Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2025 Aug 18:15:411-428.
doi: 10.2147/PTT.S535900. eCollection 2025.

The Skin-Brain Axis in Psoriasis and Depression: Roles of Inflammation, Hormones, Neuroendocrine Pathways, Neuropeptides, and the Microbiome

Affiliations
Review

The Skin-Brain Axis in Psoriasis and Depression: Roles of Inflammation, Hormones, Neuroendocrine Pathways, Neuropeptides, and the Microbiome

Lipeng Tang et al. Psoriasis (Auckl). .

Abstract

Psoriasis, a common chronic inflammatory skin disease affecting approximately 2-3% of the global population, frequently co-occurs with depression. This highly prevalent comorbidity significantly impairs patients' quality of life. Despite the substantial physical and mental health burden imposed by psoriatic depression, the underlying pathophysiological mechanisms connecting psoriasis and depression remain poorly understood. In this review, we explored several pathological processes that may contribute to psoriasis-associated depression, including immune cells dysregulations, hormones imbalances, hypothalamic-pituitary-adrenal (HPA) axis dysfunctions, neuropeptides expression abnormalities, and gut dysbiosis. The primary purpose of this review was to present a comprehensive overview of the pathogenic mechanisms linking psoriasis and depression. These insights may guide trans-disciplinary interventions aimed at both skin and mood symptoms.

Keywords: HPA axis; Th17 cell; depression; gut microbiota; neuropeptides; psoriasis.

PubMed Disclaimer

Conflict of interest statement

The authors have declared no conflicting interests in this work.

Figures

None
Graphical abstract
Figure 1
Figure 1
Th17 cells / γδ T cells and cytokines as a bridge among psoriasis and depression. By Figdraw.
Figure 2
Figure 2
Hormones imbalance in psoriasis and depression. By Figdraw. The dashed line represents the inability to exert the regulatory effect. The solid line represents the ability to play a moderating role. The red characters mean an increased expression of specific hormones. Additionally, the blue characters indicate a decreased expression of specific hormones.
Figure 3
Figure 3
The overactive HPA axis is a crucial link bridging psoriasis and depression. By Figdraw.
Figure 4
Figure 4
Neuropeptides and neurotransmitters play a vital role in the etiology of psoriasis and depression. By Figdraw. The red characters mean an increased expression of specific neuropeptides and neurotransmitters. Additionally, the blue characters indicate a decreased expression of specific neuropeptides and neurotransmitters.
Figure 5
Figure 5
The gut dysbiosis is a pivotal bridge linking psoriasis and depression. By Figdraw. The red characters mean an increased expression of specific gut microbiota and its metabolites. Additionally, the green characters indicate a decreased expression of specific gut microbiota and its metabolites. Gut microbiota is shown in italics.

Similar articles

References

    1. Armstrong AW, Blauvelt A, Callis Duffin K, et al. Psoriasis. Nat Rev Dis Prim. 2025;11(1). doi: 10.1038/s41572-025-00630-5 - DOI - PubMed
    1. Griffiths CEM, Armstrong AW, Gudjonsson JE, Barker JNWN. Psoriasis. Lancet. 2021;397(10281):1301–1315. doi: 10.1016/S0140-6736(20)32549-6 - DOI - PubMed
    1. Taliercio M, Lebwohl M. Psoriasis comorbidities and their treatment impact. Dermatol Clin. 2024;42(3):405–416. doi: 10.1016/j.det.2024.02.007 - DOI - PubMed
    1. Yamazaki F. Psoriasis: comorbidities. J Dermatol. 2021;48(6):732–740. doi: 10.1111/1346-8138.15840 - DOI - PMC - PubMed
    1. Mrowietz U, Sumbul M, Gerdes S. Depression, a major comorbidity of psoriatic disease, is caused by metabolic inflammation. J Eur Acad Dermatol Venereol. 2023;37(9):1731–1738. doi: 10.1111/jdv.19192 - DOI - PubMed

LinkOut - more resources