Inflammation in older subjects with early- and late-onset depression in the NESDO study: a cross-sectional and longitudinal case-only design

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Inflammation in older subjects with early- and late-onset depression in the NESDO study : a cross-sectional and longitudinal case-only design. / Rozing, M P; Veerhuis, R; Westendorp, R G J; Eikelenboom, P; Stek, M; Marijnissen, R M; Oude Voshaar, R C; Comijs, H C; van Exel, E.

In: Psychoneuroendocrinology, Vol. 99, 01.2019, p. 20-27.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Rozing, MP, Veerhuis, R, Westendorp, RGJ, Eikelenboom, P, Stek, M, Marijnissen, RM, Oude Voshaar, RC, Comijs, HC & van Exel, E 2019, 'Inflammation in older subjects with early- and late-onset depression in the NESDO study: a cross-sectional and longitudinal case-only design', Psychoneuroendocrinology, vol. 99, pp. 20-27. https://doi.org/10.1016/j.psyneuen.2018.08.029

APA

Rozing, M. P., Veerhuis, R., Westendorp, R. G. J., Eikelenboom, P., Stek, M., Marijnissen, R. M., ... van Exel, E. (2019). Inflammation in older subjects with early- and late-onset depression in the NESDO study: a cross-sectional and longitudinal case-only design. Psychoneuroendocrinology, 99, 20-27. https://doi.org/10.1016/j.psyneuen.2018.08.029

Vancouver

Rozing MP, Veerhuis R, Westendorp RGJ, Eikelenboom P, Stek M, Marijnissen RM et al. Inflammation in older subjects with early- and late-onset depression in the NESDO study: a cross-sectional and longitudinal case-only design. Psychoneuroendocrinology. 2019 Jan;99:20-27. https://doi.org/10.1016/j.psyneuen.2018.08.029

Author

Rozing, M P ; Veerhuis, R ; Westendorp, R G J ; Eikelenboom, P ; Stek, M ; Marijnissen, R M ; Oude Voshaar, R C ; Comijs, H C ; van Exel, E. / Inflammation in older subjects with early- and late-onset depression in the NESDO study : a cross-sectional and longitudinal case-only design. In: Psychoneuroendocrinology. 2019 ; Vol. 99. pp. 20-27.

Bibtex

@article{4b615251cd384b04b9d7e385e161d84e,
title = "Inflammation in older subjects with early- and late-onset depression in the NESDO study: a cross-sectional and longitudinal case-only design",
abstract = "OBJECTIVE: Different biological mechanisms may underlie depression beginning in early life (early-onset) and depression beginning later in life (late-onset). Although the relation between inflammation and depression has been studied extensively, the distinct role of inflammation in early and late-onset depression in older patients has not been addressed before. In the cross-sectional part of this study, we explored differences in levels of circulating inflammatory markers and cytokine levels in lipopolysaccharide (LPS) stimulated whole blood between older subjects with a late-life onset depression (≥60 years) and older subjects with an early-onset depression (<60 years). Secondly, in a 2-year follow-up study, we examined if circulating and stimulated inflammatory markers influenced the change in Inventory of Depressive Symptomatology (IDS) scores, and if this relation was different for early- and late-onset depression.METHODS: The study was part of the Netherlands Study of Depression in Older Persons (NESDO). We included 350 patients, all aged 60 and older, with a depressive episode in the previous 6 months: 119 with a late-onset depression and 231 with an early-onset depression. Blood samples were collected and CRP, IL-6, NGAL, GDF15, and, LPS plasma levels were determined and whole blood was LPS stimulated and cytokine levels IL-1β, IL-6, TNFα, IFNγ, IL-10, and IL-1 receptor antagonist (IL-1ra) were determined.RESULTS: After adjustment for demographics, health indicators, and medication use, increased plasma CRP levels were more strongly associated with late-onset depression than early-onset depression (OR [95{\%} CI]: 1.43 [1.05-1.94]). In the longitudinal analyses, higher circulating IL-6 levels were associated with a significantly slower decline in IDS scores in the crude and the adjusted models (p ≤ 0.027). This relation was not different between late- and early-onset depression. Other circulating and stimulated inflammatory markers were not associated with late- and/or early-onset depression.CONCLUSIONS: This study provides preliminary evidence that low-grade inflammation is more strongly associated with late-onset than early-onset depression in older adults, suggesting a distinct inflammatory etiology for late-onset depression. Cytokine production capacity did not distinguish between early- and late-onset depression.",
author = "Rozing, {M P} and R Veerhuis and Westendorp, {R G J} and P Eikelenboom and M Stek and Marijnissen, {R M} and {Oude Voshaar}, {R C} and Comijs, {H C} and {van Exel}, E",
note = "Copyright {\circledC} 2018. Published by Elsevier Ltd.",
year = "2019",
month = "1",
doi = "10.1016/j.psyneuen.2018.08.029",
language = "English",
volume = "99",
pages = "20--27",
journal = "Psychoneuroendocrinology",
issn = "0306-4530",
publisher = "Pergamon Press",

}

RIS

TY - JOUR

T1 - Inflammation in older subjects with early- and late-onset depression in the NESDO study

T2 - a cross-sectional and longitudinal case-only design

AU - Rozing, M P

AU - Veerhuis, R

AU - Westendorp, R G J

AU - Eikelenboom, P

AU - Stek, M

AU - Marijnissen, R M

AU - Oude Voshaar, R C

AU - Comijs, H C

AU - van Exel, E

N1 - Copyright © 2018. Published by Elsevier Ltd.

PY - 2019/1

Y1 - 2019/1

N2 - OBJECTIVE: Different biological mechanisms may underlie depression beginning in early life (early-onset) and depression beginning later in life (late-onset). Although the relation between inflammation and depression has been studied extensively, the distinct role of inflammation in early and late-onset depression in older patients has not been addressed before. In the cross-sectional part of this study, we explored differences in levels of circulating inflammatory markers and cytokine levels in lipopolysaccharide (LPS) stimulated whole blood between older subjects with a late-life onset depression (≥60 years) and older subjects with an early-onset depression (<60 years). Secondly, in a 2-year follow-up study, we examined if circulating and stimulated inflammatory markers influenced the change in Inventory of Depressive Symptomatology (IDS) scores, and if this relation was different for early- and late-onset depression.METHODS: The study was part of the Netherlands Study of Depression in Older Persons (NESDO). We included 350 patients, all aged 60 and older, with a depressive episode in the previous 6 months: 119 with a late-onset depression and 231 with an early-onset depression. Blood samples were collected and CRP, IL-6, NGAL, GDF15, and, LPS plasma levels were determined and whole blood was LPS stimulated and cytokine levels IL-1β, IL-6, TNFα, IFNγ, IL-10, and IL-1 receptor antagonist (IL-1ra) were determined.RESULTS: After adjustment for demographics, health indicators, and medication use, increased plasma CRP levels were more strongly associated with late-onset depression than early-onset depression (OR [95% CI]: 1.43 [1.05-1.94]). In the longitudinal analyses, higher circulating IL-6 levels were associated with a significantly slower decline in IDS scores in the crude and the adjusted models (p ≤ 0.027). This relation was not different between late- and early-onset depression. Other circulating and stimulated inflammatory markers were not associated with late- and/or early-onset depression.CONCLUSIONS: This study provides preliminary evidence that low-grade inflammation is more strongly associated with late-onset than early-onset depression in older adults, suggesting a distinct inflammatory etiology for late-onset depression. Cytokine production capacity did not distinguish between early- and late-onset depression.

AB - OBJECTIVE: Different biological mechanisms may underlie depression beginning in early life (early-onset) and depression beginning later in life (late-onset). Although the relation between inflammation and depression has been studied extensively, the distinct role of inflammation in early and late-onset depression in older patients has not been addressed before. In the cross-sectional part of this study, we explored differences in levels of circulating inflammatory markers and cytokine levels in lipopolysaccharide (LPS) stimulated whole blood between older subjects with a late-life onset depression (≥60 years) and older subjects with an early-onset depression (<60 years). Secondly, in a 2-year follow-up study, we examined if circulating and stimulated inflammatory markers influenced the change in Inventory of Depressive Symptomatology (IDS) scores, and if this relation was different for early- and late-onset depression.METHODS: The study was part of the Netherlands Study of Depression in Older Persons (NESDO). We included 350 patients, all aged 60 and older, with a depressive episode in the previous 6 months: 119 with a late-onset depression and 231 with an early-onset depression. Blood samples were collected and CRP, IL-6, NGAL, GDF15, and, LPS plasma levels were determined and whole blood was LPS stimulated and cytokine levels IL-1β, IL-6, TNFα, IFNγ, IL-10, and IL-1 receptor antagonist (IL-1ra) were determined.RESULTS: After adjustment for demographics, health indicators, and medication use, increased plasma CRP levels were more strongly associated with late-onset depression than early-onset depression (OR [95% CI]: 1.43 [1.05-1.94]). In the longitudinal analyses, higher circulating IL-6 levels were associated with a significantly slower decline in IDS scores in the crude and the adjusted models (p ≤ 0.027). This relation was not different between late- and early-onset depression. Other circulating and stimulated inflammatory markers were not associated with late- and/or early-onset depression.CONCLUSIONS: This study provides preliminary evidence that low-grade inflammation is more strongly associated with late-onset than early-onset depression in older adults, suggesting a distinct inflammatory etiology for late-onset depression. Cytokine production capacity did not distinguish between early- and late-onset depression.

U2 - 10.1016/j.psyneuen.2018.08.029

DO - 10.1016/j.psyneuen.2018.08.029

M3 - Journal article

VL - 99

SP - 20

EP - 27

JO - Psychoneuroendocrinology

JF - Psychoneuroendocrinology

SN - 0306-4530

ER -

ID: 203560252