The acute‐phase mediator serum amyloid A is associated with symptoms of depression and fatigue. (4th April 2017)

• Record Type: Journal Article
• Authors: Bryleva, E. Y.; Keaton, S. A.; Grit, J.; Madaj, Z.; Sauro‐Nagendra, A.; Smart, L.; Halstead, S.; Achtyes, E.; Brundin, L.
• Is Part Of: Acta psychiatrica Scandinavica. Volume 135:Number 5(2017:May)
• Page Start: 409
• Page End: 418
• Publication Date: 2017-04-04
• Subjects: inflammation -- C‐reactive protein -- interleukin‐6 -- biomarker -- mood disorders; Psychiatry -- Periodicals; 616.89
• DOI: 10.1111/acps.12730
• Languages: English
• ISSNs: 0001-690X

Abstract

Abstract : 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.