Also called hot piss or tickling, gonorrhea is a sexually transmitted infection that usually affects men under the age of thirty. It is caused by a bacteria, gonococcus, which is transmitted during unprotected sex. A priori, therefore, gonorrhea did not benefit the evolution of our species. And yet…
Grandma’s guess
While most animal species are able to reproduce throughout their lives, some species develop menopause. Humans are affected, as are orcas, pilot whales, narwhals and belugas. One of the evolutionary reasons cited to explain the development of this behavior is the grandmother effect, also called the grandmother hypothesis. In these species, including ours, researchers have noted that women or postmenopausal women play a very important role in the survival of grandchildren.
For us, however, it is still not clear where this ability comes from, genetically speaking. A study recently published in the journal Molecular Biology offers a puzzling and exciting hypothesis.
Researchers at the University of California School of Medicine have previously discovered several genetic mutations in humans that protect the elderly against cognitive decline and dementia. In this new study, they found that these helpful gene variants may have evolved in response to resistance to pathogens, including gonorrhea.
The CD33 gene
By comparing the human and chimpanzee genomes, the researchers found that humans have a unique version of the CD33 gene that codes for a receptor expressed by immune cells. In detail, a standard CD33 receptor binds to a type of sugar called sialic acid found in human cells. This process allows the immune system to recognize which cells are “safe”, thus protecting our body from attack. However, all this biological machinery is not perfect.
Because it helps protect human cells from self-attacks, the CD33 receptor on immune cells in the brain also prevents our defense system from cleaning up damaged cells and associated amyloid plaques. in Alzheimer’s disease.
In response, people have developed a CD33 gene variant with receptors that do not respond to sialic acids in damaged cells and plaques. So this variant gives us a specific resistance against Alzheimer’s disease by delaying the progression of the disease as much as possible.
But we know that Neisseria gonorrhoeae is a species of flowering plant (the bacteria responsible for gonorrhea) is the same packed with the same sugar where CD33 receptors bind. This is why the immune system does not detect them.
A happy accident?
What the researchers suggest here is that the mutated version of CD33 may have emerged as a human adaptation in response to gonorrhea. In other words, its ability to protect against dementia is actually a “happy accident” that allows us to live healthier lives as we age.
” It is possible that CD33 is one of many genes selected for their survival advantages against infectious pathogens early in life, but later second choice for their protective effects against dementia and other age-related diseases“, specified Pascal Gagneux, lead author of the study.
Looking at the genomes of Neanderthals or Denisovans, our closest evolutionary cousins, the team also pointed out that they lacked this badly mutated version of CD33. Thus we imagine that the protection against dementia enjoyed by Homo Sapiens would have provided a useful advantage over our extinct hominid relatives, allowing the young to enjoying the wisdom and care of healthy grandparents.