Aging is very much a human problem. Animals in the wild rarely live long enough to experience it. New research hints at genes that might be involved in protecting our aging brains.
In the vast majority of animals, once reproductive ability has passed, they are, evolutionarily speaking, void.
Creatures who can no longer pass on their genes are essentially pointless, as far as nature is concerned.
Genes that favor vigorous youths, reproductive fitness and survival to adulthood are passed on preferentially – even if they are detrimental to an animal as it ages.
Humans (and certain whales) are different from other species. Our reliance on accumulated knowledge makes an aging individual incredibly useful to the group.
New research published in Proceedings of the National Academy of Sciences may have found a genetic marker signposting our species’ ancient reliance on the wisdom of older members.
The current research, lead by Prof. Ajit Varki at the University of California-San Diego School of Medicine, found intriguing evidence of uniquely human gene variants.
These genes seem to be involved in staving off neurodegenerative disease in the elderly population to help ensure they are able to maintain their vital advisory role. They help prevent the aging individual from becoming a burden and, potentially, giving misinformation that could put the entire group in jeopardy.
Dr. Varki says:
“We unexpectedly discovered that humans have evolved gene variants that can help protect the elderly from dementia.
Such genes likely evolved to preserve valuable and wise grandmothers and other elders, as well as to delay or prevent the emergence of dependent individuals who could divert resources and effort away from the care of the young.”
The gene at the center of this study codes for a protein – CD33.
CD33 is is a sialic acid-binding immunoglobulin-like lectin (siglecs). It is a receptor that spans the membrane of immune cells and plays a part in preventing the body from generating unwanted immune reactions.
Siglecs mediate cell-cell interactions that inhibit or restrict immune responses. In other words, they protect the body from overreacting and damaging itself.
There are a number of CD33 variants, most of which have been shown to increase the risk of Alzheimer’s disease. One specific variant, however, has the opposite effect and appears to be protective.
Previous research discovered that this particularly positive variant of CD33 plays a role in preventing the build up of beta-amyloid peptide.
The accumulation of amyloid beta peptide plays a pivotal role in the etiology of late-onset Alzheimer’s.
Beta-amyloid normally aggregates to form soluble clumps. In Alzheimer’s, it is thought that these clumps are occasionally folded incorrectly. The badly packed molecules then act as a “seed,” encouraging other packages of protein to become similarly folded in a chain reaction.
The plaques that are formed by this cascade are toxic to nerve cells.
Researchers believe that, in Alzheimer’s patients, the mechanisms by which beta-amyloid peptide is normally removed are faulty in some way.
The research team compared levels of the protective CD33 variant in humans with our nearest relatives, chimpanzees. Humans were found to have four times the levels of the protective CD33 variant.
Levels of this variant were not the only human-specific differences of note. The team also found human-specific variants in APOE genes.
The presence of APOE4 is known to be a risk factor for cerebral vascular disease and Alzheimer’s. APOE2 and APOE3, however, appear to have evolved only in humans, to help stave off dementia.
Interestingly, all of the variants mentioned are found in Africa and, therefore, predate the birth of humanity.
“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,” says Pascal Gagneux, PhD, who ran the study alongside Dr. Varki.
It is not possible to conclude that these protective genes evolved as a method of staving off cognitive decline in the elderly. Much more research is needed before those types of conclusions can be drawn.
“Our study does not directly prove that these factors were involved in the selection of protective variants of CD33, APOE and other genes, but it is reasonable to speculate about the possibility.
After all, inter-generational care of the young and information transfer is an important factor for the survival of younger kin in the group and across wider social networks or tribes.”
The study gives a fascinating glimpse into one of the many factors that might have aided humanity’s bewildering ascent to culture, society and intelligence.
Medical News Today recently covered a study on a drug that reversed the effects of Alzheimer’s in rats.