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Blocking This RNA Reverses Signs Of Aging, And Disease In Mice, Says New Study

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In addition to reversing signs of aging and extending the lifespan of mice, the newly found target also reverses disease.

Researchers from the King Abdullah University of Science and Technology (KAUST) in Saudi Arabia and the Salk Institute have found that a piece of DNA that hops across the human genome contributes to disorders of premature aging.

In those with progeria, or premature aging, RNA encoded by this mobile DNA accumulates inside cells. Furthermore, the researchers discovered that in mice, inhibiting this RNA restores the condition.

The research, published today in Science Translational Medicine, focuses on an RNA fragment called LINE-1.

LINE-1 RNA is important in normal aging, according to co-corresponding author Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and the head of the Altos Labs San Diego Institute of Science. “These findings provide new insight into progeroid syndromes and how to treat them,” he adds.

Werner syndrome and Hutchinson-Gilford progeria syndrome are two examples of progeroid diseases that accelerate aging in kids and teenagers. Along with stunning physical features, patients also develop illnesses and symptoms that are generally seen in older people, such as heart disease, cataracts, type 2 diabetes, osteoporosis, and cancer. Progeroid disorders are currently without viable treatments.

Izpisua Belmonte and his colleagues were aware that altered overall DNA organization is a molecular marker of both normal aging and progeroid disorders. When DNA is packed differently into the nucleus of cells, it alters which genes are accessible to the cell and, as a result, dramatically alters the behavior and function of the cell.

Additionally, researchers were aware that the human genomes include a large number of LINE-1 elements, which spread across the genome and encode LINE-1 RNA. These substances change and proliferate with age, as well as in disorders including cancer and cardiovascular disease, but their role is poorly known. Izpisua Belmonte’s team wondered if they changed in progeroid disorders as well.

The impacts of LINE-1 RNA that worsen with aging in the nuclei are often ignored, according to co-first author Pradeep Reddy, a former Salk staff member and current principal scientist at Altos Labs. “The repeat sequences like LINE-1 make up a large percentage of our genomes,” he says.

The researchers showed that progeroid syndrome patients’ cells had four to seven times more LINE-1 RNA than healthy persons’ cells. They also demonstrated that the key DNA structural modifications that were already linked to progeria began before the buildup of LINE-1 RNA.

The group then created compounds that could precisely bind to LINE-1 RNA, stopping the RNA from amassing and having an effect on the cells. This type of therapy increased the lifespan of mice with genetic abnormalities that generally cause early aging and cured the molecular symptoms of progeria in isolated cells. In all situations, therapy boosted the expression of genes linked to DNA structure and cell proliferation while decreasing the expression of genes linked to aging, inflammation, and DNA damage.

According to Izpisua Belmonte, holder of the Roger Guillemin Chair, “Targeting LINE-1 RNA may be an effective way to treat progeroid syndromes, as well as other age-related diseases that have been connected to LINE-1, including neuropsychiatric, eye, metabolic disorders and cancers. Eventually, we think that this approach may lead to treatments to help extend human health span.”

Future research is being planned to learn more about the factors that contribute to the buildup of LINE-1 RNA and how it can be treated medically in patients. A patent application has been filed for the current study targeting the LINE-1 RNA.

Image Credit: Getty

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