Nobody likes the idea of aging. But the alternative — which is to die young — doesn’t have too many fans either.

That’s why a study that offers possible new ways to prevent and treat age-related diseases such as cancer, diabetes and Alzheimer's disease has attracted attention.

The study was published today in the journal Science.

But don’t throw out that bottle of Gray Be Gone just yet. The scientists at the Salk Institute for Biological Studies in La Jolla, California, and the Chinese Academy of Sciences, Beijing, have some new clues, not a magic bullet.


“Aging is complex,” according to Alejandro Ocampo, Ph.D., a member of the institute’s Gene Expression Laboratory. “What scientists do is study premature aging syndromes.”

In this case, they focused on Werner syndrome, a rare genetic disorder that causes rapid aging. It affects about one in every 20,000 people in the United States. Its victims experience age-related diseases early in life, including cataracts, type 2 diabetes, hardening of the arteries, osteoporosis, and cancer. Most die in their late 40s or early 50s.

The disease is caused by a mutation to the Werner syndrome RecQ helicase-like gene (known as the WRN gene), which generates the WRN protein. The mutated protein in Werner syndrome disrupts the replication and repair of DNA and the expression of genes, which was thought to cause premature aging. However, it was unclear exactly how the mutated WRN protein disrupted these critical cellular processes.

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Study Focuses on DNA Bundles

The new study honed in on the deterioration of tightly packaged bundles of cellular DNA.

“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,” said Juan Carlos Izpisua Belmonte, a senior author on the paper. “This has implications beyond Werner syndrome, as it identifies a central mechanism of aging —heterochromatin disorganization — which has been shown to be reversible.”

The team created a stem cell model into which they could introduce mutations. Since stem cells can convert into different cell types, the researchers could examine its progress in fat, cartilage, or bones, said Ocampo.

They created a cellular model of Werner syndrome by using a cutting-edge gene-editing technology to delete WRN genes in human stem cells. Werner cells have markers for premature aging, and the Werner protein has been identified.

“How is the marking important?” Ocampo asked. “Is it a cause or a result of the aging process?”

“We can use a model to collect stem cells and analyze those marks,” added Pradeep Reddy, Ph.D., another member of the investigative team.

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Can We Prevent Aging?

Izpisua Belmonte says more extensive studies will be needed to fully understand the role of heterochromatin disorganization in aging. That includes how it interacts with other cellular processes implicated in aging, such as the shortening of the end of chromosomes known as telomeres.

“[The] 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.”

“It’s all very complex,” Ocampo added, stressing that they are a long way from human solutions. “We know some of the drivers of aging. We are learning about drivers to develop ways to prevent changes, to slow down aging process, or reverse those changes. You must always remember that we are studying in vitro.”

That means moving on to tests in mice or, eventually, in people.

“In a dish you don’t have a whole complex body,” Ocampo says.

Eventually the researchers hope to figure out how to reprogram somebody to a younger state. Then, you can toss the bottle of Gray Be Gone.

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