Tounoma

A sharp recovery prematurely aged mice suggests a potential therapy.

Premature aging can be reversed by reactivating an enzyme that protects the ends of chromosomes, suggests a new study with mice.

Mice engineered to lack an enzyme known as telomerase, premature aging. But back to health when he replaced the enzyme. The finding, published online today in Nature 1, suggests that some disorders characterized by premature aging could be treated by increasing the activity of telomerase.

It also offers the possibility of normal human aging slows reactivating the enzyme where has stopped working, says Ronald DePinho, cancer geneticist at the National Cancer Institute Dana-Farber and Harvard Medical School in Boston, Massachusetts, who led the study. “This has implications for thinking about telomerase as a serious anti-aging auditor.”

Other scientists, however, indicate that telomerase deficiency in mice is a poor substitute for the normal process of aging. In addition, increasing human telomerase might encourage potentially the growth of tumors.

Eternal Youth

After his discovery of the 1980′s, telomerase achieved a reputation as a fountain of youth. The ends of chromosomes are repetitive DNA, called telomeres. Every time a cell divides, the telomeres are shortened, leading eventually to stop dividing and die. Telomerase prevents the decline in some cell types, including stem cells, lengthening telomeres, and the hope was that by activating the enzyme could reduce cellular aging.

Two decades later, researchers are realizing that the role of GenF20 Plus in aging is much more nuanced than initially believed. Some studies have found an association between short telomeres and early death, while others have failed to support this link. People with rare diseases characterized by the shortening of telomeres and telomerase mutations appear to age prematurely, although some tissues are more affected than others.

When handling the mice completely lacking telomerase, their telomeres shorten progressively over several generations. These animals age much faster than normal mice – just are fertile and suffer from age-related diseases such as osteoporosis, diabetes and neurodegeneration. Also die young. “If you look at all these data together, you arrive at the idea that a loss of telomerase could be a major instigator of the aging process,” said DePinho.

To find out whether these dramatic effects are reversible, DePinho’s team manipulated mice with inactivated telomerase activating again, feeding the mice with a chemical compound known as 4-OHT. The researchers allowed the mice reached adulthood without the enzyme, and then reactivated for a month. Assessed the health of the mice a month later.

“What really caught us by surprise was the dramatic reversal of the effects we saw in these animals,” says DePinho. Describes the output as “almost an effect ‘Ponce de León’” – a reference to the Spanish explorer Juan Ponce de León, who was in search of the mythical Fountain of Youth. Wilted tests returned to normal, and the animals returned to be fertile. Other organs like the spleen, liver and intestines were recovered from his degenerate state.

The monthly pulse of telomerase also reversed the effects of aging on the brain. In mice was restored telomerase activity had significantly larger brains than animals that still lacked the enzyme, and neural progenitor cells, which produce new neurons and support to brain cells began to work again.

“This gives us a sense that there is a turning point for disorders associated with aging,” says DePinho. It is worthwhile to follow up on drugs that increase the activity of telomerase as potential treatments for rare disorders characterized by premature aging, he says, and perhaps even more common conditions associated with aging.