Year: 2025
Type: article
Abstract: DOI: https://doi.org/10.46296/gt.v8i16.0314 Abstract Major psychiatric disorders such as major depressive disorder (MDD), schizophrenia, and bipolar disorder have been linked to alterations in immune and inflammatory pathways. Numerous studies in the past decade show that psychiatric patients exhibit elevated levels of pro-inflammatory cytokines (e.g., interleukin-6, tumor necrosis factor-alpha) and markers of low-grade systemic inflammation, such as C-reactive protein, compared to healthy individuals (1–3). This critical literature review examines the relationship between peripheral cytokines, microglial activation in the central nervous system, the neuroimmune axis, and subclinical inflammation in psychiatric disorders. Key findings are discussed: the “neuroinflammation hypothesis” of depression, which postulates that overproduction of cytokines may contribute to depressive symptoms; the involvement of microglia (resident immune cells of the brain) in synaptic regulation and their aberrant activation in disorders like depression and bipolar disorder; the bidirectional communication between chronic stress (HPA axis) and immune response; and the presence of chronic subclinical inflammation associated with metabolic alterations in psychiatric patients. Finally, emerging therapeutic implications are addressed, including adjunctive anti-inflammatory treatments, and the need for future research is emphasized to clarify whether immuno-inflammatory alterations are a cause, consequence, or part of specific subtypes of psychiatric illness. Keywords: Neuroimmunology; Cytokines; Microglia; Subclinical inflammation; Psychiatric disorders; Neuroimmune axis.
Language: Spanish
Subfield: Biological Psychiatry
Field: Neuroscience
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W7217764330