Drug for Alzheimer’s Disease Could Relieve Migraines

Hi Everyone,

I made some research online the other day, I came across this paper from UCLA. Have anyone heard of this treatment for migraine? The Alzhemier’s drug is called Namenda.
I think it’s quit interesting. Go and read here uclahealth.org/body.cfm?xyzp … il&ref=517

from UCLA paper: hartp.neurology.ucla.edu/IMAGES/ … andout.pdf

Is there anything new for migraine?
There are a variety of new potential treatments that are in development. As our understanding of migraine
advances, we have been able to identify new targets for treatment. One example is the medication memantine
(Namenda). Memantine inhibits the waves of brain activity that are believed to be a trigger for migraine.
Because it was already on the market for the treatment of memory and cognition problems due to Alzheimer’s
disease, and known to be well tolerated, we have begun to use it to treat patients with migraine. We have now
treated hundreds of patients with the medication, and with some we have had excellent results. Some patients
experience dizziness, and because the medication can be energizing, some patients have found that it interferes
with sleep if they take it too close to bedtime. In general, however, most patients have no side effects.
Memantine has not been proven with formal clinical trials to be effective for migraine prevention, but we
believe it is an excellent candidate for further study. It may be worth a try for patients who have tried other
standard migraine treatments.

Emma

Hi Emma,
This could make sense as a potential therapeutic. Below is the mechanism of action of mematine and as you can see it “tone’s down” the CNS which is how so many of the other migraine preventives work as well.

MECHANISM OF ACTION — Glutamate, the primary excitatory amino acid in the CNS, may contribute to the pathogenesis of Alzheimer’s disease (AD) by overstimulating various glutamate receptors leading to excitotoxicity and neuronal cell death. Memantine is an uncompetitive antagonist of the N-methyl-D-aspartate (NMDA) type of glutamate receptors, located ubiquitously throughout the brain. Under normal physiologic conditions, the (unstimulated) NMDA receptor ion channel is blocked by magnesium ions, which are displaced after agonist-induced depolarization. Pathologic or excessive receptor activation, as postulated to occur during AD, prevents magnesium from reentering and blocking the channel pore resulting in a chronically open state and excessive calcium influx. Memantine binds to the intra-pore magnesium site, but with longer dwell time, and thus functions as an effective receptor blocker only under conditions of excessive stimulation; memantine does not affect normal neurotransmission.

Thanks for keeping us up to date,
Lisa