BG09 The skin–brain axis: exploring the role of neuroinflammation in dermatological and neurological disorders

Abstract

The skin–brain axis describes bidirectional neuroimmune communication in which psychological stress alters skin inflammation and, conversely, chronic cutaneous inflammation can influence central nervous system (CNS) function. Psoriasis is increasingly linked to neurodegenerative disease risk, including Alzheimer disease, through shared inflammatory pathways. We review mechanistic links between psoriasis and Alzheimer disease across the skin–brain axis, and summarize emerging diagnostic and therapeutic implications for dermatology. A comprehensive literature search was conducted using PubMed, Google Scholar, ScienceDirect, Scopus and Web of Science to identify peer-reviewed English-language articles relevant to neuroimmune interactions, psoriasis, Alzheimer disease, neuroinflammation, immune signalling, biomarkers and treatment within the skin–brain axis context. Stress-mediated activation of the hypothalamic–pituitary–adrenal axis and neuropeptides (corticotropin-releasing hormone, cortisol and substance P) modulate keratinocyte, mast-cell and T-cell activity, amplifying cutaneous inflammation. Circulating cytokines central to psoriasis – interleukin (IL)-17, IL-23, tumour necrosis factor (TNF)-α and IL-6 – are also implicated in Alzheimer disease-associated neuroinflammation and may contribute to blood–brain barrier dysfunction and downstream microglial and astrocyte activation. Systemic inflammatory burden is further shaped by common comorbidities (obesity, type 2 diabetes, hypertension and dyslipidaemia), which may accelerate later-life cognitive decline. Therapeutic overlap is emerging: biologics targeting TNF-α or IL-17 and agents modulating Janus kinase–signal transducer and activator of transcription signalling may plausibly attenuate inflammatory crosstalk across skin and CNS compartments. Diagnostic innovation includes skin-based detection of pathological tau/amyloid signatures and artificial intelligence-assisted phenotyping to refine classification and support personalized risk stratification. Shared neuroendocrine and cytokine-driven mechanisms support a biologically plausible link between psoriasis and AD. Prospective longitudinal studies are needed to clarify causality, validate clinically actionable skin biomarkers and determine whether systemic anti-inflammatory treatment modifies long-term cognitive outcomes. Dermatology-led screening for neuropsychiatric symptoms and collaborative care pathways may improve holistic patient management.