May 15 (UPI) — Researchers have found a genetic link between rheumatoid arthritis and Huntington’s disease, which shows promise of new therapeutic targets and drugs for both conditions.

Researchers at University of California San Diego School of Medicine and the Icahn School of Medicine at Mount Sinai were decoding the epigenetic landscape of RA when they found an overlap between its causes and Huntington’s disease, which is an inherited incurable genetic brain disease. Their findings were published Monday in the journal Nature Communications.

People with Huntington’s disease are born with a defective gene that causes it, but symptoms generally don’t appear until middle age. And while medications can offer some relief from symptoms, the drugs do not prevent the physical, mental and behavioral decline linked to the condition.

RA is an autoimmune disease that affects more than 1.3 Americans, causes pain and swelling in joints, and can affect other organs, including the heart and blood vessels. Between 10 percent and 20 percent of RA patients do not respond to any available medicines.

The researchers found a link in the epigenome, the proteins and molecules that decorate DNA and help turn genes on and off.

“We did not expect to find an overlap between rheumatoid arthritis and Huntington’s disease, but discovering the unexpected was the reason that we developed this technology,” Dr. Gary S. Firestein, dean and associate vice chancellor of translational medicine at UC San Diego School of Medicine, said in a press release. “Now that we have uncovered this connection, we hope that it opens a door for treatment options for people living with either disease.”

The research team developed an algorithm called EpiSig, which integrated and reduced the number of epigenetic combinations in the genes of patients with RA.

The researchers studied the epigenome in cells from the joints of patients with RA. In the control group were patients with osteoarthritis, which is a disease of cartilage degeneration.

“Comparing different types of epigenomic data is difficult because it involves a variety of different data subsets that cannot normally be analyzed together, including various methods in which DNA gets modified,” said Dr. Wei Wang, a professor of chemistry, biochemistry and cellular and molecular medicine at UC San Diego School of Medicine.

Frestein said the researchers have gained a better understanding of RA and people with other immune-mediated diseases may also benefit from the findings if the potential for new treatments is realized.

“As genes involved are discovered, researchers can potentially identify new treatment options and even repurpose existing drugs,” he said.

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