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Re: falconer66a post# 333243

Tuesday, 10/19/2021 12:00:18 PM

Tuesday, October 19, 2021 12:00:18 PM

Post# of 462572
The fellow’s “activator” was actually toxic.

Actually, the finding that the author’s particular sigma-1 receptor ligand caused the production of amyloid beta proteins, which cause Alzheimer’s symptoms, is actually a confirmation of the mechanism of action (MOA) of the Anavex molecules, blarcamesine and Anavex 3-71.

Again, the good fellow failed to tell the specific sigma-1 receptor ligand he used. It surely wasn’t either of the Anavex molecules. He did claim that his molecule “activated” the sigma-1 receptor protein. But, so clearly, not in the same way. In effect, it disabled the receptor, keeping it from favorably modulating the protein’s several downstream biochemical outcomes. The fellow’s molecule (whatever it was) disrupted the normal function of the sigma-1 receptor protein. It was toxic. Hence, amyloid beta was produced.

This rather clearly proves that if sigma-1 receptor activity is disrupted, shut down, or diverted, amyloid wastes are produced or are not cleared; Alzheimer’s symptoms are generated.

The Anavex molecules have a propitious MOA at the sigma-1 receptor protein. Other sigma-1 receptor ligands have the opposite result. To treat (or prevent) Alzheimer’s, the sigma-1 receptor protein must function fully and favorably. Anavex has the molecules that facilitate this. Other sigma-1 receptor ligands fail.

Pharmacologically, Anavex has the winning molecular hand.
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