Replies to post #211028 on Anavex Life Sciences Corp (AVXL)

[falconer66a]

Is Exosome Facility Determined by Endoplasmic Reticular Function?

Very interesting information regarding the role of exosomes, produced in neurons, to communicate or control external nerve or neuron processes. Most important is the report that selected, exogenous (external) exosomes can restore or promote proper neuron growth and function. Restoration or promotion of normal nerve function — significant implications for all Central Nervous System diseases and conditions.

In the case of exosome dysfunction (and consequent CNS disease), might that be often caused by poorly synthesized proteins within the exosome? Might those development-controlling proteins be mis-formed if their sites of final topology (shape, folding) in the endoplasmic reticulum were compromised by the lack of a normal endogenous sigma-1 receptor agonist or a related chaperone?

It is now well understood that Anavex 2-73 restores, facilitates proper protein folding in the endoplasmic reticulum. Properly-folded proteins (primarily as functional enzymes) control biochemical reactions. If mis-folded in the neuron, cellular chemistry goes awry; nerve pathology results (CNS disease).

Is there, then, the possibility that Anavex 2-73 so facilitates normalized exosome production that all of the downstream processes they control function normally? Might this be the mechanism by which Anavex 2-73 (or other Anavex sigma-1 receptor agonists) might have such a wide, diverse set of positive therapeutic results for a diversity of otherwise unconnected CNS and other diseases?

I’ve contended previously that the Anavex drugs will not be confined to just Rett, Parkinson’s Disease Dementia, or Alzheimer’s; the three diseases now in clinical trial. The Anavex pipeline displays a number of other diseases and conditions that will be targeted. I’m certain that Anavex has tested their molecules against a host of diseases in murines (rats and mice). It will be surprising if in the next several years a good number of other diseases and conditions are not clinically targeted.

Lastly, how much of geriatric decline is caused by exosome dysfunction? As we age, is exosome function compromised, resulting in any or all of the debilities of older age? If so, what, then, might be the implications of prophylactic administration of Anavex 2-73, to facilitate the suitable production of functioning exosomes, to slow the aging process (if that might be possible)?

Let’s watch. The Anavex story is still in the first chapter.