A genetic breakthrough into the underlying causes of arthritis could mean a simple blood test could predict whose wellbeing is at risk of the crippling disease. This is according to US and Swedish researchers, who have found that certain genes and the “tags” that regulate them conspire together to promote the development of arthritis.
The disease is both caused by, and causes, these tags, and so wellness experts at the Karolinska Institute in Sweden and Johns Hopkins University School of Medicine in the United States separated the two groups of tags, which helped them to identify the specific DNA sequences which are vital for arthritis to progress. The hope is that now, armed with this insight, they might be able to spot people who go on to suffer from arthritis, as well as other non-infectious conditions such as type 2 diabetes and heart disease.
Dr Andrew Feinberg, professor of molecular medicine at Johns Hopkins` Institute for Basic Biomedical Sciences, explained, ‘Since rheumatoid arthritis is a disease in which the body’s immune system turns on itself, current treatments often involve suppressing the entire immune system, which can have serious side effects. The results of this study may allow clinicians to directly target the culpable genes and/or their tags.’
Of the 10 DNA sites that were tagged differently in arthritis patients, and affected risk for developing the disease, nine were in a region known to play an important role in autoimmune diseases. However, site number 10 was on a gene that has never before been associated with the disease. Lead researcher, Dr Yun Liu, said, ‘Our method allows us to predict which tagging sites are most important in the development of a disease.’
There are several known DNA mutations that increase your risk for rheumatoid arthritis, but the researchers found that additional factors appear to suppress or enhance that risk. The chemical tags that attach to DNA sequences are one of these factors. They work as part of an epigenetic system that helps regulate when and how DNA sequences are “read”, how they are used to create proteins and how they affect the onset or progress of disease.
In more than 300 people with and without arthritis, the researchers managed to catalogue DNA sequences and their tagging patterns in the white blood cells. This enabled them to identify DNA sequences that were more prevalent in patients with the disease, which could shed further light on how it operates. Tomas Ekstrom, professor of molecular cell biology at Karolinska Institute’s Department of Clinical Neuroscience, commented, ‘This could explain why risk genes assert themselves and cause disease and why some people are affected more easily than others.’
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