We Are Meant to Live Long and Lucid Lives!
Humans (and certain whales) are unique among vertebrates in that we typically live long past our reproductive years, and most of us stay sharp well into old age. Now researchers at the University of California, San Diego have discovered the reason for this happy phenomenon. In a paper published November 30th 2015 in Proceedings of the National Academy of Sciences, the team reports that humans evolved unique gene variants that protect older adults from neurodegenerative disease, thus preserving their valuable contributions and delaying dependency. In other words, we stick around because we continue to have a lot to give to society in general and to our families in particular. What a welcome and upbeat take on aging that is as we head into the holiday season!
A release from the university quotes Ajit Varki, MD, Distinguished Professor of Medicine and Cellular and Molecular Medicine at UC San Diego School of Medicine, adjunct professor at the Salk Institute for Biological Studies and co-director of the UC San Diego/Salk Center for Academic Research and Training in Anthropogeny (CARTA), as saying, “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.” Varki led the study, along with Pascal Gagneux, PhD, associate professor of pathology and associate director of CARTA.
The release explains that the standard model of natural selection predicts that once the age of reproduction ends, individuals die. That’s because selection early in life strongly favors variants that benefit reproductive success, even at the cost of negative consequences late in life — one major reason we age. This is indeed the case in almost all vertebrates. Humans (and certain whales) are an exception to this rule, living decades beyond reproductive age. Such elders contribute to the fitness of younger individuals by caring for grandchildren and also by passing down important cultural knowledge. Age-related cognitive decline compromises these benefits, and eventually burdens the group with the need to care for dependent older members.
In this first-of-its kind discovery, Varki, Gagneux and their teams initially focused on the gene that encodes the CD33 protein. CD33 is a receptor that projects from the surface of immune cells, where it keeps immune reactions in check, preventing “self” attack and curtailing unwanted inflammation. Previous studies suggested that a certain form of CD33 suppresses amyloid beta peptide accumulation in the brain. Amyloid beta accumulation is thought to contribute to late-onset Alzheimer’s disease, a post-reproductive condition that uniquely affects humans and is aggravated by inflammation and cerebral vascular disease.