(ORDO NEWS) — American scientists have discovered a set of mutations in certain genes that protect older people from dementia and cognitive decline.
It turned out that the appearance of these genes in our ancestors is associated with pressure from infectious pathogens, such as gonococcus, which causes gonorrhea.
According to the researchers, such bacteria could have contributed to the fact that women began to live to menopause, while maintaining a sound mind. This literally helped our ancestors raise children.
The so-called grandmother hypothesis is held by many paleoanthropologists and other experts in human evolution. It is intended to explain the origin of menopause in women (in fact, Homo sapiens is one of the few species that survives to such a biological state).
If we take a wild society, it is easy to imagine that immediately after the death of a mother, for whatever reason, her young children are probably also doomed to death – from hunger, disease, attacks by predators or even relatives.
Therefore, the closer biological death is, from an evolutionary point of view, it is more profitable for female individuals to change their strategy – to stop the reproduction of their own offspring and invest in what they already have, that is, grandchildren. In this way, grandmothers help maintain their own genes in the population.
Scientists from the Universities of California and Princeton (USA) decided to find out what features of human biology make such long-term health of women possible. They presented their findings in the journal Molecular Biology and Evolution.
Previously, scientists have compared the human and chimpanzee genomes, finding that humans have a unique version of the CD33 gene, a receptor expressed in immune cells.
The standard CD33 receptor binds to the so-called sialic acid, which covers all human cells. And when an immune cell perceives this acid through the aforementioned receptor, it recognizes another cell as part of the body and does not attack it, preventing an autoimmune response.
The same receptor is expressed in the brain’s immune cells, microglia, where it helps control neuroinflammation.
These same microglia play an important role in the removal of damaged brain cells and amyloid plaques associated with Alzheimer’s disease.
By binding to sialic acid on these plaques, conventional CD33 receptors, in effect, suppress this important microglia function and increase the risk of developing dementia.
And here a new gene variant enters the biological arena – the CD33 mutation, which lacks a sialic acid binding site.
That is, the mutated receptor no longer reacts to this acid and allows microglia to destroy damaged brain cells and plaques. The higher the level of this gene, the better it protects against the onset of Alzheimer’s disease.
Scientists have found that neither Denisovans nor Neanderthals had this version of the gene. So the researchers speculated that such a mutation might actually help our ancestors better adapt to the survival of their offspring, such as having older women to help raise the children.
As the authors of the work believe, the change in the CD33 receptor is associated with pathogenic bacteria, for example, with the microorganism that causes gonorrhea.
The fact is that gonococci coat themselves with the same sialic acid that the CD33 gene binds to. And the bacteria are able to fool the human immune cells so as not to be destroyed.
According to scientists, the mutated version of CD33 arose as a human adaptation to molecular mimicry of the gonorrhea bacterium and other pathogens.
They confirmed that the mutation of the above gene is able to completely level the interaction between it and bacteria, and this allows immune cells to attack the latter again. Thus, having protected from gonorrhea, our ancestors received an additional “bonus” – a certain protection against senile dementia.
Contact us: [email protected]