To age and rejuvenate
Injection of old blood suppressed the mental abilities of mice
Polina Loseva, "The Attic"
Under its action, signs of inflammation appeared in the blood vessels of the brain, and the precursor cells of neurons stopped dividing.
It is known that blood from younger animals improves the health of older ones. The opposite is also true: "old" blood has a detrimental effect on a young body. However, the exact mechanisms of its action remain controversial. Scientists from Germany and the USA tracked changes in the brains of mice that received an infusion of "old" plasma. Their number of dividing cells decreased and their mental abilities deteriorated, but the immune cells of the brain were activated. However, scientists have also found a way to reverse these effects.
Scientists began to find out how blood of different ages affects the body of animals in the middle of the twentieth century. First, they stitched the blood vessels of different mice, creating a system of heterochronic parabiosis, then moved on to transfusion of blood and its individual components.
Since then, scientists have accumulated a lot of data on how the blood of a younger animal acts on the body of an older one, and vice versa. These effects are sometimes called "rejuvenation" and "aging", although there are few reasons to think so: transfusion of blood of another age acts only pointwise. In some mice, for example, young blood helped to improve the sense of smell, in others – to stop the loss of muscle mass. In the experiment most quoted now, which is often cited as an argument in favor of blood transfusion and between people, under the influence of young blood, memory improved in mice.
Anyway, it is not necessary to talk about a real "rejuvenation" yet. With "aging" the situation is a little easier: since it is not proposed to be used in humans, in order to conclude that it occurs, a small effect is enough – for example, a decrease in the rate of wound healing. However, the mechanisms of both effects are still unclear.
A team of researchers from the USA and Germany, led by the author of the same cited experiment, studied in detail how the plasma of old blood (which does not contain blood cells and clotting proteins) affects the young brain. The researchers suggested that the key role in their interaction may be played by the wall of the brain vessels, or rather, the endothelial cells lining the vessels from the inside.
They found that under the action of old blood, a protein molecule VCAM1 (vascular cell adhesion molecule 1) appears on the surface of endothelial cells. Normally, it participates in the migration of immune cells into the tissue: they float in the blood stream, cling to VCAM1, stop, attach to endothelial cells, and then crawl through the vessel wall to destroy the pathogen or cellular debris there.
However, in the brain of mice, immune cells do not migrate to the brain tissue, but remain "hanging" on the endothelium. There, they apparently secrete pro-inflammatory proteins, that is, they cause local inflammation. These proteins penetrate the vessel wall, activate the brain's own immune cells (microglia) and block the division of stem cells in the hippocampus. As a result, the mental abilities of mice decrease.
Mice are not alone in this, elderly people have a similar effect: the more VCAM1 on the cells, the worse the brain works. At the same time, if you introduce antibodies to mice that block VCAM1 and prevent immune cells from attaching to it, then the harmful effects of old blood are leveled.
The authors of the work do not point to a specific "criminal" – a molecule from old blood that causes endothelial cells to produce more VCAM1. But they believe that other pro-inflammatory proteins may be to blame, the amount of which in the blood increases with age. Thus, with blood, the old organism transmits its inflamed state to the young, and the walls of the vessels transmit this inflammation to the brain tissue.
Article by Yousef et al. Aged blood impairs hippocampal neural precursor activity and activates microglia via brain endothelial cell VCAM1 published in the journal Nature Medicine.
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