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Re: blu_1 post# 80808

Wednesday, 11/23/2016 5:02:05 PM

Wednesday, November 23, 2016 5:02:05 PM

Post# of 463610
No, Anavex has not specifically mentioned enzymes, misfolded or otherwise. That’s a molecular chemistry detail that is not specifically characterized in any of the 2-73 studies. But cellular biologists know of this well. No need to mention it. Enzymes are complex proteins, with three structures: primary structure, the simple sequence of constituent amino acids; secondary structure, the twisted or bend arrangements of the amino acid sequences; and lastly the tertiary structure, the complex folding of the coils and other structures of the secondary structure.

Virtually all chemical reactions in any cell occur because of the presence of specific reaction-controlling enzymes, of which there are thousands. Those enzymes are made in ribosomes, which are attached during protein synthesis to the rough endoplasmic reticulum (RER), which is attached to the mitochondria, where ATP’s are available to power the protein-synthesizing reactions. Disconnect the RER from the mitochondria and the attached ribosomes have a difficulty producing well-formed, functioning enzyme proteins. Here’s where 2-73 uniquely works; it functionally reconnects the RER with mitochondria, allowing normalized and fully-functioning enzymes to be made. No other drug does this. With 2-73, no excessive waste proteins are made to clog up and suppress normal neuron function.

No, amyloid plaque proteins are not “misfolded.” They are chemical wastes the neuron failed to discard or dysfunctionally produced. Yes, amyloid plaques lead to neuron dysfunction, resulting in Alzheimer’s symptoms. Presently, most drug companies have been targeting the plaques, presuming their prevention or elimination would be an Alzheimer’s cure. Problem is, no drug effectively does this. Any drug capable of dissolving or disintegrating the plaques is too big and too delicate to cross the blood-brain barrier (and it probably would mess with other good proteins – side effects).

This is crucial. Anavex does not target either amyloid plaques nor A-beta tangles (other protein waste accumulations). Both are seen in virtually every Alzheimer’s case. But Anavex’s approach attacks the problem at its start, even before protein wastes can accumulate; by reconnecting and maintaining (“homeostasis”) proper mitochondrial-RER connections.
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