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dc.contributor.authorRyan, J
dc.contributor.authorPilkington, L
dc.contributor.authorNeuhaus, K
dc.contributor.authorRitchie, K
dc.contributor.authorAncelin, M-L
dc.contributor.authorSaffery, R
dc.date.accessioned2020-12-21T03:57:41Z
dc.date.available2020-12-21T03:57:41Z
dc.date.issued2017-10-25
dc.identifierpii: 10.1186/s12888-017-1515-8
dc.identifier.citationRyan, J., Pilkington, L., Neuhaus, K., Ritchie, K., Ancelin, M. -L. & Saffery, R. (2017). Investigating the epigenetic profile of the inflammatory gene IL-6 in late-life depression. BMC PSYCHIATRY, 17 (1), https://doi.org/10.1186/s12888-017-1515-8.
dc.identifier.issn1471-244X
dc.identifier.urihttp://hdl.handle.net/11343/257428
dc.description.abstractBACKGROUND: It is well established that there is a link between inflammation and depression, with several studies reporting increased circulating levels of the pro-inflammatory cytokine, interleukin-6 (IL6), in depressed individuals. Peripheral epigenetic marks, including DNA methylation, hold promise as biomarkers for a range of complex conditions, with potential to inform diagnosis and tailor interventions. The aim of this study was to determine whether individuals with depression display differential methylation of the IL6 gene promoter compared to individuals without depression. METHODS: The ESPRIT study of later life neuropsychiatric disorders used a random sampling framework to select non-institutionalised participants aged ≥65 years and over living in the Montpellier region of France. Major depressive disorder (MDD) was assessed using the Mini International Neuropsychiatric Interview (MINI) according to DSM-IV criteria. High levels of depressive symptoms were defined as a score of ≥16 on the Centre for Epidemiologic Studies Depression Scale (CES-D). IL6 promoter DNA methylation was measured on a sub-sample of 380 participants who provided buccal samples. RESULTS: Individuals with depression (current MDD or high depressive symptoms) had lower IL6 methylation levels at one of the four sites investigated, however the effect size was small (∆ 2.4%, SE 0.009, p = 0.006). Interestingly, antidepressant use was independently associated with higher IL-6 methylation at the same site (∆ 4.6%, SE 0.019, p = 0.015). In multivariate linear regression analyses adjusting for covariates, including sex and smoking status, these associations remained. There was no effect modification when considering IL6 genotype. CONCLUSION: This study presents evidence that IL6 methylation may be a marker of depression status in older individuals, however further work is now needed to replicate these findings and to assess the association with inflammatory status of individuals.
dc.languageEnglish
dc.publisherBMC
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleInvestigating the epigenetic profile of the inflammatory gene IL-6 in late-life depression
dc.typeJournal Article
dc.identifier.doi10.1186/s12888-017-1515-8
melbourne.affiliation.departmentPaediatrics (RCH)
melbourne.source.titleBMC Psychiatry
melbourne.source.volume17
melbourne.source.issue1
dc.rights.licenseCC BY
melbourne.elementsid1273124
melbourne.contributor.authorSaffery, Richard
melbourne.contributor.authorRyan, Joanne
dc.identifier.eissn1471-244X
melbourne.accessrightsOpen Access


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