Mice that received a gene encoding a telomere-producing enzyme extended their lifespan by forty percent, compared to a control group. Treatment with another gene, one that codes for the follistatin protein, resulted in a thirty-six percent extension of their lifespan
[Translation by Dr. Moshe Nachmani]
Both types of treatments were able to increase glucose tolerance, improve physical performance and curb the decrease in body mass and fur loss. The extension of life expectancy came as a surprising result for the researchers. "We wanted to see what the results of gene therapy would be," said researcher Hua Zhu of Rutgers School of Medicine in New Jersey. "At this time we saw that all the control mice (24 in number) died, while all the experimental mice (36 in number) survived, a finding that clearly proves that there was a significant increase in the life expectancy of the mice."
telomeres (Wikipedia) They are old DNA sequences that repeat themselves and serve as a protective region on the chromosomes and which tend to shorten with age. Efforts to extend the lifespan and health of humans are a particularly active area of research, and they include a variety of methods, such as calorie restriction and the use of small molecules that adjust to age-related metabolic pathways. The researchers injected the mice with the gene for telomerase reverse transcriptase (the enzyme responsible for re-lengthening the telomere, which protects the cell's chromosomes and shortens them in place, with each cell division), an action that caused the activation and encouragement of telomere elongation, as well as polystatin, a protein which is secreted in the body and has an important role in muscle development and maintenance, all through the shingles virus (herpes) as a carrier.
The monthly treatment started in 18-month-old mice. After two months, the treated mice appeared stronger and had shinier, healthier fur than the control mice, which began to lose their fur and suffered from a decrease in body mass. The injections were repeated every month in order to maintain high concentrations of the protein. All the mice in the control group died within 29 months, while the mice in the experimental group died only after 38-42 months.
Liz Parrish, the chief executive of the biotech company "BioViva" which provided the funding for this research, comments that the next step will be to test the safety and effectiveness of the gene therapy in monkeys using more weakened strains of the rhesus virus. "Based on the research findings in monkeys, we will submit our report to the US Food and Drug Administration in order to allow us to begin clinical trials in humans," she explains.
There are serious hurdles for any researcher interested in treating aging with a gene therapy approach, says Ilaria Bellantuono, a professor of muscle aging at the University of Sheffield in the UK. "We found difficulties with the drug treatment approach, which is a much less expensive and dangerous approach, so it is likely that the gene therapy approach will encounter greater resistance." The researcher says that it is still difficult for any anti-aging treatment to compete with diet and exercise. Therefore, the researcher claims, the best approach would be to focus on conditions related to age and aging, such as loss of muscle mass or dementia. Such an approach would require a clinical trial to test whether the medical intervention prevents any of these conditions. "A preventive trial is a very complex matter - you have to give the treatment and then wait for the disease to appear," explains the researcher. It is necessary to use biological markers, which will be able to determine within three to six months if the intervention by the gene therapy or the drug has indeed been beneficial.
Molecular biologist Peter Lansdorp from the University of British Columbia in Canada points out that aging is a multi-causal phenomenon and it seems unlikely that a single protein would have such great consequences on life expectancy. He adds and also notes that negative side effects following repeated activation of the immune system by a viral carrier are a concern in humans, but not particularly in mice. "First, the effects of a modified gene on the negative activity of the virus must be examined. In the next step, it will be necessary to repeat the experiment in mice by other independent research groups."
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