Replies to post #134714 on Anavex Life Sciences Corp (AVXL)

[polarbear77]

Nidan appreciated your & sokol’s postings re that PD article, and I’ve a combo PD/MS theory.

“Anavex 2-73, an investigational therapy being evaluated in clinical trials for Alzheimer’s disease, was found to restore the function of damaged nerve cells in mouse models of Parkinson’s disease.”

“The drug candidate has the potential to restore the molecular balance of cells by targeting misfolded proteins and mitochondria dysfunction. This ultimately prevents oxidative stress, inflammation, and cellular stress, processes that are shared by many neurological disorders and known to contribute for nerve cell degeneration.”

https://parkinsonsnewstoday.com/2017/10/31/anavex-2-73-investigational-therapy-restored-nerve-cell-function-in-mice-with-parkinsons-disease-in-lab-study/

And if I may parlay the quote above in the Parkinson’s Disease article to the Multiple Sclerosis front, ....”This ultimately prevents oxidative stress, inflammation, and cellular stress, processes that are shared by many neurological disorders and known to contribute for nerve cell degeneration.”

Well, OFP provided an interesting MS article and link from Nature.com regarding possibly inhibiting fibrinogen from entering the brain which may then allow for cells to repair myelin sheaths; I can’t explain it very well, but it’s an interesting read: https://www.nature.com/articles/d41586-017-08232-2?WT.mc_id=TWT_newsandviews

The POINT is that the article made a key contention:

“Demyelinated areas that arise in MS can also be considered as local ‘brain injuries’. Although there is no bleeding and subsequent blood clotting involving coagulation factors in MS, chronic inflammation causes a persistent opening of the blood–brain barrier (BBB), across which these factors might pass in large amounts. Could the permanent entry of blood-borne coagulation factors prevent OPC differentiation and myelin repair?”

So chronic inflammation is the likely cause of the problem (per the nature article)??

So can I take the logical next step that perhaps a2-73 is effective in promoting remyelination in MS because of its ability to prevent INFLAMMATION? Thereby reducing the persistent opening in the blood brain barrier, which helps to stop the entry of blood-borne coagulation factors, etc etc??

Again I reference the above quote re the MOA of a2-73: “This ultimately prevents oxidative stress, inflammation, and cellular stress, processes that are shared by many neurological disorders and known to contribute for nerve cell degeneration.”

Any BP possibly interested in this remyelination concept?

Possibly the National MS Society wants to further some research in this area?

Piggyback on Dr Lisak’s years of a2-73 MS study in the WSU labs and his positive conclusions regarding same?