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A dermo-hypothalamic axis driven by TNF-α mediates sleep disturbances in psoriasis
Dandan Chen1,2, Ying Ma3, Jiliang Lu1
1Department of Dermatology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Communications Biology
|June 17, 2026
Summary
Psoriasis causes sleep disturbances through brain inflammation, not just itching. Targeting tumor necrosis factor-alpha in the brain may treat psoriasis-related insomnia.
Area of Science:
- Neuroscience
- Immunology
- Sleep Medicine
Background:
- Sleep disturbances are common in psoriasis patients.
- The cause of sleep disruption in psoriasis (itching vs. brain inflammation) is unclear.
Purpose of the Study:
- To investigate the direct link between skin inflammation and sleep disturbances in psoriasis.
- To identify the specific brain mechanisms and inflammatory mediators involved.
Main Methods:
- Utilized clinical data and a mouse model of psoriasis-like inflammation.
- Examined sleep patterns, neuronal activity in the anterior hypothalamic area, and local inflammatory markers.
- Administered a tumor necrosis factor-alpha inhibitor directly into the brain.
Main Results:
- Psoriatic mice showed increased wakefulness and fragmented sleep, independent of itching.
- Overactivity of wake-promoting neurons in the anterior hypothalamic area was observed.
- Evidence of local inflammation, including activated microglia and elevated tumor necrosis factor-alpha, was found in this brain region.
- Inhibiting tumor necrosis factor-alpha in the anterior hypothalamic area restored normal sleep patterns.
Conclusions:
- Skin inflammation directly impacts sleep-regulating brain circuits in psoriasis.
- Tumor necrosis factor-alpha plays a key role in mediating these sleep disturbances.
- Tumor necrosis factor-alpha is a potential therapeutic target for managing insomnia in psoriasis patients.
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