Listen, folks, we’ve got a situation with brain tumors causing seizures, and it’s a big deal, a huge deal. We’re talking about drug-resistant epilepsy here, and it’s not good, not good at all. Now, the brain, it’s complicated, very complicated, but we’ve got these things called glutamate transporters, glutamine synthetase, and pyruvate carboxylase – they’re supposed to keep everything in balance, but sometimes, they don’t work like they should.

Our previous research, it was tremendous, we found out that these angiocentric gliomas, they didn’t have the main glutamate transporter, EAAT2. But the other stuff, the glutamine synthetase and pyruvate carboxylase, they were mostly doing okay. Now, in this study, we looked at a bunch of different tumors, 25 of them, all kinds of names – dysembryoplastic neuroepithelial tumors, gangliogliomas, you name it. And we checked for EAAT2, glutamine synthetase, and pyruvate carboxylase.

What did we find? EAAT2 was missing in 36% of these tumors. That’s a lot, a third of them! And glutamine synthetase, it was gone in 8%. But pyruvate carboxylase, that was mostly doing fine, except in these rosette forming glioneuronal tumors. We also did some digging in this PedcBioPortal, very advanced stuff, and out of over 2300 brain tumors, less than 1% had issues with the EAAT2 gene.

So, what’s the bottom line? Unlike those angiocentric gliomas, where EAAT2 is always missing, other tumors only sometimes have this problem. And when EAAT2 is gone, it might be causing these seizures. The good news is pyruvate carboxylase is there, fighting the good fight, but sometimes it’s not enough. And this EAAT2 problem, it’s probably not in your genes, it’s more about what’s happening around the genes – epigenetics, very cutting-edge.

In conclusion, we’re dealing with a complex issue, but we’re making progress, the best progress, and we’re going to figure this out. We’re going to make brain health great again, believe me.