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Tuesday, October 19, 2021 11:24:22 AM
Ok, the good doctor’s research discovered this: “Conversely, a drug that activated S1R triggered an increase in beta secretase cleavage of palAPP and increased production of amyloid beta in axons.”
Not good, at all. A-beta in axons causes Alzheimer’s symptoms. And, according to this statement, activation of the sigma-1 receptor protein produced amyloid beta.
Who’s got it right? Anavex, whose sigma-1 receptor activator, blarcamesine, in human trials, reduces the symptoms caused by amyloid beta; or, this researcher, whose particular sigma-1 activator—whatever it was—did just the reverse?
Key is this. Any number of molecules can be sigma-1 receptor ligands, having the ability to bind to that molecule and thereby change its biochemical functions. Some, such as blarcamesine and Anavex 3-71, after binding to the sigma-1 receptor, produce propitious (favorable) downstream outcomes. Pretty clear, the particular molecule used in the author’s study clearly complicated, suppressed the normal, favorable mechanisms of the sigma-1 receptor protein.
Might it be curious that the sigma-1 receptor ligand used in the study, which produced results exactly opposite to the Anavex molecules, was not identified? Could it be supposed that the researcher, working with the sigma-1 receptor protein, should be aware of the Anavex science centered on that protein; and the two Anavex molecules that produce results exactly opposite to his? Is the man merely ignorant (failing to scrutinize all relevant sigma-1 science, for which Anavex leads the way)? Or, for convenience to his purposes (whatever they are) has he deliberately failed to mention the Anavex successes, while at the same time deliberately failing to simply tell the name of his sigma-1 ligand?
Inquiring minds wish to know.
Informed, knowledgeable minds already know of blarcamesine’s successes, which do not in any way increase amyloid beta production; just the opposite. For Anavex, the “research” is irrelevant.
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