Inflammation in psychiatric disorders: what comes first?

Abstract

Neuropsychiatric disorders (i.e., mood disorders and schizophrenia) and inflammation are closely intertwined, and possibly powering each other in a bidirectional loop. Depression facilitates inflammatory reactions and inflammation promotes depression and other neuropsychiatric disorders. Patients with neuropsychiatric disorders exhibit all cardinal features of inflammation, including increased circulating levels of inflammatory inducers, activated sensors, and inflammatory mediators targeting all tissues. Inflammation may contribute to the pathophysiology and clinical progression of these disorders. Of note, proinflammatory cytokines modulate mood behavior and cognition by reducing brain monoamine levels, activating neuroendocrine responses, promoting excitotoxicity (increased glutamate levels), and impairing brain plasticity. What are the sources of this chronic inflammation? Increasing evidence indicates that changes in neuroendocrine regulation, metabolism, diet/microbiota, and negative health behaviors are important triggers of inflammation. Finally, recent data indicate that early-life stress is associated with overt inflammation prior to the development of neuropsychiatric disorders.

Profiling of the Peripheral Blood Mononuclear Cell Proteome in Schizophrenia and Mood Disorders for the Discovery of Discriminatory Biomarkers: A Proof-of-Concept Study

“…In parallel, a considerable number of diagnostic protein candidates are involved in immune process-es. While this is not unexpected, considering the immunomodulatory function of PBMC, it is in line with the recently reemerging hypothesis about the role increased inflammatory processes play in mediating psychiatric afflictions (review [31][32][33][34][35]). Some points must be considered when contemplating these data.…”

A Pro-Inflammatory Diet Is Associated With an Increased Odds of Depression Symptoms Among Iranian Female Adolescents: A Cross-Sectional Study

“…Several metabolic and inflammatory processes, such as reduced insulin sensitivity, elevations in plasma homocysteine levels and, perhaps more importantly, increased production of pro-inflammatory cytokines and endothelial dysfunction, seem to be the major factors responsible for the depression (3, 4). Proinflammatory cytokines like c-reactive protein and interleukin-6 act by reducing brain monoamine levels, activating neuroendocrine responses, promoting excitotoxicity (increased glutamate levels), and impairing brain plasticity modulate mood behavior which can result in depression (6). Various dietary components have different effects on inflammation (7–9).…”

Decoding the multimorbidities among psychiatric disorders and cognitive functioning

“…However, these phenotypes are associated with physiological changes at the level of the whole body, e.g. with impaired functioning of endocrine 27 , immune 28,29 and cardiometabolic 30 systems. Therefore, tissue-specific spatial regulatory interactions of eQTL SNPs with their target genes may be important in understanding the multimorbidities among psychiatric and cognitive phenotypes.…”