Many of us treasure our grandparents, but it turns out they’re so precious that humans have evolved gene variants that help protect them against certain age-related diseases, like Alzheimer’s. By keeping the older generation healthier, it not only reduces their burden on others but also allows them to keep contributing to society.
“When elderly people succumb to dementia, the community not only loses important sources of wisdom, accumulated knowledge and culture, but elders with even mild cognitive decline who have influential positions can harm their social groups by making flawed decisions,” co-lead researcher Pascal Gagneux from the University of California, San Diego, explained in a statement.
Reproduction is the name of the game for life on Earth. For the vast majority of species, if your reproductive organs are knackered, there is no point in hanging around. Humans are an exception here: We can live for an extremely long time after we pass reproductive age. And that is a good thing for the species, as they can look after their kids and grandkids, help gather food, and bestow their valuable knowledge unto others.
Of course, this is all dependent on the elderly being physically and mentally capable of doing so. Age-associated conditions like dementia and heart disease threaten these contributions to families and are costly. So is there a genetic mechanism that helps keep the brain and body healthy enough so that they can confer these benefits to groups? That indeed seems to be the case, according to this latest study.
As described in the Proceedings of the National Academy of Sciences, the team was initially interested in the contribution of a gene called CD33 to Alzheimer’s disease, which only occurs post reproductive age. The receptor produced by this gene helps regulate the immune system, preventing potentially harmful responses after infection or injury. Interestingly, earlier work has suggested that a particular variant of CD33 might help protect against Alzheimer’s by preventing the build-up of toxic protein bundles in the brain, which are associated with disease progression.
Looking into the origins of this particular variant, the researchers examined CD33 in our closest relatives – chimpanzees. While both species had similar levels of “normal” CD33, levels of the protective variant were four times higher in humans than chimps. That’s surprising, because you wouldn’t expect strong selection pressure for something that benefits those in old age, since elderly females are no longer able to reproduce.
Interestingly, their findings didn’t end with CD33. They also found human-specific variants of numerous other genes that have been implicated in age-related cognitive deterioration. For example, genes that have been linked with neurodegenerative diseases like dementia or impaired blood flow to the brain were found to have protective variants in humans of different ethnicities, but not our closest evolutionary relatives. This means these variants must be older than the ancestral genes, and their widespread presence across ethnicities indicates they probably arose before Homo sapiens appeared.
For these genes to have been strongly selected in post-reproductive individuals, they must have played an important role in our evolution. This role, the researchers suggest, is to protect against age-associated diseases that could impede the ability of older individuals to look after younger kin. Perhaps in the future, scientists can use this new information to help develop treatments for the diseases that burden the elderly.
