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 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.

The role of inflammation in suicidal behaviour.

OBJECTIVE: Over the past decade, clinical data have accumulated showing that inflammation might contribute to the pathophysiology of suicide. To evaluate the associations and to identify the support for pathways linking inflammatory processes with suicidal behaviour, a comprehensive review of the literature was undertaken. METHOD: The search terms 'cytokine', 'risk factors', 'kynurenine', 'asthma', 'allergy', 'autoimmunity', 'traumatic brain injury', 'infection' along with the terms 'inflammation' and 'suicide' were entered into PubMed, and a thorough analysis of the publications and their reference lists was performed. RESULTS: The effects of inflammation on mood and behaviour could partially be mediated by kynurenine pathway metabolites, modulating neuroinflammation and glutamate neurotransmission. At the same time, the triggers of the inflammatory changes documented in suicidal patients may be attributed to diverse mechanisms such as autoimmunity, neurotropic pathogens, stress or traumatic brain injury. CONCLUSION: Targeting the inflammatory system might provide novel therapeutic approaches as well as potential biomarkers to identify patients at increased risk. For the goal of improved detection and treatment of suicidal individuals to be achieved, we need to develop a detailed understanding of the origin, mechanisms and outcomes of inflammation in suicidal behaviour.