According to the University of California, San Diego School of Medicine, a variety of human gene variants have specifically evolved to avoid neurodegenerative and cardiovascular disease, thus preserving their contributions to society.
Ajit Varki, MD, who is a Distinguished Professor of Medicine and Cellular and Molecular Medicine at the UC San Diego School of Medicine, and the lead author of the study says that 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.
According to the standard model of natural selection, if the age of reproduction is passed, individuals die. The reason behind this is that selection in early life prefers variants that favor reproductive success, even if there will be consequences later in life, which is one major reason why we age. This case can be seen in almost all vertebrates. On the other hand, humans (and some species of whale), are actually exceptions to this rule, and can live decades beyond the age for reproduction. The elder population is able to contribute to this fitness of the younger generation by caring for the grandchildren and also help by passing down important cultural knowledge. Human aging is accompanied by cognitive decline, and unfortunately, this interferes with the benefits previously mentioned, and makes the elderly population a burden instead, because the younger population has to care for them.
Memory Loss Genes
Varki and his team cooperated with Pascual Gagneux, PhD, who is an associate professor of pathology
and associate director of CARTA, and his team. They focused on the expression of the CD33 protein, which
is a receptor that is seen in the surface of immune cells. The function of this receptor is to maintain
immune reactions, prevent self-inflicting damage, and also prevented unwanted inflammation. Studies
previously conducted have shown that a certain type of CD33 prevents amyloid-beta accumulation in the
brain, which is associated with Alzheimer's disease.
The researchers compared levels of CD33 in the brain to our closest living relatives, the chimpanzees. They
discovered that the levels of CD33 are around four-times higher in humans than in the primates.
Apart from CD33, the researchers also found human-specific variations in genes that are also involved in
the inhibition of cognitive decline. One of the genes that they found is APOE, but the ancestral form of
the genes, APOE4, is actually a risk factor for Alzheimer's and cardiovascular disease. However, other
variants such as APOE2 and APOE3 have actually evolved in order to prevent dementia.
Our study does not directly prove that these factors (negative effects of cognitive decline in elderly) 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,