What do a terminal brain disease and a painful autoimmune condition have in common?
More than we thought.
Scientists from the University of California San Diego (UCSD) School of Medicine and the Icahn School of Medicine at Mount Sinai in New York have discovered an apparent epigenetic overlap between the origins of Huntington’s disease and that of rheumatoid arthritis (RA).
The researchers shared their findings last month in the journal, Nature Communications.
Using cutting-edge analytical tools, the scientists analyzed the epigenomic landscape of RA and compared it to other conditions.
They discovered the overlap between the origins of Huntington’s and the origins of RA. They proclaimed it a potential common cause.
Or at least a partial commonality.
Huntington’s is a fatal and incurable brain disease with a wide and disabling array of neurological and functional implications and deficits.
Rheumatoid arthritis is a painful and chronic inflammatory autoimmune disease that primarily affects the joints as well as some organs.
Other than depression and muscle stiffness, there are virtually no known similarities between the diseases.
While the diseases themselves may not be similar — Huntington’s is far more disabling than RA — researchers say their origins are, in fact, epigenetically linked.
This may be where the common ground ends for these two illnesses, but it was noteworthy enough for researchers to address the overlap.
“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 Firestein, a senior study investigator and dean and associate vice chancellor of translational medicine at the UCSD School of Medicine, said in a statement. “Now that we have uncovered this connection, we hope that it opens a door for treatment options for people living with either disease.”
At least, that’s the hope.
This method of research and discovery could also yield other connections and thus, potential new targeted approaches in disease management.
“This methodology can also be used to find connections between other diseases, not just rheumatoid arthritis,” Firestein said. “As genes involved are discovered, researchers can potentially identify new treatment options and even repurpose existing drugs.”
But it isn’t always easy.
“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,” Wei Wang, PhD, a co-senior study investigator and professor of chemistry, biochemistry, and cellular and molecular medicine at UCSD School of Medicine, said in a statement.
The researchers are now thinking about the role that epigenetics may play in treating diseases such as RA and Huntington’s.
“By revealing the comprehensive epigenetics behind RA, we now have a better understanding of this disease. More importantly, our new approach could not only help patients with RA, but also people with other immune-mediated diseases,” Firestein said.
Huntington’s isn’t categorized as an immune disease, but rather, a neurodegenerative disorder.
Some scientists have proposed that it may actually be autoimmune in nature, but the jury is still out on that notion.
The recent connection between the epigenetic origins of RA and Huntington’s may shed more light on this area of research and disease treatment.
Discoveries like this may also yield more unexpected novel therapeutic drug targets for many diseases such as rheumatoid arthritis, which is sometimes treated by targeted therapies and precision medicine.