Dermatology researcher Nicole Ward earned her third National Institutes of Health grant in a year, including two that scored in the first percentile. With this most recent award, an R21 (exploratory/developmental research grant), she will investigate the role the nervous system plays in psoriasis—an inflammatory autoimmune disease characterized by raised areas of red, scaly, itchy and sometimes painful patches of skin.
“The National Institute of Arthritis and Musculoskeletal and Skin Diseases’ enthusiasm for, and commitment to, psoriasis research is very exciting, and I am thrilled to be one of their supported investigators,” Ward said. “Over the course of the next five years, we have the unique opportunity to identify new therapeutic avenues for treating the disease, moving the field forward and ultimately improving patient care.”
Ward, an associate professor of dermatology, plans to build upon her existing research by investigating the nervous system proteins that help sustain the skin disease. Anecdotal reports suggest that accidental injury to the skin resulting in damage or removal of its nerves—known as denervation—lead to improvement of the psoriasis. These reports indicate that the nervous system may play a significant role in maintaining and exacerbating the disease.
“For decades, dermatologists have observed the disappearance of psoriasis on a patient’s skin following knee replacement surgery or other injury that resulted in accidental or inadvertent denervation,” Ward said.
Ward and her team recently pinpointed the mechanisms underlying psoriasis remission after denervation and identified two nerve-derived peptides critical in sustaining the disease. The group published its findings in the Journal of Investigative Dermatology. The studies were conducted using an innovative psoriasis mouse model engineered in Ward’s lab. The mouse, coupled with Ward’s training in neuroscience, enabled this highly innovative experimental approach, which explained this previously inexplicable occurrence.
The new grant will allow Ward to investigate how nerves and their released proteins mediate psoriasis skin inflammation. Specifically, she and her team will examine how nerves contribute to psoriasis. They will investigate whether the immune cells or keratinocytes, or both, respond directly or indirectly to sensory nerve derived proteins—specifically calcitonin gene related peptide and Substance P, to elicit the chronic inflammation and cell proliferation that are characteristics of psoriasis. This may lead to the identification of new targets for drug development.
As the nation’s most prevalent autoimmune disease, psoriasis affects as many as 7.5 million Americans. It impacts quality of life, often causing significant physical pain and disability. Research has shown chronic inflammation—like that seen in psoriasis—puts individuals at risk for other co-morbidities, including cardiovascular disease, depression, obesity and diabetes. Even more troubling, psoriasis patients generally die seven to 10 years earlier than those without the disease.