dc.contributor.coauthorSquassina, A.
dc.contributor.departmentSchool of Medicine
dc.contributor.departmentKUTTAM (Koç University Research Center for Translational Medicine)
dc.contributor.departmentGraduate School of Health Sciences
dc.contributor.kuauthorFettahoğlu, İbrahim
dc.contributor.kuauthorCeylan, Deniz
dc.contributor.schoolcollegeinstituteResearch Center
dc.contributor.schoolcollegeinstituteGRADUATE SCHOOL OF HEALTH SCIENCES
dc.contributor.schoolcollegeinstituteSCHOOL OF MEDICINE
dc.date.accessioned2026-07-02T07:03:32Z
dc.date.available2026-03-27
dc.date.issued2026
dc.description.abstractBipolar disorder (BD) has been associated with accelerated biological aging, potentially driven by genetic and environmental factors. Long non-coding RNAs (lncRNAs), key regulators of epigenetic, telomere attrition, and cellular aging processes, may play a role in accelerated aging in BD. This review summarizes current evidence on aging-associated lncRNAs and their relevance to BD. We searched PubMed for English-language original studies published up to June 2, 2025, using keywords related to lncRNAs, aging-related mechanisms, and agingassociated neuropsychiatric disorders. A total of 112 articles reported 163 lncRNAs, of which 19 were common to aging-related mechanisms and aging-associated neuropsychiatric disorders. Among these, ANRIL, HOTAIR, TUG1, MALAT1, NEAT1, and GAS5 have been reported in both aging-related contexts and BD; however, their relevance to BD requires further confirmation in independent and well-characterized cohorts. The remaining overlapping lncRNAs may represent additional candidates of interest for future investigation rather than established contributors to BD pathophysiology.
dc.description.fulltextNo
dc.description.harvestedfromManual
dc.description.indexedbyWoS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.openaccessN/A
dc.description.publisherscopeInternational
dc.description.readpublishN/A
dc.description.sponsoredbyTubitakEuN/A
dc.description.versionPublished version
dc.identifier.WoSQuartileN/A
dc.identifier.doi10.1016/j.nsa.2026.106990
dc.identifier.eissn2772-4085
dc.identifier.embargoNo
dc.identifier.pubmed41768529
dc.identifier.scopus2-s2.0-105034904546
dc.identifier.urihttps://doi.org/10.1016/j.nsa.2026.106990
dc.identifier.urihttps://hdl.handle.net/20.500.14288/32852
dc.identifier.volume5
dc.identifier.wos1701560500001
dc.keywordsAccelerated aging
dc.keywordsAging-associated neuropsychiatric disorders
dc.keywordsBipolar disorder
dc.keywordsLong non-coding RNAs
dc.languageeng
dc.publisherElsevier
dc.relation.affiliationKoç University
dc.relation.collectionKoç University Institutional Repository
dc.relation.ispartofNeuroscience Applied
dc.relation.openaccessN/A
dc.rightsN/A
dc.rights.uriN/A
dc.subjectNeurosciences
dc.subjectPsychiatryv
dc.titleLong non-coding RNAs and accelerated aging in bipolar disorder
dc.typeReview
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