ReviewFrontiers in psychiatry2026
Comorbid mechanisms of psoriasis and mental disorders: an analysis of inflammatory and psychosocial interactions.
Review in Frontiers in psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
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Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Psoriasis is a long-lasting, immune-related inflammatory skin disorder that has been increasingly recognized to be a systemic disorder with significant neuropsychiatric symptoms. Objective: To critically evaluate the emerging neuroimmune and immune systems that link psoriasis and psychiatric comorbidities, and to assess the implications for treatment. Methods: A comprehensive literature review was conducted to identify biological, neuroendocrine, and psychosocial pathways linking psoriasis to mental illness. We searched PubMed, Web of Science, and Scopus databases for articles published between January 2000 and December 2025 using keywords including "psoriasis", "depression", "anxiety", "neuroinflammation", "IL-23/Th17", and "psychosocial stress". Studies were included if they addressed human or relevant animal models of psoriasis with psychiatric outcomes, and excluded if they were case reports, editorials, or not published in English. References from retrieved articles were also screened to identify additional relevant studies. This approach ensures reproducibility and minimizes selection bias, consistent with narrative review standards. Results: The most recent research indicates that psoriasis-related psychological vulnerability is mediated primarily by IL-23/Th17-driven inflammation, dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, microglial activation, and neuroinflammation. These autoimmune conditions are linked by bidirectional skin-to-brain loops and central-peripheral immune crosstalk, which together lead to cytokine-mediated disruption of neurotransmission and maladaptive stress responses. In addition, stressors in psychosocial contexts and gut and brain interaction have been shown to further exacerbate chronic inflammation, emotional dysregulation, and psychological vulnerability. Immune-targeted biologics and structured psychotherapy may serve as complementary vehicles for the simultaneous treatment of skin inflammation and neurobehavioral outcomes. Conclusion: This synthesis of mechanisms suggests that neuroimmune circuitry may serve as a unifying construct for understanding psoriasis-related psychiatric illnesses and provides a framework for developing integrated dermatology-psychiatry treatment models. Future work should focus on biomarker-driven, interdisciplinary clinical trials to facilitate the development of tailored treatment approaches.
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