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Title
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Inflammatory markers and cortisol parameters across depressive subtypes in an older cohort
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Author
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Abstract
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| Background: There is growing evidence that inflammatory and cortisol dysregulation are underlying pathophysiological mechanisms in the aetiology of major depressive disorder, particularly in younger adults. However, findings of biological disturbances in late-life depression have been divergent, probably due to the even greater heterogeneity of depression in older adults with aging processes influencing biological factors. Using empirically derived subtypes may enable the identification of biological disturbances underlying depression in older adults. Methods: Data were used from the Netherlands Study of Depression in Older Persons (NESDO) of 359 persons aged 60 years or older, with a current diagnosis of major depressive disorder (MDD). Depressive subtypes (severe atypical, severe melancholic, and moderate severe subtype) that were previously identified through latent class analysis (LCA), were examined on differences in inflammatory markers including C-reactive protein (CRP), in-terleukin-6 (IL-6), and neutrophil gelatinase-associated lipocalin (NGAL), as well as cortisol parameters. Results: No differences in measures for inflammation and cortisol across subtypes were observed in uncorrected or for putative confounders corrected models. Limitations: Several subjects had missing cortisol and inflammatory data, decreasing the power. However, results did not change after imputation analysis. Discussion: In this cohort of depressed older adults, no differences in inflammation and cortisol measures between depression subtypes were observed. This is probably due to the many (patho) physiological processes that are involved in aging, thereby clouding the results. |
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Language
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English
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Source (journal)
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Journal of affective disorders. - Amsterdam
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Publication
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Amsterdam
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Elsevier science bv
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2018
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ISSN
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0165-0327
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DOI
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10.1016/J.JAD.2018.02.080
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Volume/pages
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234
(2018)
, p. 54-58
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ISI
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000429308000009
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Pubmed ID
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29522944
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Full text (Publisher's DOI)
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Full text (open access)
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Full text (publisher's version - intranet only)
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