From wiki: https://en.wikipedia.org/wiki/Quinolinic_acid
"The fact that NMDA receptor antagonists possess antidepressant properties suggests that increased levels of quinolinic acid in patients with depression may overactivate NMDA receptors.[11] By inducing increased levels of quinolinic acid in the cerebral spinal fluid with interferon ?, researchers have demonstrated that increased quinolinic acid levels correlate with increased depressive symptoms."
This is interesting, so kynurenic acid blocks glycine site NMDA receptors, yet quinolinic acid overactivates it? How would I then have them both increased? Shouldn't I be afraid that agonizing the NMDAr would induce depressive properties? That seems paradoxical a bit.
Hi Nas, sorry for the delay, but as I have said in my previous post, I was on vacations, and just got back yesterday to do on return. Whenever you have a question for me, please be patient, it will usually takes far less than one month before I get back to you
About what you see as a paradox, I refer you again at the diagram I have linked to my January 2015 post, at
http://fr.slideshare.net/adonissfera/tryptophan-and-madness/17-Cytokines_Come_in_Two_FlavorsProInflammatory . If you look carefully, you will see that the 2 kynurenine pathways tryptophan is shunt to happen in two different cell types:
the KMO enzyme leading to quinolinic acid is active in the microglia and produces quinolinic acid, and causes emotional symptoms
and the KAT enzyme is present in the astrocytes, leading to kynurenic acid production, and cause cognitive symptoms
so, 2 different cell types, having a different distribution in the brain.
both enzymes, KMO and KAT, have kynurenine as substrate ( = "input" substance).
Back in 2015, I search a lot to find natural KMO inhibitor, which would have been great to test my hypothesis on quinolinic acid causing my emotional symptoms , but did not find any ( KAT inhibitor were not interesting for me since I have no cognitive symptoms). So, I then went back up in the chain and decided to work on blocking TDO and IDO, so there would be less tryptophan turned into kynurenine, so less substrate available for KMO and KAT, to turn TRP in QUIN or kynureninc acid, as explained above.
This worked for me, in addition to all other substance in my pre-pack and with my overall method, as described in detail in my detailed post on that subject, so I stayed at that.
My hypothesis have still many questions attached to it, but not a lot of discussions have followed my presentation of it on the forum, in 2015, so many stones have been left unturned. I had read dozens and dozens of scientific articles around this subject, 4 years ago, but not since. I am not an expert on this topic, so I cannot answer all questions about this. I just see that my method works for me, and it may be in part because it helps tryptophan not to be changed in kynurenine, and then in too much quinolonic acid (and too much kynurenic acid, but this is not of concern in my case).
I hope this will help you get further in your own research, Nas .
