There are ways we can target the glutamatergic system indirectly, rather than directly blocking the glutamate receptors, which as we said, will have considerable side effects. One way, for example, is through the kynurenic acid, which has been known to have a binding site on the NMDA receptor. Also, studies have shown that kynurenic acid and metabolites are found in the plasma of migraine patients during an attack, hence using kynurenic acid analogs, a lot of preclinical studies have shown that it can be an effective modulators...
There are ways we can target the glutamatergic system indirectly, rather than directly blocking the glutamate receptors, which as we said, will have considerable side effects. One way, for example, is through the kynurenic acid, which has been known to have a binding site on the NMDA receptor. Also, studies have shown that kynurenic acid and metabolites are found in the plasma of migraine patients during an attack, hence using kynurenic acid analogs, a lot of preclinical studies have shown that it can be an effective modulators. They can be effective modulators of the trigeminal activation, hence this can be one of the indirect strategies to modulate glutamatergic transmission in the future.
Another way, it could be with the novel development of recombinant botulinum toxin, as you know, Botox, botulinum toxin is a well-established preventive treatment for migraine. And these days biochemical engineering has been evolutionary in terms of synthesizing novel botulinum toxin molecules that can have specific targets. So potentially, such a novel botulinum toxin could be designed to specifically target the vesicular glutamate transporters, hence it will specifically block glutamatergic transmission from the peripheral branch of the trigeminal nerve.