Posted by SLS on May 1, 2014, at 12:20:00
In reply to Can someone explain Namenda's MOA?, posted by zonked on April 30, 2014, at 13:29:24
Guess:
There is probably an excess of glutamate being leaked out of cells and causing progressive deterioration through neurotoxicity and oxidative damage. Memanting would dampen this at NMDA glutamate receptors.
I would seriously look at minocycline to reduce inflammation, buffer glutamate release, and reduce neurotoxic degenerative processes, including oxidative damage produced by free radicals. Lamictal might help with mood by reducing active release of glutamate.
1. Is neuroprotective.
2. Reduces brain inflammation
3. Reduces the number of glutamate receptors.
4. Demonstrates antidepressant properties in mouse models of depression.
5. Is reported to act synergistically with noradrenergic antidepressants to treat depression - desipramine (but not fluoxetine).
6. Is reported to act synergistically with NMDA antagonists.
7. Reduces glutamate excitotoxicity by reducing the formation of quinolic acid, a NMDA agonist.
8. Reduces mitochondrial release of cytochrome C.
9. Modulates several signaling pathways.
10. Reduces microglial activation.
11. Has been reported anecdotally to successively treat depression.
12. Reduces the expression of lipopolysaccharide-induced pro-inflammation cytokines, an effect that acts as an antidepressant in animal models.
13. Increases neurite growth in response to nerve growth factor (NGF).
14. Inhibits high levels of PKC and GSK-3 alpha;
15. Decreases nitric oxide synthetase, thereby reducing free radicals which damage neurons and glia.
16. Reduces glutamate release.
- ScottSome see things as they are and ask why.
I dream of things that never were and ask why not.- George Bernard Shaw
poster:SLS
thread:1064975
URL: http://www.dr-bob.org/babble/20140419/msgs/1065024.html