The acute‐phase mediator serum amyloid A is associated with symptoms of depression and fatigue
Objective Establish whether inflammatory biomarkers—serum amyloid A (SAA), C‐reactive protein (CRP), interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α)—are related to key symptoms of depression, including anxiety and fatigue, in a cross‐sectional, out‐patient setting to identify biomarkers th...
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Published in | Acta psychiatrica Scandinavica Vol. 135; no. 5; pp. 409 - 418 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Blackwell Publishing Ltd
01.05.2017
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Subjects | |
Online Access | Get full text |
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Summary: | Objective
Establish whether inflammatory biomarkers—serum amyloid A (SAA), C‐reactive protein (CRP), interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α)—are related to key symptoms of depression, including anxiety and fatigue, in a cross‐sectional, out‐patient setting to identify biomarkers that reflect psychiatric symptomatology in a naturalistic, real‐life population.
Methods
We measured SAA, CRP, IL‐6, and TNF‐α in plasma samples from 89 adult psychiatric out‐patients by multiplex, high‐sensitivity electrochemiluminescent assays. Psychiatric symptoms were evaluated using the Hamilton Depression Rating Scale (HAMD‐17), the Patient Health Questionnaire (PHQ‐9), and the Center for Epidemiological Studies Depression Scale (CES‐D).
Results
Plasma SAA was most robustly associated with depressive symptoms across diagnostic boundaries in this cohort of out‐patients. Elevated SAA was significantly associated with higher total scores on the HAMD‐17 scale and correlated with multiple scale items that rated symptoms of fatigue and depressed mood, but not with anxiety‐related items.
Conclusions
SAA might constitute a cross‐diagnostic marker indicative of depressed mood and fatigue in a naturalistic patient setting. Because SAA activates Toll‐like receptors 2 and 4, present on macrophages and glial cells, its association with depression severity could also implicate this inflammatory mediator in the pathogenesis of mood disorders. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0001-690X 1600-0447 |
DOI: | 10.1111/acps.12730 |