Ever heard of a drug which may slow aging? Well if this happens in the future, it will be a huge leap in technology for mankind.
The lifespan of a mice is somewhat increased by a fifth by scientists and they have apparently somehow managed to decrease the amount of age-related diseases the animals suffer. This is put forth by a study from the University College London that supposedly involved obstructing a vital molecular pathway. It apparently imitated the health gains of decreasing calorie intake and claims that drug treatments for aging and age-related diseases are apparently viable.
In the 1930’s, experts demonstrated that dropping the calorie intake of laboratory rats even as sustaining adequate amounts of vitamins, minerals and other vital nutrients could have health gains. So-called ‘calorie restriction’ seemed to augment the life-span of the animals, and a new study illustrated that this may be the case for primates. Evidence also proposes that calorie restriction may have health benefits for humans, too, though it is uncertain whether it could boost prolonged existence.
Scientists from the Institute of Healthy Ageing at University College London have found alterations in the ageing process in a strain of knockout mice, which were supposedly not able to generate a particular protein called S6 Kinase 1 (S6K1). This protein is apparently caught up in the body’s reaction to changes in levels of the food that we eat. Such nutrient sensing systems may be essential in facilitating the body to react suitably to altering food levels in terms of development and reproduction, and also, apparently, ageing.
Professor Dominic Withers and colleagues established that removing the S6K1 protein in mice supposedly has an extensive variety of health benefits which seems to impersonate the action of calorie constraint. Nevertheless, even as the outcome was drastic in female mice, their male counterparts exhibited slight disparity in lifespan but displayed few of the health benefits, although the causes for these differences between the two sexes is apparently vague.
Professor Withers explained, “Blocking the action of the S6K1 protein helps prevent a number of age-related conditions in female mice. The mice lived longer and were leaner, more active and generally healthier than the control group. We added ‘life to their years’ as well as ‘years to their lives’.”
The knockout mice were compared with the normal mice when they were 600 days old, which is apparently corresponding of middle age in humans. It was seen that the female knockout mice were leaner and apparently had stronger bones. They supposedly did not display the general age-related decline in insulin sensitivity and they were hence shielded from type 2 diabetes. They gave a better performance at motor tasks which is a measure of qualities like balance, strength and coordination. They appeared to be prying and investigative, signifying that their senses and cognition were enhanced. Even their T-cells, a significant part of the immune system, seemed more ‘youthful’, hinting slowing of the standard age decline in immunity.
The male knockout mice were also leaner, had less insulin and had healthier T-cells as compared to their normal counterparts.
On average, the female knockout mice apparently survived for about 950 days, over 160 days longer than the control group. Their lifespan supposedly increased by 20 percent.
The findings claim that calorie restriction may act using the S6K1 pathway. Additional studies showed that the useful effects of jamming S6K1 were mediated by increased activity of a second molecule, AMPK, which is apparently known as master ‘fuel gauge’ as it may adjust energy levels inside cells.
Drugs that trigger AMPK are by now used for human patients to treat type 2 diabetes. Metformin, an extensively used drug for the disease, is believed to function by activating AMPK.
Metformin is apparently not the only drug in use that may influence the ageing process. A new study in the journal ‘Nature’ exhibited that the drug rapamycin supposedly increased the lifespan of mice. Rapamycin is said to be used in humans as an immunosuppressant and so could not be administered as an anti-ageing drug in its present form. However, rapamycin obstructs the activity of S6K1 and thus it may increase lifespan through its effects on S6K1.
Together these studies supply proof that this may be a drug-sensitive pathway which apparently regulates mammalian ageing and propose new approaches for the treatment of age-related diseases.
The next step by the experts is to see that if the drugs like metformin could slow the ageing process in humans.
The findings of the study are published in the journal ‘Science’.