Experimental treatment developed by researchers at Harvard Medical School turned weak and feeble old mice into healthy animals by regenerating their aged bodies. The surprise recovery of animals has raised hopes among scientists that it may be possible to achieve a similar feat in humans — or at least to slow down the ageing process. An anti-ageing therapy could have a dramatic impact on public health by reducing burden of age-related health problems, such as dementia, stroke, heart disease, and prolonging quality of life for an increasingly aged population. “What we saw in these animals was not a slowing down or stabilization of ageing process. We saw a dramatic reversal — and that was unexpected,” said Ronald DePinho, who led the study, published in Nature journal. “This could lead to strategies that enhance regenerative potential of organs as individuals age and so increase their quality of life. Whether it serves to increase longevity is a question we are not yet in a position to answer.”
Ageing process is poorly understood, but scientists know it is caused by many factors. Highly reactive particles called free radicals are made naturally in body and cause damage to cells, while smoking, ultraviolet light, other environmental factors contribute to ageing. Harvard group focused on a process called telomere shortening. Most cells in body contain 23 pairs of chromosomes, which carry our DNA. At ends of each chromosome is a protective cap called a telomere. Each time a cell divides, telomeres are snipped shorter, until eventually they stop working and cell dies or goes into a suspended state called “senescence”. Process is behind much of wear and tear associated with ageing. At Harvard, they bred genetically manipulated mice that lacked an enzyme called telomerase that stops telomeres getting shorter. Without enzyme, mice aged prematurely and suffered ailments, including a poor sense of smell, smaller brain size, infertility and damaged intestines and spleens. But when DePinho gave mice injections to reactivate enzyme, it repaired damaged tissues and reversed signs of ageing.
“These were severely aged animals, but after a month of treatment they showed a substantial restoration, including growth of new neurons in their brains,” said DePinho. Repeating trick in humans will be more difficult. Mice make telomerase throughout their lives, but enzyme is switched off in adult humans, an evolutionary compromise that stops cells growing out of control and turning into cancer. Raising levels of telomerase in people might slow ageing process, but it makes risk of cancer soar. DePinho said treatment might be safe in humans if it were given periodically and only to younger people who do not have tiny clumps of cancer cells already living, unnoticed, in their bodies. He said none of Harvard’s mice developed cancer after treatment. Team is now investigating whether it extends lifespan of mice or enables them to live healthier lives into old age.
