Research on a condition called Werner syndrome, which causes premature aging, has discovered what may be one of the major causes of cellular aging.

In a collaboration between the Salk Institute for Biological Studies in California and the Chinese Academy of Sciences in Beijing, scientists introduced mutations mimicking those that occur in Werner syndrome into a stem cell model. They found that this mutation caused disorganization in the replication and repair of DNA, leading to accelerated aging. Specifically, the study found that much of the cellular aging in Werner syndrome is due to the deterioration of bundles of cellular DNA known as heterochromatin.

Werner syndrome, also known as adult progeria, causes rapid aging and early onset of aging-related diseases, like osteoporosis, type 2 diabetes and hardening of the arteries. It affects about one in 20,000 people in the U.S., but researchers believe the results of this study could be used to find a way of reversing aging in people without the disease.

"Our findings show that the gene mutation that causes Werner syndrome results in the disorganization of heterochromatin, and that this disruption of normal DNA packaging is a key driver of aging," wrote senior author Juan Carlos Izpisua Belmonte. "This has implications beyond Werner syndrome, as it identifies a central mechanism of aging —heterochromatin disorganization — which has been shown to be reversible."

However, more research is still required to determine why exactly heterochromatin disorganization is associated with premature aging, and how it interacts with other aging processes in the body.

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