Scientists have named the age after which the brain begins to age much faster
At a certain point, large-scale changes are initiated in the brain, with cells playing a key role that was not expected of them before.

For a long time, brain aging was imagined as a more or less gradual process: with age, its cells slowly change, and some functions begin to work worse. However, new research by American scientists casts doubt on such a simple picture. Neue Zürcher Zeitung provides details.
In one of the studies, American scientists, using modern biotechnology and artificial intelligence, analyzed traces of gene activity in tens of thousands of cells from donated human brains.
Donors were between 20 and 100 years old and had no neurological diseases before death. All studied cells came from the hippocampus — a brain region important for memory and particularly vulnerable to age-related changes.
The result surprised the researchers themselves. Around the age of 50, hundreds of genes suddenly switch on or off in various brain cells. Processes related to the immune system change particularly noticeably in this regard.
Cells begin to lack energy
Some of the notable changes occur in astrocytes. These are star-shaped cells that perform a number of supporting functions in the brain: they support neurons and participate in maintaining the blood-brain barrier.
With age, mitochondria in astrocytes, which provide cells with energy, begin to work less efficiently. As a result, astrocytes weaken and can no longer perform their functions as effectively.
The blood-brain barrier, which astrocytes help maintain, also suffers from this. It becomes more permeable, and immune cells from the blood gain the ability to enter the brain. With age, their numbers increase.
Normally, microglia cells perform immune function in brain tissues. Among other things, they get rid of cellular waste.
However, with age, the situation changes significantly. As another study by scientists from Stanford University showed, immune cells from the blood gradually fill not only the hippocampus but also other brain regions. By the age of 80, they almost completely displace microglia cells.
The problem is not just their presence. Cells that come from the blood take on the functions of microglia, but at the same time, they produce a large number of signaling molecules that support inflammation. As a result, numerous small foci of inflammation can arise around neurons. These can disrupt the function of nerve cells and even lead to their death.
What does dementia have to do with it?
Many researchers believe that chronic inflammation in the brain can contribute to the development of Alzheimer's disease, other forms of dementia, and Parkinson's disease. Some go even further and believe that small foci of inflammation may be the direct cause of these diseases.
According to this hypothesis, continuous exposure to inflammation-supporting substances can so severely disrupt the function of nerve cells that toxic protein clots, characteristic of Alzheimer's disease and other neurodegenerative diseases, begin to form in them. Eventually, the cells may die.
Normally, the immune system maintains a balance: some cells enhance the inflammatory response, while others suppress it. However, in the aging brain, this balance may be disrupted. One of the reasons could be changes in gene activity that begin around the age of 50.
At the same time, the brain also has a mechanism capable of suppressing excessive inflammation. A recent study by scientists from the Max Planck Institute for Biology of Ageing in Cologne showed that a separate group of microglia cells, upon detecting toxic protein clots, begins to suppress the inflammatory response and restrain other immune cells. Whether this ability of microglia is preserved with age is not yet known.
How they want to turn a problem into a treatment
Researchers see the ability of immune cells from the blood to penetrate the brain not only as a problem but also as an opportunity for future therapy.
The idea is to extract such immune cells from the blood and modify them in the laboratory. They could be altered to stop producing inflammation-supporting substances, begin to restrain the excessive activity of other immune cells, or neutralize existing substances that cause an inflammatory reaction.
After this, the modified cells could be returned to the body. Once they reach the brain via the bloodstream, they should weaken or even eliminate existing inflammation.
The main advantage of this approach is that blood cells are much easier to modify outside the body than to directly intervene in the brain's function.
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