Anavex Life Sciences Corp (AVXL)

[blu_1]

OK, what you say makes sense mostly it is what I figured too. So, toxic a-beta gets produced even by normal cells at homeostasis. Cells eject a-beta into the extracellular space where they clump with other a-beta. Normal cells produce enzymes that (I assume?) go extracellular and can then help digest the a-beta and amyloid? But, in a stressed cell not at homeostasis, those enzymes are misfolded and then can't do their job. Is this summary correct? If so, Anavex should have spelled this out long time ago! a-beta formation

Caveat - I also know the endoplasmic reticulum (ER) functions to get rid of waste proteins, besides just packaging proteins. A cell not at homeostasis will lose the ability of the ER's to break down waste proteins I'm guessing. I thought maybe this aspect is why the a-beta could persist; however, right after a-beta is formed in the plasma membrane, it is ejected from the cell so I assume the ER wouldn't then be able to digest a-beta? It has to get digested some other way? Need to research how it is normally gotten rid of. Do specialized cells do this, do enzymes go extracellular to act on a-beta and amyloid in space, etc?

As an aside, damaged prions inside neurons act like a-beta. They can cause CJD (Creutzfeldt-Jakob disease) in elderly people. Damaged prions also cause Mad Cow Disease, which can affect even teens and punch holes in their brains. The prions act like infectious agents, spreading from cell to cell. I wonder, if damaged prions act like a-beta, why can't a teen's brain, assuming it's healhty, get rid of the prions? Maybe the teens that died were in the minority of teens whose neurons weren't at homeostasis and thus couldn't deal with the prions? IDK.

amyloid and Tau formation