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frrol

11/28/21 8:53 AM

#337849 RE: jimmy_mcyoloswag #337836

AD is likely quite complex. Our hope is that activating S1 and modulating some muscarinic receptors will be therapeutic. The hypothesis is that it will promote ionic homeostasis in the neurons, reduce protein misfoldings, tau hyperphosphorylation, and other pathologies. We're one of many, many approaches, and biotechs and pharmas are using clinical trials to figure which, if any, are helpful.

nidan7500

11/28/21 9:31 AM

#337850 RE: jimmy_mcyoloswag #337836

jimmy_mc

https://neurosciencenews.com/alzheimers-3-types-19711/

Thx for link. Cannot help but think how discussions like this one must lead to a fuller discussion on the composite linked body of knowledge (BOK) which must certainly be at the core of the AXVL CNS MOA. We are on the correct path here folks...BTD is not a comprehensive enough concept, IMO.

xodcode

11/28/21 9:58 AM

#337855 RE: jimmy_mcyoloswag #337836

Thanks jimmym.

Great read.

The article does seem to parallel the ANVX approach to targeting AD.

HMB2010

11/28/21 10:37 AM

#337857 RE: jimmy_mcyoloswag #337836

Confirmation many have said here. Science catching up to what Missling is attempting, will make more readily acceptable rather than casually brushed off.

Thanks for sharing, excellent read!

Steady_T

11/28/21 3:11 PM

#337882 RE: jimmy_mcyoloswag #337836

I think this article is less meaningful than it appears on the surface.

The first group identified carries a clearly identified genetic mutation. That doesn't explain the pathway of the disease process. The same can be said of the disease pathway of the other two groups.

These groupings don't describe the mechanism of AD which is very likely to be different in each group and multiple mechanisms within the last more general grouping.

It is looking more and more like AD is a group of symptoms that are similar in outcome. The symptoms most like arise from a number of different causes and may take different pathways that have the same end result.

The genetic markers identified provide clues as to where to go looking for the disease pathway involved. They don't tell what the disease mechanisms are.

The focus on A beta has been a focus on one of the few tangible physiological results available in AD research. Only recently have other means of identifying AD begun to be available. Technology has advanced a huge amount in the last 10 years and that makes research into the pathways of AD possible that simple were not possible prior.