It means that there was a time when everybody in the human population had that allele and its been reducing in frequency over time because the other alleles have some advantage. So when we look today at things that make you susceptible to long-term chronic diseases like Alzheimers and Type 2 diabetes a lot of those alleles are the ancestral forms. Ancient people just were not well adapted to today's circumstances. And the alleles aren't gone, they have been reducing but they are still here and they are causing what we consider to be problems although 50,000 years ago they weren't problems, people lived a different lifestyle.This is a great point to make, and actually represents the flip side of usual way of thinking. Instead of viewing a novel alleles that is increasing in frequency as advantageous, we can think of the old (ancestral) allele as disadvantageous in the new circumstances.
Sometimes people think that our ancestral forms "work just fine", until some new mutation comes along that works better, somewhat like a new car model replacing an old but effective one. In this view, humans are "perfecting themselves" by acquiring new and better abilities.
But, evolution doesn't work that way. Some of the new alleles favored by recent evolution could have arisen several times in the past in earlier Homo or even more distant ancestors. But, selection did not favor them then because the circumstances weren't right.
John also talks about why Neanderthals may have been the source for FOXP2 in humans:
It seems to me we've got a 50/50 chance that it originated in modern humans and was passed to Neanderthals.and:
If it came from Neanderthals we would have to propose that FOXP2 arose about 100,000 years ago when modern humans and Neanderthals were in contact in the Near East. The key is that if FOXP2 is more recently fixed than the common ancestor of humans and Neanderthals who lived 300,000 or 400,000 years ago, then it had to be transferred in one direction or the other. Given that it's there in several Neanderthal specimens and it's globally dispersed in humans, this transfer, if it happened, had to happen early enough for FOXP2 to get to where it was. So I'm thinking in the time frame of 100,000 years ago, but I'm waiting to see a date.
If I were to meet somebody who lived 50,000 years ago, how would that person be different from me?
Well number one, somebody from 50,000 years ago who was transported to today in a time machine would probably be dead within two years from some infectious disease. That's the number one difference, we have resistance to all kinds of diseases that have emerged during the process of civilization that never existed before. The smallpox that killed many of the Native Americans, the susceptibility was there for genetic reasons. There would be some digestive changes. When we look at the diversity among people in the world to day in terms of Type 2 diabetes, and obesity susceptibility, some of those differences are going to be explained by recently selected genes that have to do with diet. I suspect there would be some behavioral changes. We're looking at a large category of genes that effect the central nervous system, we don't know what they do but I can expect there must be some behavioral differences that have influenced human populations across the last 50,000 years.