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Tuesday, November 30, 2021 10:08:42 AM
-dated Pr yet ALS still on the drawing board--what say you for possibilities ??
Thanks. I accessed the abstract in Neuroscience Letters (entire article was a subscription service; so didn't read it).
SA4503, an Anavex molecule (don't know which one, if related to any of the current ones in test) was shown in both in vitro (cells in glassware) and in vivo (cells in living organisms) to suppresses motor neuron damage in amyotrophic lateral sclerosis animal models.
What I found interesting is the mechanism by which this appeared to occur. ALS, amyotrophic lateral sclerosis (Lou Gehrig's disease), is generally understood to be caused by the loss of the myelin sheath that surrounds nerves, acting in the manner of an electrical insulator, allowing electrical signals to progress along the nerve. With the loss of the myelin sheath, nerve signals short out, are lost. ALS symptoms set in.
Loss of the myelin sheath is generally regarded to be caused by inflammation or an immunological pathology, where the immune system attacks, eats away at the myelin. But in this study, "One important mechanism by which motor neuronal injury is caused involves inhibition of specific components of the mitochondrial electron transfer chain. Therapeutic measures aimed at protecting mitochondrial respiratory chain function may be useful in related familial and possibly other forms of ALS." Apparently, the drug was facilitating proper electron transfer within the mitochondria, which apparently resolved the neuropathology. Wonderful.
But, of course, this was published in 2014. I haven't seen any follow-up studies. Certainly, the Anavex people are aware of this study. To be clinically useful, a lot of work yet remains to be done. It's much lower on the long list of Anavex studies yet to be done. But, in time, Anavex may have a treatment for this, another severe central nervous system disease.
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