short story by F. Scott Fitzgerald, "The Curious Case of Benjamin Button," an old man becomes young with each passing day, a fantastic concept recently brought to life on film by Brad Pitt. In a laboratory in Boston, a research team used genetic engineering to accomplish something similar curious, transforming frail mouse in younger versions of themselves by stimulating the regeneration of certain tissues. The study helps explain why some organs and tissues break down with age, researchers say, provides hope that this deterioration related to age may one day be thwarted and even reversed.
As we age, many of our cells stop dividing. Our bodies are no longer able to regenerate, fail slowly. Scientists do not fully understand what triggers, but many researchers suspect the gradual shrinking of telomeres, the protective DNA caps on the ends of chromosomes. A bit of telomere is lost each time a cell divides, and telomerase, the enzyme that maintains caps, is generally not active in adult tissues. Another evidence. People with longer telomeres tend to live longer, healthier lives, while those with shorter telomeres suffer more diseases associated with age, such as diabetes, Alzheimer's and heart disease there
Several years Ronald DePinho, molecular biologist and director of the Belfer Institute Dana-Farber cancer Institute, and colleagues from Harvard Medical School in Boston mice genetically modified to miss working copy of the telomerase gene. The animals died at about 6 months to young mice, who usually live until they are about 3 years old and appeared to age prematurely. At an early age, liver and spleen faded, their brains have fallen, and they have become infertile. By adulthood, these mice exhibited a large number of diseases observed in 80 humans.
DePinho said he wondered what would happen to the aging process in these mice if they suddenly began again to telomerase. "Does [we] slow down, stabilize, or would we overthrow?" He and his colleagues genetically engineered a new batch of mice with the same disability, but this time they added a telomerase gene that became active when the mice were given a drug. The researchers kept off the gene during development and let these mice prematurely age, like previous had. But then to 6 months, the team placed on the telomerase gene.
The burst of telomerase production stimulated almost complete recovery. The rodents became fertile, their livers and spleens increased in size, and new neurons appeared in their brains, the researchers reported online yesterday in Nature .
The ability to reverse the deterioration of age in the mutant mice indicates that the cells that divide to replenish the tissues are not only not die when their telomere clock expires, said DePinho. They apparently persist in a dormant state from which they can be reactivated. "One could imagine applying this approach to man," he said, focusing therapy on specific types of tissues such as the liver, where telomerase appears to play an important role in regeneration after damage hepatitis, parasitic infection, and alcoholism.
K. Lenhard Rudolph, who studies stem cell aging at the University of Ulm in Germany, says the results are encouraging for people with diseases that cause accelerated aging, such as progeria, because the mice in this study were saved despite already suffering the effects of chronic disease. "It is a proof of principle that telomeres are at work here."
pharmaceutical companies and researchers are looking for ways to restore, protect or extend the telomeres of a person, but the jury is still out on whether such interventions can slow down the symptoms of aging, much less the reverse. Telomeres investigator Maria Blasco of the National Research Center on the Spanish cancer in Madrid warned that the experience of DePinho should not raise even just people's expectations of anti-aging therapies. "This study used genetically modified mice," she said. "It remains a very important issue in the area is that you can delay aging in a normal mouse?"
DePinho agrees with these concerns. It also warns that his approach has potential drawbacks, that increasing telomerase activity beyond its natural levels can cause cancer. However, this can not be an insurmountable problem if levels telomerase can be carefully monitored. DePinho noted that mice in the study, telomerase activity has returned to a natural level, do not develop tumors.
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