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Posted On: 10/13/2019 9:08:43 PM
Post# of 1460
A post copied from IHUB from falconer66a .......
How low will PPS drop? I’m holding and may add more if it drops much more,
Fletch
falconer66a Sunday, 10/13/19 08:22:48 PM
Re: XenaLives post# 214337 0
Post # of 214369
Anavex 2-73 Moderation of Glutamate and GABA.
Quote:
I believe the glutamate/GABA improves because of corrected protein misfolding. Can someone confirm?
As noted by those who have read the report on the clinical findings of the six young ladies with Rett syndrome, treated with but 5 mg of Anavex 2-73, two very significant metrics were discovered. Simply, glutamate generally decreased during the short six-week trial, and gamma aminobutyric acid (GABA) increased. Very, very favorable.
Elevated or excess glutamate, simply, causes all sorts of problems in nerves and is associated with many central nervous system diseases and conditions. “... glutamate has excitatory effects on nerve cells, and that it can excite cells to their death in a process now referred to as “excitotoxicity”. Read the details in the abstract and journal article here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133642/
Too much glutamate, simply, is pathogenic. In the girls with Rett syndrome, Anavex 2-73 significantly reduced glutamate levels (in a very short treatment period, at a very low dose; 5 mg).
To the contrary was gamma aminobutyric acid, GABA. GABA works in the opposite way; it slows the firing of neurons across synapses. Decreased levels of GABA are found in a variety of CNS diseases. Decreased levels of GABA are pathogenic; increased levels are therapeutic (and in properly functioning nerves, normal).
Now, does Anavex 2-73 specifically optimize concentrations of these neurotransmitters by restoring or controlling the proper folding of proteins (enzymes) that control virtually all of the chemical reactions of cells? Perhaps. But I’ve seen no specific descriptions of the involved proteins. The absence of the precisely-known biochemical mechanisms by which Anavex 2-73 optimizes GABA and glutamate levels in diseased nerves does not in any way affect those outcomes. The only important thing is that the drug does, indeed, suppress excess glutamate and promote optimized levels of GABA.
This, of course, would be a homeostatic process, where cellular processes are controlled to a static or normalized state — normal cell health and function. It could involve proper protein folding in the endoplasmic reticulum, allowing the production of functioning enzymes, which control chemical reactions. Or, it might in some way cause the expression of normal genes; or suppress the expression of pathogenic ones (epigenetics).
No matter what the actual mechanics of glutamate suppression and GABA elevation might be, both (particularly in combination) are extremely important in affected nerves. Glutamate and GABA disruptions are pathogenic in a variety of CNS and other diseases. Their moderation by Anavex 2-73 is extremely important. Let’s see if similar metrics are found in both the Parkinson’s Disease Dementia study in Spain and the expanded Alzheimer’s study in Australia. Very, very high probability.
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How low will PPS drop? I’m holding and may add more if it drops much more,
Fletch
falconer66a Sunday, 10/13/19 08:22:48 PM
Re: XenaLives post# 214337 0
Post # of 214369
Anavex 2-73 Moderation of Glutamate and GABA.
Quote:
I believe the glutamate/GABA improves because of corrected protein misfolding. Can someone confirm?
As noted by those who have read the report on the clinical findings of the six young ladies with Rett syndrome, treated with but 5 mg of Anavex 2-73, two very significant metrics were discovered. Simply, glutamate generally decreased during the short six-week trial, and gamma aminobutyric acid (GABA) increased. Very, very favorable.
Elevated or excess glutamate, simply, causes all sorts of problems in nerves and is associated with many central nervous system diseases and conditions. “... glutamate has excitatory effects on nerve cells, and that it can excite cells to their death in a process now referred to as “excitotoxicity”. Read the details in the abstract and journal article here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133642/
Too much glutamate, simply, is pathogenic. In the girls with Rett syndrome, Anavex 2-73 significantly reduced glutamate levels (in a very short treatment period, at a very low dose; 5 mg).
To the contrary was gamma aminobutyric acid, GABA. GABA works in the opposite way; it slows the firing of neurons across synapses. Decreased levels of GABA are found in a variety of CNS diseases. Decreased levels of GABA are pathogenic; increased levels are therapeutic (and in properly functioning nerves, normal).
Now, does Anavex 2-73 specifically optimize concentrations of these neurotransmitters by restoring or controlling the proper folding of proteins (enzymes) that control virtually all of the chemical reactions of cells? Perhaps. But I’ve seen no specific descriptions of the involved proteins. The absence of the precisely-known biochemical mechanisms by which Anavex 2-73 optimizes GABA and glutamate levels in diseased nerves does not in any way affect those outcomes. The only important thing is that the drug does, indeed, suppress excess glutamate and promote optimized levels of GABA.
This, of course, would be a homeostatic process, where cellular processes are controlled to a static or normalized state — normal cell health and function. It could involve proper protein folding in the endoplasmic reticulum, allowing the production of functioning enzymes, which control chemical reactions. Or, it might in some way cause the expression of normal genes; or suppress the expression of pathogenic ones (epigenetics).
No matter what the actual mechanics of glutamate suppression and GABA elevation might be, both (particularly in combination) are extremely important in affected nerves. Glutamate and GABA disruptions are pathogenic in a variety of CNS and other diseases. Their moderation by Anavex 2-73 is extremely important. Let’s see if similar metrics are found in both the Parkinson’s Disease Dementia study in Spain and the expanded Alzheimer’s study in Australia. Very, very high probability.
Respond | No replies
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