Study
NAD+ augmentation by nicotinamide riboside engages SLIT2/ROBO1 signaling to attenuate Th17 inflammation in psoriasis.
In psoriasis, 4 weeks of nicotinamide riboside altered Th17 signalling; the abstract gives no N or clinical outcome.
Summary Does nicotinamide riboside improve psoriasis by changing immune signals? Show / hide ↓
Researchers gave people with mild-to-moderate psoriasis either 500 milligrams of nicotinamide riboside twice daily or a placebo for four weeks. The abstract does not say how many people took part or report changes in psoriasis symptoms. Blood tests suggested that nicotinamide riboside reduced activity linked to Th17 cells, immune cells involved in inflammation. It also increased SLIT2, a protein involved in cell-to-cell communication, and affected its ROBO1 receptor. Additional tests in isolated human cells suggested these changes could reduce inflammatory activity, but they were not proof of better psoriasis.
What this means for you: This is early laboratory evidence, not evidence that nicotinamide riboside improves psoriasis or extends lifespan. You can ignore it when deciding whether to buy a supplement, especially because the participant number and clinical results are missing.
early evidenceThis placebo-controlled study examined nicotinamide riboside (NR) in people with mild-to-moderate psoriasis. Participants received oral NR 500 mg twice daily or matching placebo for four weeks, with blood collected before and after supplementation. The abstract does not report the participant number, allocation numbers, a clinical psoriasis score, or symptom results. Instead, its central outcome is immune target engagement. NR reduced Th17 immune responsiveness, and bulk CD4+ T-cell RNA sequencing identified induction of the SLIT-ROBO signalling pathway. Circulating SLIT2 increased after NR supplementation, and the abstract reports increased SLIT2 production in dermal fibroblasts. Pharmacological and genetic experiments in CD4+ T cells and fibroblasts implicated SLIT2 acting through ROBO1, with inhibition of Rho GTPase signalling, reduced canonical Th17 polarisation, and reduced inflammatory activation in fibroblasts. These findings are mechanistic and disease-specific. They do not establish an improvement in psoriasis symptoms, clinical outcomes, or ageing-related outcomes. The funding listed is the NHLBI Division of Intramural Research. A four-week immunology study cannot support broad claims about NAD augmentation for longevity.
NAD+ augmentation had anti-inflammatory effects in psoriasis through SLIT2-ROBO1-mediated crosstalk that suppressed Th17-driven inflammation.
The abstract does not state N and reports no clinical psoriasis endpoint. Follow-up was four weeks, and the main findings are mechanistic immune markers in a psoriasis population.
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