ScienceDaily (May 14, 2012) A new study consisting of inducing cells to express telomerase, the enzyme which -- metaphorically -- slows down the biological clock -- was successful. The research provides a \"proof-of-principle\" that this \"feasible and safe\" approach can effectively \"improve health span.\" <\/p>\n
A number of studies have shown that it is possible to lengthen the average life of individuals of many species, including mammals, by acting on specific genes. To date, however, this has meant altering the animals' genes permanently from the embryonic stage -- an approach impracticable in humans. Researchers at the Spanish National Cancer Research Centre (CNIO), led by its director Maria Blasco, have demonstrated that the mouse lifespan can be extended by the application in adult life of a single treatment acting directly on the animal's genes. And they have done so using gene therapy, a strategy never before employed to combat aging. The therapy has been found to be safe and effective in mice. <\/p>\n
The results were recently published in the journal EMBO Molecular Medicine. The CNIO team, in collaboration with Eduard Ayuso and Fatima Bosch of the Centre of Animal Biotechnology and Gene Therapy at the Universitat Autonoma de Barcelona (UAB), treated adult (one-year-old) and aged (two-year-old) mice, with the gene therapy delivering a \"rejuvenating\" effect in both cases, according to the authors. <\/p>\n
Mice treated at the age of one lived longer by 24% on average, and those treated at the age of two, by 13%. The therapy, furthermore, produced an appreciable improvement in the animals' health, delaying the onset of age-related diseases -- like osteoporosis and insulin resistance -- and achieving improved readings on aging indicators like neuromuscular coordination. <\/p>\n
The gene therapy consisted of treating the animals with a DNA-modified virus, the viral genes having been replaced by those of the telomerase enzyme, with a key role in aging. Telomerase repairs the extreme ends or tips of chromosomes, known as telomeres, and in doing so slows the cell's and therefore the body's biological clock. When the animal is infected, the virus acts as a vehicle depositing the telomerase gene in the cells. <\/p>\n
This study \"shows that it is possible to develop a telomerase-based anti-aging gene therapy without increasing the incidence of cancer,\" the authors affirm. \"Aged organisms accumulate damage in their DNA due to telomere shortening, [this study] finds that a gene therapy based on telomerase production can repair or delay this kind of damage,\" they add. <\/p>\n
'Resetting' the biological clock <\/p>\n
Telomeres are the caps that protect the end of chromosomes, but they cannot do so indefinitely: each time the cell divides the telomeres get shorter, until they are so short that they lose all functionality. The cell, as a result, stops dividing and ages or dies. Telomerase gets around this by preventing telomeres from shortening or even rebuilding them. What it does, in essence, is stop or reset the cell's biological clock. <\/p>\n
But in most cells the telomerase gene is only active before birth; the cells of an adult organism, with few exceptions, have no telomerase. The exceptions in question are adult stem cells and cancer cells, which divide limitlessly and are therefore immortal -- in fact several studies have shown that telomerase expression is the key to the immortality of tumour cells. <\/p>\n
It is precisely this risk of promoting tumour development that has set back the investigation of telomerase-based anti-aging therapies. <\/p>\n<\/p>\n
Visit link: ScienceDaily (May 14, 2012) A new study consisting of inducing cells to express telomerase, the enzyme which -- metaphorically -- slows down the biological clock -- was successful. The research provides a \"proof-of-principle\" that this \"feasible and safe\" approach can effectively \"improve health span.\" A number of studies have shown that it is possible to lengthen the average life of individuals of many species, including mammals, by acting on specific genes. To date, however, this has meant altering the animals' genes permanently from the embryonic stage -- an approach impracticable in humans. Continue reading
\nFirst gene therapy successful against aging-associated decline: Mouse lifespan extended up to 24% with a single ...<\/a><\/p>\n","protected":false},"excerpt":{"rendered":"