Thursday, 3 December 2015

How Evolution Gave Us Grannies

Human-specific derived alleles of CD33 and other genes protect against postreproductive cognitive decline

There's something special about a granny. Granddads are special too of course, but not quite like a granny. Ask my grandchildren.

Grandparents are biologically, on the face of it, a little bit of a mystery especially in a social species and especially in one like humans where for most people for most of the time until the discovery of agriculture, life consisted mostly of hunting and gathering food. Anyone not capable of joining in would have been a drain on the resources of those who could so it seems logical to suppose that any process which removed surplus people from the group after their fertile and productive years were over would be advantageous to the group and so would be expected to evolve. In fact, when you look at our closest relatives, chimpanzees, you find that the females tend to die soon after their fertility ceases.

And yet human females live for perhaps another 30 to 40 or more years after the menopause. Their post-fertile years may even be longer than their fertile years.

Of course, many people remain fit and active and able to be productive and would probably have been able to hunt and gather along with the younger people for some considerable time, even producing a surplus that could be shared with children and nursing mothers, but there comes a time when physical fitness deteriorates and productivity falls and at that point they would have become a burden on the rest of the group.

The reason humans don't die off naturally in 'middle age' may well be a result of humans evolving a larger brain and particularly the means to communicate stored information to others. Before written communication, the old people in the group would have been the repository of group wisdom. They would be where the sum total of accumulated human knowledge resided. They would also have the experience and time, especially the grannies, to help look after the children and to take over care of weaned children so freeing up the mother to have more babies. Because there were grannies (and granddads) the group as a whole, together with the genes which enabled it, would have been more successful than one in which 'surplus' adults died soon after they ceased breeding.

But what this all depended on was a brain which continued to function and remain alert and communicative, but, as the human brain ages so it tends to deteriorate especially with degenerative conditions such as Alzheimer's, which is where this latest piece of research comes in.

Ajit Varki a physician-scientist and Pascal Gagneux, an evolutionary biologist, of the University of California, San Diego, USA have accidentally discovered that there is a protective form of the CD33 gene which prevents Alzheimer's. The 'normal' form is thought to predispose to it. The team were studying genes which control the body's responses to inflammatory conditions when they came across this protective variant.

So to understand how this may have arisen the team searched the 1000 Genomes Project to discover its occurrence in chimpanzees as well as in diverse human ethnic groups. They found it to be absent in chimpanzees but present in a diverse range of human ethnic groups. This suggests that it evolved after the human branch diverged from the chimpanzees.

Significance
Most vertebrates die soon after they stop reproducing, but humans are an exception. Postreproductive humans care for offspring, assist in foraging, and communicate ecological and cultural knowledge, increasing the survival of younger individuals. Loss of cognitive capacity disrupts these benefits and burdens the group with the care of older members. We studied how the immunoregulatory receptor CD33 contributes to Alzheimer’s disease, a human-specific postreproductive condition. Surprisingly, a protective CD33 allele is derived and unique to humans, despite weak direct selection on older individuals. We identified several genes with derived alleles that protect against neurodegenerative disease and cerebrovascular insufficiency in old age. Selection by inclusive fitness may be strong enough to favor alleles that protect against cognitive decline in postreproductive humans.

Abstract
The individuals of most vertebrate species die when they can no longer reproduce. Humans are a rare exception, having evolved a prolonged postreproductive lifespan. Elders contribute to cooperative offspring care, assist in foraging, and communicate important ecological and cultural knowledge, increasing the survival of younger individuals. Age-related deterioration of cognitive capacity in humans compromises these benefits and also burdens the group with socially costly members. We investigated the contribution of the immunoregulatory receptor CD33 to a uniquely human postreproductive disease, Alzheimer’s dementia. Surprisingly, even though selection at advanced age is expected to be weak, a CD33 allele protective against Alzheimer’s disease is derived and unique to humans and favors a functional molecular state of CD33 resembling that of the chimpanzee. Thus, derived alleles may be compensatory and restore interactions altered as a consequence of human-specific brain evolution. We found several other examples of derived alleles at other human loci that protect against age-related cognitive deterioration arising from neurodegenerative disease or cerebrovascular insufficiency. Selection by inclusive fitness may be strong enough to favor alleles protecting specifically against cognitive decline in postreproductive humans. Such selection would operate by maximizing the contributions of postreproductive individuals to the fitness of younger kin.


It is beginning to look like, in evolution's mindlessly and ruthlessly efficient way, dementia evolved as a way to kill off elderly apes who were no longer producing young, so freeing up resources for their offspring and their offsprings' offspring. It's quite easy to see how a 'eugenic' gene which doesn't deliver it's fatal load until after reproduction ceases, could have been selected for because this strategy would have produced more copies of itself in the long run.

Entirely 'selfishly', of course because genes don't have morals or the ability to plan. The ones which make most copies are the ones which survive and it matter not how that comes about. But, with the evolution of a brain good at learning and communicating, there now was an advantage in the old folks not dying off too soon, so there was now selection pressure to evolve the means of switching off this eugenic gene or at least delaying it.

The result is grandparents, who, in all human cultures, are an essential part of the social structure and who are often still looked up to as 'seniors' and founts of wisdom and experience. The interesting thing from an evolutionary biology perspective is that this may well be an example of there being selection pressure acting not immediately on the carrier of a gene but on the carriers of that gene two or even three generations later who benefit from the grandparents and great grandparents carrying it, hence selection pressure can apply even after reproduction ceases in a social species.

So, creationists, should we thank your invisible designer friend for designing the Alzheimer's gene to kill off the grannies, or for designing the different version so it doesn't work anymore?

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