So even though PS and PE are not in their specific panel, I posit that they DO show up externally on the stressed neural cells, which are becoming Alzheimer’s, just like they do on any/all stressed/sick cells. Therefore I posit that Bavi will have some effect in that disease also. (it helps that PPHM has already mentioned Alzheimer’s and Bavi so it is not a stretch for me to “agree” with them)
I would agree there and a couple publications I came across:
Although much attention has been given to the link between cholesterol and AD pathogenesis, growing evidence suggests that other lipids, such as phosphoinositides and phosphatidic acid, have an important role.
Lipids in Alzheimer’s disease brain (pg 565) ... but interesting reading from 564/565/566...see Table 2.1 also
2 Lipids in Plasma Membranes
Plasma membranes contain a wide diversity of lipids, all of which are amphipathic. There are three main types of membrane lipids: phosphoglycerides, sphingolipids, and cholesterol. Most membrane lipids contain a phosphate group, which makes them phospholipids, and as they are built on glycerol backbone, they are called phosphoglycerides. Membrane phosphoglycerides have an additional group linked to the phosphate, most commonly choline (forming phosphatidylcholine, PtdCho), ethanolamine (forming phosphatidylethanol- amine, PtdEtn), serine (forming phosphatidylserine, PtdSer), or inositol (forming phosphatidylinostol, PtdIns). Each of these groups is small and hydrophilic and together with the negatively charged phosphate to which they are attached, forms a, highly water-soluble domain at one end of the molecule, called the head group. At physiological pH, the head groups of PtdSer and PtdIns have an overall negative charge, whereas those of PtdCho and PtdEtn are zwitterions. Phosphoglycerides most often contain one saturated (a-chain) and one unsaturated fatty acyl chain (b-chain).
My first thought when I think of Phosphatidylserine and Alzheimer's Disease, is that PS is a communicator, or facilitator between cognitive intactness to aMCI or AD.
In the 10 lipid panel AD article that you provided, this quote was made>>
“directly disrupt bilayer integrity” by interacting with phospholipids"
If this is true, then how is it possible that PS is NOT involved?
How do I come to this conclusion?
Because, it is common knowledge that when asymmetry of plasma membrane occurs, metamorphic changes transpose phospholipids, and asymmetry is lost, which exposes phosphatidylserine externally.
That's a fact jack, and I'm sticking to my theory!!