A new, genetic-level discovery at Brigham and Women’s Hospital offers a potential pathway toward better treatments for psoriasis, an often-debilitating condition impacting at least 100 million individuals worldwide.

A Brigham research team initially found that the trademark skin thickening that occurs in psoriasis is elicited through a build-up of dysregulated stem cells. With that in mind, the team sought to better understand the dysregulation through further research focused on the epigenome, the methylated wrapping covering each DNA strand that directs individual gene behavior. The investigators found a defect in that covering that resulted in loss of 5-hmC, a DNA methylation hydroxymethylation mark, only in psoriasis patients. Previous findings suggest that this 5-hmC loss in the skin epigenome can be reprogrammed using such agents as ascorbic acid, commonly known as vitamin C—offering a potential therapeutic pathway targeting a root cause behind psoriasis.

“Psoriasis places social and psychological stress on patients and is associated with risk of diabetes, cardiovascular disease, and more,” says study co-senior author George Murphy, MD, director of the Program in Dermatopathology, Department of Pathology, the Brigham. “If successful, our epigenetic stem cell explanation for psoriasis hopefully could transform therapy, allowing for more personalized, targeted approaches directed at the very cells that accumulate to form the heartbreak of this devastating skin condition.”

Read more about the research, published in the Journal of Investigative Dermatology, here.

Topics: Clinical Trials

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