Anavex Life Sciences Corp (AVXL)

[falconer66a]

A distant but viable conjecture—ALS.

Ok, this is entirely conjectural; should not be a factor in considering the holding or purchase of AVXL shares. But most science begins with well-formed conjectures, which are then tested. What I describe below may, someday, be tested, with blarcamesine or another Anavex sigma-1 receptor activator.

Just read a research report that showed that the accumulation of specific waste or toxic proteins in the axons of nerve cells with amyotrophic lateral sclerosis (ALS) cause the disease symptoms. The paper claimed, “Clearance of axonal TDP-43 or dissociation of G3BP1 condensates restored local translation and resolved TDP-43-derived toxicity in both axons and NMJs. ... Clearance of axonal TDP-43 or dissociation of G3BP1 condensates restored local translation and resolved TDP-43-derived toxicity in both axons and NMJs.”
https://pubmed.ncbi.nlm.nih.gov/34824257/

Simply, if nerve cells can clear, remove the toxic proteins, the ALS (“ Lou Gehrig's Disease”) is resolved; a cure, dare I say.

Might it be that for those of us who do not have Lou Gehrig’s disease our nerves normally and continually clear away the toxic proteins? With this normal autophagy our nerves work properly. But, for some reason (genetic, chemically-induced, etc.), this normal autophagy fails in the neurons of those with ALS.

Might ALS be caused by a specific failure of normal autophagy? Moreover, might blarcamesine’s ability to restore autophagic processes in diseased cells be a treatment or cure for the disease?

That conjecture can’t be known until a lot of detailed, precise work is done. I note that there are mice that are animal models of amyotrophic lateral sclerosis (ALS). Won’t be inordinately expensive to test various dosages and treatment regimens of blarcamesine on them, to see if the diseased mice respond in any positive way. If they do, human trials would be next.

Again, the strength (not magic) of blarcamesine centers on its unique ability to favorably activate the sigma-1 receptor protein’s ability to modulate autophagy, thereby restoring healthful, normal homeostasis within the diseased neuron.