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Anyone have success with KYNA inhibitors?

kyna nmda

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#1 experimenting

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Posted 08 December 2018 - 09:30 AM


Is this perhaps the holy grail of cognition? Seeing as KYNA inhibits AMPA and NMDA. Has anyone reduced it with any great effect?

#2 mono

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Posted 08 December 2018 - 01:56 PM

I would also like to hear about this. It would seem galantamine and memantine have been used with some success in schizophrenia.

 

"Galantamine is an acetylcholinesterase inhibitor and a positive allosteric modulator of the α7nicotinic receptors. Memantine is an N-methyl-D-aspartate (NMDA) receptor antagonist. There is evidence to suggest that the combination of galantamine and memantine may be effective in the treatment of cognitive impairments in schizophrenia. There is a growing body of evidence that excess kynurenic acid (KYNA) is associated with cognitive impairments in schizophrenia. The α-7 nicotinic and the NMDA receptors may counteract the effects of kynurenic acid (KYNA) resulting in cognitive enhancement. Galantamine and memantine through its α-7 nicotinic and NMDA receptors respectively may counteract the effects of KYNA thereby improving cognitive impairments."

https://www.ncbi.nlm...les/PMC4824953/


Edited by mono, 08 December 2018 - 01:58 PM.


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#3 experimenting

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Posted 08 December 2018 - 05:33 PM

Anyone tried it?

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#4 mono

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Posted 09 December 2018 - 12:22 AM

"Data revealed demonstrate the ability of Cerebrolysin to lower KYNA formation in homogenates. We suggest that the anti-dementia effect of Cerebrolysin observed in Alzheimer patients could be due to Cerebrolysin induced reduction of KYNA levels, thus enhancing the cholinergic and glutamatergic neurotransmissions."

"Interestingly, we found that D-cycloserine blockes significantly KATs activities in rat liver and brain homogenates and in the frontal cortex homogenate of human post mortem tissue, as well. These results allowed us to propose that lowering of KYNA content likely due to D- cycloserine inhibition of KATs activities might be involved in the postulated mechanism for D- cycloserine to act as a partial agonist at the glycine site of the NMDA receptor."

"Interestingly, we found that Jerusalem balsam blocks significantly KATs activities, too. Lowering of KYNA synthesis by Jerusalem balsam represents notable biochemical effect since it might influence KYNA levels."

https://www.omicsonl...rugs-79326.html

 

 

"Brain KYNA levels were dose-dependently increased by tryptophan intake, and these increase were consistent with kynurenine (KYN), the precursor to KYNA, levels in the brain, plasma and liver. Administration of the 1.5% tryptophan added diet reduced the extracellular DA level to 60%, and increased the extracellular KYNA to 320% in the striatum. The DA reduction was atten- uated through inhibiting KYNA synthesis with 2-aminoadipic acid. These results indicate that a high tryptophan diet can induce KYNA production and suppress DA release."

https://onlinelibrar...59.2011.07369.x

 

"Ten out of 19 amino acids (specifically, leucine, isoleucine, phenylalanine, methionine, tyrosine, alanine, cysteine, glutamine, glutamate, and aspartate) significantly reduced KYNA formation at 1 mmol/L. These amino acids showed inhibitory effects in a dose-dependent manner, and partially inhibited KYNA production at physiological concentrations. Leucine, isoleucine, methionine, phenylalanine, and tyrosine, all LAT substrates, also reduced tissue KYN concentrations in a dose-dependent manner, with their inhibitory rates for KYN uptake significantly correlated with KYNA formation. These results suggest that five LAT substrates inhibit KYNA formation via blockade of KYN transport, while the other amino acids act via blockade of the KYNA synthesis reaction in brain. Amino acids can be a good tool to modulate brain function by manipulation of KYNA formation in the brain. This approach may be useful in the treatment and prevention of neurological and psychiatric diseases associated with increased KYNA levels."

https://www.ncbi.nlm...les/PMC4318830/

 

"The non-selective COX-inhibitor diclofenac (50 mg/kg, i.p.) or indomethacin (50 mg/kg, i.p.), a non-selective inhibitor with a preferential selectivity for COX-1, produced an elevation in brain KYNA. In contrast, the COX-2 selective inhibitors parecoxib (25 mg/kg, i.p.) or meloxicam (5 mg/kg, i.p.) decreased brain KYNA."

https://www.ncbi.nlm...pubmed/15517427


Edited by mono, 09 December 2018 - 12:45 AM.

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