Young mice show signs of old age after receiving blood from an elder mouse
- Young mice were infused with blood from a much older mouse
- After a week, their physical endurance dropped, and fatigue increased
- Certain components in old blood could be making other cells feel 'older'
Researchers at the University of California, Berkley, have shown that young mice begin to display characteristics of older mice after just one blood transfusion from an old mouse, ScienceAlert reported.
Scientists worldwide are looking for solutions that may delay or even prevent aging. This work hasn't made major breakthrough so far, and one of the reasons for this might be how little we know about our age in the first place. Therefore, researchers also focus on determining what really makes us old in a bid to understand the processes that one day could be reversed or stopped to prevent aging.
Can young mice be made old?
In 2005, a team of researchers at the University of California created conjoined mice which had one old mouse and one young, where both shared the same organs and blood. During the experiment, older mice showed signs of reversal of their aging. In a recent experiment, researchers wanted to know if the reverse was true.
To test whether young mice could be turned older, the researchers infused them with blood from an old mouse. All mice who received blood were three months of age, while the old mouse was between 22-24 months of age. After seven days of the infusion, the mice were tested for their physical endurance on a treadmill.
To determine the impact of the infusion, a control group was used where the mice received blood from a younger mouse and compared their treadmill performances.
What did the researchers find?
The researchers found that mice that received old blood became fatigued faster and ran shorter distances on the treadmill. To probe into the causes of the decline in their physical endurance, the researchers tested the blood samples in the mice and found that mice who had received old blood also had markers for kidney damage and aging of the liver.
Conversely, when older mice were given younger blood, lipids and fibrosis declined, along with fatigue, while there was an increase in muscle endurance. Therefore, the researchers hypothesize that the cells from the older mice were releasing a 'senescence-associated secretory phenotype (SASP) that promoted muscle weakness, loss of endurance, and tissue damage, all signs of aging.
It is also likely that older cells in the blood, which have stopped reproducing but haven't been cleared from the body, could potentially be affecting cells in the younger individual and making them behave as though they are older, while they actually weren't.
To compare the result in human cells, the researchers placed human kidney cells in plasma taken from individuals who were between 60-70 years of age. Within six days of this placement, the researchers found multiple biomarkers of aging, which were found to be absent when the experiment was carried out with plasma taken from individuals aged between 20-30.
The researchers, therefore, concluded that adjusting factors such as SASP could be used as a therapeutic strategy when aiming for longevity.
The research was published in the journal Nature Metabolism.
Ageing is the largest risk factor for many chronic diseases. Studies of heterochronic parabiosis, substantiated by blood exchange and old plasma dilution, show that old-age-related factors are systemically propagated and have pro-geronic effects in young mice. However, the underlying mechanisms how bloodborne factors promote ageing remain largely unknown. Here, using heterochronic blood exchange in male mice, we show that aged mouse blood induces cell and tissue senescence in young animals after one single exchange. This induction of senescence is abrogated if old animals are treated with senolytic drugs before blood exchange, therefore attenuating the pro-geronic influence of old blood on young mice. Hence, cellular senescence is neither simply a response to stress and damage that increases with age, nor a chronological cell-intrinsic phenomenon. Instead, senescence quickly and robustly spreads to young mice from old blood. Clearing senescence cells that accumulate with age rejuvenates old circulating blood and improves the health of multiple tissues.
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