Technology to prevent ageing has moved a step closer, with the identification of DNA bundles that play a vital role in the process.

While studying Werner syndrome, which results in premature ageing and death, scientists found that the bundles, known as heterochromatin, experience significant deterioration.

The scientists, from the Salk Institute and the Chinese Academy of Science, believe that their findings have has wider implications for ageing research and treatment.

“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,” explained Salk professor and study 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.”

This means that further research into heterochromatin could eventually result in treatments that either slow or reverse the ageing process.

“[The study] suggests that accumulated alterations in the structure of heterochromatin may be a major underlying cause of cellular aging,” said Izpisua Belmonte.

“This begs the question of whether we can reverse these alterations – like remodeling an old house or car – to prevent, or even reverse, age-related declines and diseases.”

The research, which was published today in the journal Science, used gene editing technology that has only been made possible very recently.

The scientists were able to create a stem cell model of Werner syndrome by deleting a gene known as WRN from human stem cells.

WRN, which is short for Werner syndrome RecQ helicase-like gene, is normally responsible for maintaining DNA’s structure, but in Wener sufferers is mutated, affecting the repair and replication of DNA.

By deleting the gene, the researchers were able to mimic the genetic process that occurs in Werner syndrome to zone in on the areas of DNA it affects.

They also performed follow-up research that confirmed WRN directly interacts with the structures responsible for stabilising heterochromatin, a finding that Salk describes as the “smoking gun”.

“Our study connects the dots between Werner syndrome and heterochromatin disorganization, outlining a molecular mechanism by which a genetic mutation leads to a general disruption of cellular processes by disrupting epigenetic regulation,” said Izpisua Belmonte.

The next research step will be to find out the full extent of the role heterochromatin plays in the ageing process.

This will include determining how the DNA bundles interact with other processes known to affect ageing, including telomeres, the ends of chromosomes, which have been found to shorten as we age.