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Tuesday, October 19, 2021 12:44:25 PM
Ok, as a competent reviewer of research should do, I pulled up the actual paper telling the research:
https://www.cell.com/cell-reports/fulltext/S2211-1247(21)00473-3?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124721004733%3Fshowall%3Dtrue
Those who wish are welcome to scrutinize the presented information. Lots of it. The sigma-1 receptor agonist in the study was “PRE-084.” Information on this molecule here:
https://www.selleckchem.com/products/pre-084-hydrochloride.html
Ok, then, did the paper show that activation of the sigma-1 receptor actually caused the production of amyloid wastes, which cause Alzheimer’s. Yes, it did—with the PRE-084 molecule. (For those discounting murine [lab rodent] research, read no further. All of this was in mice.)
So, now pretty clear. Merely getting some molecule to stick to the sigma-1 receptor protein, thereby “activating’ it in some way, does not necessarily, in every case produce good therapeutic results. A few sigma-1 receptor agonists, those of Anavex, do. Others do not.
The take-home message is this, confirmed by this (and other) studies. To prevent the production or accumulation of amyloid beta wastes in neurons, to prevent or treat Alzheimer’s, the sigma-1 receptor protein must function normally and completely. Disrupting that function with a ligand (attached molecule) with a toxic “activator” allows the production of amyloid beta wastes. Facilitating sigma-1 receptor function with the Anavex molecules produces favorable therapeutic outcomes. In reality, this research further substantiates the unique, propitious Anavex mechanism of action (MOA) at the sigma-1 receptor protein.
As the human clinical results will show, Anavex has it.
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