Dr. Sergiu Pașcă

I think in children, it's much more difficult.

And in fact, many of the genes that were early on identified for autism were identified in these populations, in the Amish populations, for instance.

There is a very classic example of a gene that is associated with severe epilepsy and autism that was identified there for the first time.

It's present in other places as well.

So, yeah, I think, of course, the complexity of the problem is that you also want to make sure that you don't just associate something.

You also want to reverse it in a way, right?

So you would want to do the other experiment where you change it and it goes away.

But you can never do that in the human brain.

We can't just turn things on and off to see whether they're truly causal.

And then, of course, human brain development also takes an incredibly long period of time.

Right.

If anything, it seems that the human nervous system has done everything possible to slow down that process.

I mean, we myelinate all the way to the third decade.

Neurons are born and migrating through the nervous system into early postnatal years.

There's evidence that myelination, especially in the frontal areas of the brain, are continuing up to the third decade.

Yeah, no, the prevalence for autism has been actually reported to be higher in other countries even before this.

Some of the early reports many years ago showed that in Korea, for instance, the prevalence was very high.

Now that the studies are done, also like in Scandinavian countries, it shows that it's probably around the same, you know, kind of like rate, 1 in 30 to 1 in 40, so somewhere between.

And perhaps another argument, which is very important to bring, is that we find the same mutations.

I mean, the same mutations, if we're talking, let's say, a mutation in a specific calcium channel, you'll find it in a patient in Denmark, as well as one in Africa or in, let's say, Australia.