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Getting Back ON Track

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#1 Q did it!

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Posted 16 August 2015 - 11:15 PM

I have reached a low in my life. That is putting it simply as possible. Below is a link describing in part my absence from theses forums and YouTube. This link HERE is to my blog where I will become quite active also a doc attached as well. My absence to this community, my blog, and YouTube is coming to an end! I will be making dual post to here and the blog for a while I am thinking. This thread is about my recovery, nootropics and your guys input! I am quite serious about committing myself to becoming an entrepreneur in BioHacking.

            There is a lot to say but ill leave it to other posts. One day at a time!


LOVE THIS GUY AND HIS MESSAGE!!!!!!!!!!!!! (Also should check out his books)

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#2 lostfalco

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Posted 18 August 2015 - 04:15 AM

Hey Q, I know you're trying to steer clear of nootropics and that's totally cool. If you ever choose to look into them again I would suggest looking into the role of kyneurenic acid in schizophrenia and the ability of galantamine, exercise, and amino acids to ameliorate it. Just a possible thought for the future. =)


I wish you nothing but health and happiness!


Check out the studies in this thread.  http://www.longecity...ad/#entry716469





Neuroscience. 2013 May 15;238:19-28. doi: 10.1016/j.neuroscience.2013.01.063. Epub 2013 Feb 6.

Early developmental elevations of brain kynurenic acid impair cognitive flexibility in adults: reversal with galantamine.


Levels of kynurenic acid (KYNA), an endogenous α7 nicotinic acetylcholine receptor (α7nAChR) antagonist, are elevated in the brain of patients with schizophrenia (SZ) and might contribute to the pathophysiology and cognitive deficits seen in the disorder. As developmental vulnerabilities contribute to the etiology of SZ, we determined, in rats, the effects of perinatal increases in KYNA on brain chemistry and cognitive flexibility. KYNA's bioprecursor l-kynurenine (100mg/day) was fed to dams from gestational day 15 to postnatal day 21 (PD21). Offspring were then given regular chow until adulthood. Control rats received unadulterated mash. Brain tissue levels of KYNA were measured at PD2 and PD21, and extracellular levels of KYNA and glutamate were determined by microdialysis in the prefrontal cortex in adulthood (PD56-80). In other adult rats, the effects of perinatal l-kynurenine administration on cognitive flexibility were assessed using an attentional set-shifting task. l-Kynurenine treatment raised forebrain KYNA levels ∼3-fold at PD2 and ∼2.5-fold at PD21. At PD56-80, extracellular prefrontal KYNA levels were moderately but significantly elevated (+12%), whereas extracellular glutamate levels were not different from controls. Set-shifting was selectively impaired by perinatal exposure to l-kynurenine, as treated rats acquired the discrimination and intra-dimensional shift at the same rate as controls, yet exhibited marked deficits in the initial reversal and extra-dimensional shift. Acute administration of the α7nAChR-positive modulator galantamine (3.0mg/kg, i.p.) restored performance to control levels. These results validate early developmental exposure to l-kynurenine as a novel, naturalistic animal model for studying cognitive deficits in SZ.



Psychopharmacology (Berl). 2012 Apr;220(3):627-37. doi: 10.1007/s00213-011-2539-2. Epub 2011 Oct 26.

Acute elevations of brain kynurenic acid impair cognitive flexibility: normalization by the alpha7 positive modulator galantamine.

Cognitive deficits represent a core symptom cluster in schizophrenia (SZ) that is predictive of outcome but not effectively treated by current antipsychotics. Thus, there is a need for validated animal models for testing potential pro-cognitive drugs.


As kynurenic acid levels are increased in prefrontal cortex (PFC) of individuals with SZ, we acutely increased brain levels of this astrocyte-derived, negative modulator of alpha7 nicotinic acetylcholine receptors (α7nAChRs) by administration of its bioprecursor kynurenine and measured the effects on extracellular kynurenic acid and glutamate levels in PFC and also performance in a set-shifting task.


Injections of kynurenine (100 mg/kg, i.p.) increased extracellular kynurenic acid (1,500%) and decreased glutamate levels (30%) in PFC. Kynurenine also produced selective deficits in set-shifting. Saline- and kynurenine-treated rats similarly acquired the compound discrimination and intra-dimensional shift (saline, 7.0 and 6.3 trials, respectively; kynurenine, 8.0 and 6.7). Both groups required more trials to acquire the initial reversal (saline, 15.3; kynurenine, 22.2). Only kynurenine-treated rats were impaired in acquiring the extra-dimensional shift (saline, 8.2; kynurenine, 21.3). These deficits were normalized by administering the α7nAChR positive allosteric modulator galantamine (3.0 mg/kg, i.p) prior to kynurenine, as trials were comparable between galantamine + kynurenine (7.8) and controls (8.2). Bilateral local perfusion of the PFC with galantamine (5.0 μM) also attenuated kynurenine-induced deficits.


These results validate the use of animals with elevated brain kynurenic acid levels in SZ research and support studies of drugs that normalize brain kynurenic acid levels and/or positively modulate α7nAChRs as pro-cognitive treatments for SZ.




Edited by lostfalco, 18 August 2015 - 04:16 AM.

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#3 gamesguru

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Posted 18 August 2015 - 11:31 AM

Nicotine and acetylcholine agonise alpha7 receptors, so galantamine may exert part of its effect through boosting extracellular acetylcholine.  Fascinating compound.

An interesting RC: (S)-4-(Ethylsulfonyl)benzoylalanine is a potent and selective inhibitor of kynurenine aminotransferase


B6 may help metabolize it and control its levels:


Effects of vitamin B6 deficiency on the conversion ratio of tryptophan to niacin

The urinary excretion of kynurenic acid decreased while that of xanthurenic acid increased drastically in the two B6-deficient groups



I found studies suggesting we may not want to lower levels too drastically.


Modulation of striatal quinolinate neurotoxicity by elevation of endogenous brain kynurenic acid

nicotinylalanine exerts its effect by increasing levels of endogenous kynurenic acid in the brain. The results of this study suggest that agents which influence levels of endogenous excitatory amino acid antagonists such as kynurenic acid may be useful in preventing excitotoxic damage


Nicotinylalanine increases the formation of kynurenic acid in the brain and antagonizes convulsions

antagonism of the NMDA receptors. In fact, NAL antagonized sound-induced seizures and prevented death in DBA/2 mice. Pretreatment of the mice with D-serine (100 micrograms intracerebroventricularly), a glycine agonist and a competitive antagonist of KYNA, completely prevented the anticonvulsive action of NAL. These data suggest that changes in the extracellular concentration of KYNA in the brain are associated with a modulation of NMDA receptor function.


The Brain Metabolite Kynurenic Acid Inhibits α7 Nicotinic Receptor Activity and Increases Non-α7 Nicotinic Receptor Expression

Edited by gamesguru, 18 August 2015 - 11:34 AM.

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#4 Saffron

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Posted 03 September 2015 - 12:35 AM

Kynurenic Acid is probably good instead of bad like everyone is claiming. Theres only one other way to enhance functioning & well-being if not the Mu Pathway, mGluR Blockade. Im pretty sure Tian isnt any direct Mu agonist, probably lowers 1/5 mGluR expression. No one has ever taken tian and got pain-pill like effects. Its not like that, more like indirect dis-inhibition of endogenous mu  & D2 transmission. I dont think i believe that one study that claims Tian is a Mu Agonist. Was it a radiolabled Ligand study with radioactive tian, not something else, being the ligand? if not, i dont believe it and would go with indirect mu-peptide increase as one of the factors. why the hell would it be a mu agonist? its a Nitrogen-Tricyclic augmented small chain soap

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