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.