First, the OP seems to be about how to increase omega3 levels in the brain. If I've misinterpreted, please say so.

Second, I completely agree with the statement that the phospholipid (especially lysophospholipid) forms of omega3 have greater ability to get across the BBB and increase brain and CSF levels of omega3.

It isn't what is ingested, it's what happens when it gets digested. What happens when it gets into the enterocyte of the intestines. The LPC-omega3 gets turned into TAG-omega3.

I'm not saying the ND product doesn't contain LPC-omega3**. I think it is very easy to find EPA/DHA food and supplements that contain the LPC form. You can buy eggs from chickens fed flaxseed or fish byproducts which contain a fair amount of LPC-omega3. Biology puts LPC-omega3 into reproductive products like eggs in pretty much all species. Eat salmon roe, for example, and get a lot of LPC-omega3. Look in Table 2, column "%PL" of reference (7) to find a lot of different foods that contain various LPC-omega3 amounts. The problem is the oral route of _any_ form of omega3 requires transit across the epithelial membrane into the enterocyte and packaging into lipid droplets and chylomicrons for subsequent transport into lacteals then lymph then blood.

The process of packaging the, for example, LPC form breaks down the attachment of the, for example, DHA ligand from the LPC portion of the molecule and then re-attaches the DHA to triacylglycerol (TAG) in the transport of lipid molecule through endoplasmic reticulum (ER) then Golgi apparatus. The TAG-DHA coalesces into lipid droplets inside the enterocytes, rolls along the ER, gets some apo proteins attached then moves into the lacteals, etc.

Here's a good review including a diagram in Figure 2 that summarizes the process of oral lipid intake:

(9) https://sci-hub.se/https://doi.org/10.1038/s41575-019-0250-7 "Regulation of intestinal lipid metabolism: current concepts and relevance to disease" (2020) Here's what it says about LPC-lipids:

"Lysophospholipids released from dietary and biliary phospholipids cross the enterocyte membrane by pas­sive diffusion21. Absorbed lysophospholipids are asso­ciated with caveolin 1­-containing endocytic vesicles loaded with fatty acids and participate in intracellular lipid trafficking. Association of lysophospholipids with the surface of the vesicles activates protein kinase Cζ (PKCζ). Activated PKCζ leaves the vesicles and targets these to the ER, where the fatty acids are unloaded as substrates for TAG re­esterification74. Re­esterification of lysophospholipids to phospholipids at the ER is necessary for the subsequent process of lipid transport."

Most oral lipids get mostly re-esterified to TAG form. I think some probably make it through as LPC-lipid (or whatever was originally ingested) but it isn't much because of the transport packaging mechanism/process. Figure 1 in reference (9) shows the structure of lipids. The EPA/DHA part are the "fatty acid side chain" part. The LPC (or TAG or...) are the carriers. In Figure 1a, the three omega3 ligands are in position sn1, sn2 and sn3. In Fig.1c, the positions are sn1 and sn2.

References (2), (3) and (8) describe the difference in blood levels of, for example, DHA possible when the sn1 position of the LPC-DHA is treated with a lipase. The lipase treated molecule then protects the sn2 position from further PLA2 breakdown. Reference (3) shows stack graphs comparing DHA levels for diets consisting of chow, chow + DHA and chow + lipase-treated DHA. The chow + DHA does show more DHA than just chow. The lipase-treated DHA is much, much higher.

Getting the lipid into the non-brain/CSF part of the body is pretty much the same for all forms. Getting lipid into the brain/CSF takes either free fatty acid or phospholipid (which includes LPC) form. Mammals can produce LPC-omega3 through the PEMT part of the metabolic cycles. Reproductive age females have much more active PEMT cycles especially when producing eggs, growing fetuses or producing milk. Even when not performing reproductive activities, female PEMT cycles are more active than in males or menopausal females.

Unless an omega3 product specifically addresses the enterocyte digestion mechanism (conversion by PLA2 or other protein kinase to mostly TAG), it isn't going to substantially increase BBB accessible omega3.

The Evonik product you reference isn't an LPC-omega3. It's a lysine salt of omega3 that purports to preferentially create free form fatty acid instead of TAG. The referenced article also does not measure ability to get across the BBB. Here's the referenced research article in full:

In vitro dissolution behaviour and absorption in humans of a novel mixed L-lysine salt formulation of EPA and DHA (2021)

Keep the PEMT cycle working well and eat omega3 oil containing foods (or take supplements of some omega3 form) to get whatever absorbed omega3 converted to phospholipid-omega3 (including LPC-omega3) which will get across the BBB/CSF.

Edit: ** The ND product contains a lysine salt of DHA/EPA. It is not LPC.