GoodJohnHunting, I was thinking that PS/PE may be part of that study also. Tonight I rented the report , “Plasma phospholipids identify antecedent memory impairment in older adults” and I can’t find any mention of PS or PE in it. I did find phosphatidylinositol (PI)and phosphatidylcholine (PC), however. Even though PS and PE may not be in their ten Lipid panel, I found this statement very familiar: amyloid-ß may “directly disrupt bilayer integrity” by interacting with phospholipids
The Phopholipids are: “We posit that this ten–phospholipid biomarker panel, consisting of PC and AC species, reveals the breakdown of neural cell membranes in those individuals destined to phenoconvert from cognitive intactness to aMCI or AD and may mark the transition between preclinical states where synaptic dysfunction and early neurodegeneration give rise to subtle cognitive changes”
More specifically: “A notable finding of this targeted metabolomic and lipidomic analysis was the identification of a set of ten metabolites, comprising PCs, (PC diacyl (aa) C36:6, PC aa C38:0, PC aa C38:6, PC aa C40:1, PC aaC40:2, PC aa C40:6, PC acyl-alkyl (ae) C40:6), lysophophatidylcholine (lysoPC a C18:2), and acylcarnitines (ACs) (Propionyl AC (C3) and C16:1-OH) that were depleted in the plasma of the Converterpre participants but not in that of the NC group (Fig. 1b). These metabolites remained depleted after phenoconversion to aMCI/AD (Converterspost) and were similar to the levels in the aMCI/AD group”
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 don't even pretend to understand that report beyond that. It is out of your environement rather than mine.
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