Please use this identifier to cite or link to this item: http://hdl.handle.net/10773/38050
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dc.contributor.authorTrindade, Dáriopt_PT
dc.contributor.authorCachide, Mariapt_PT
dc.contributor.authorSoares Martins, Tâniapt_PT
dc.contributor.authorGuedes, Sandrapt_PT
dc.contributor.authorRosa, Ilka M.pt_PT
dc.contributor.authorda Cruz e Silva, Odete A.B.pt_PT
dc.contributor.authorHenriques, Ana Gabrielapt_PT
dc.date.accessioned2023-06-15T10:37:42Z-
dc.date.available2023-06-15T10:37:42Z-
dc.date.issued2023-06-
dc.identifier.urihttp://hdl.handle.net/10773/38050-
dc.description.abstractObjective: Clusterin is involved in a variety of physiological processes, including proteostasis. Several clusterin polymorphisms were associated with an increased risk of developing Alzheimer’s disease, the world-leading cause of dementia. Herein, the effect of a clusterin polymorphism, aging and dementia in the levels of clusterin in human plasma were analysed in a primary care-based cohort, and the association of this chaperone with fibrillar structures discussed. Methods: 64 individuals with dementia (CDR 1) and 64 age- and sex-matched Controls from a Portuguese cohort were genotyped for CLU rs1136000 polymorphism, and the plasma levels of clusterin and fibrils were assessed. Results: An increased prevalence of the CC genotype was observed for the dementia group, although no significant robustness was achieved. CLU rs11136000 SNP did not significantly change plasma clusterin levels in demented individuals. Instead, clusterin levels decreased with aging and even more in individuals with dementia. Importantly, plasma clusterin levels correlated with the presence of fibrillar structures in Control individuals, but not in those with dementia. Conclusion: This study reveals a significant decrease in plasma clusterin in demented individuals with aging, which related to altered clusterin-fibrils dynamics. Potentially, plasma clusterin and its association with fibrillar structures can be used to monitor dementia progression along aging.pt_PT
dc.language.isoengpt_PT
dc.publisherElsevierpt_PT
dc.relationCENTRO-01-0145-FEDER-181255pt_PT
dc.relationCENTRO-01-0145-FEDER-000003pt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UIDB%2F04501%2F2020/PTpt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UIDP%2F04501%2F2020/PTpt_PT
dc.relationBPD/UI98/7844/2017pt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/POR_CENTRO/SFRH%2FBD%2F132995%2F2017/PTpt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/POR_CENTRO/SFRH%2FBD%2F145979%2F2019/PTpt_PT
dc.rightsopenAccesspt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectClusterinpt_PT
dc.subjectAgingpt_PT
dc.subjectFibrilspt_PT
dc.subjectDementiapt_PT
dc.subjectAlzheimer’s diseasept_PT
dc.titleMonitoring clusterin and fibrillar structures in aging and dementiapt_PT
dc.typearticlept_PT
dc.description.versionpublishedpt_PT
dc.peerreviewedyespt_PT
degois.publication.titleAging Brainpt_PT
degois.publication.volume3pt_PT
dc.identifier.doi10.1016/j.nbas.2023.100080pt_PT
dc.identifier.essn2589-9589pt_PT
dc.identifier.articlenumber100080pt_PT
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