Could humans owe their relationships with grandparents to gonorrhea? Perhaps so, suggests a new study published in the journal Molecular Biology. Bear with us, the question is not as ridiculous as you might first think.
Humans (plus orcas and pilot whales) are unusual animals as they can live happy and healthy lives far beyond menopause, after their ability to reproduce fades. One of the suggested reasons for this is the so-called “grandmother hypothesis,” in which older females can help to raise infants, thereby ensuring the survival of their genes and providing stability to their community.
However, it was never clear where this handy ability of Homo Sapiens had emerged from, genetically speaking. Scientists at the University of California San Diego School of Medicine previously found a number of human gene mutations that protect older adults against cognitive decline and dementia.
In their latest study, they found that these useful gene variants perhaps evolved in response to dealing with pathogens, most notably gonorrhea.
When comparing human and chimp genomes, the team discovered that found that humans have a unique version of the CD33 gene that codes for a receptor expressed in immune cells.
The standard CD33 receptor binds to a type of sugar called sialic acid found on human cells. This allows the immune system to recognize which cells are “safe,” prompting the body not to attack itself.
It’s not a perfect system, however – because it helps to protect human cells from self-inflicted attack, the CD33 receptor in brain immune cells also prevents the immune system from cleaning up damaged brain cells and amyloid plaques associated with Alzheimer's disease.
Humans have overcome this problem through a variant of the CD33 gene that creates receptors that don’t react to sialic acids on damaged cells and plaques, thereby providing some resistance against late-onset Alzheimer's.
It’s also apparent that Neisseria gonorrhoeae (the bacteria that cause gonorrhea) are coated in the same sugars that CD33 receptors bind to, allowing them to evade detection from the immune system. The researchers suspect that the mutated version of CD33 may have emerged as a human adaptation in response to gonorrhea. Its ability to protect against dementia, they argue, was a happy accident that allowed people to live healthier lives as they entered old age.
"It is possible that CD33 is one of many genes selected for their survival advantages against infectious pathogens early in life, but that are then secondarily selected for their protective effects against dementia and other aging-related diseases," Pascal Gagneux, lead study author, and professor of pathology at UC San Diego School of Medicine and professor in the Department of Anthropology, said in a statement.
By examining genomes of Neanderthals or Denisovans, our closest evolutionary relatives, the team noticed they also lacked the mutated version of CD33. It’s not a massive leap to assume that the protection against dementia experienced by Homo Sapiens could have provided a useful advantage when competing against our extinct hominin relatives.
“For most genes that are different in humans and chimps, Neanderthals usually have the same version as the humans, so this was really surprising to us," explained co-senior author Ajit Varki, Distinguished Professor of Medicine and Cellular and Molecular Medicine at UC San Diego School of Medicine. "These findings suggest the wisdom and care of healthy grandparents may have been an important evolutionary advantage that we had over other ancient hominin species."