Table 1.
Types of PL Form | Model System | Treatment and Duration | Findings | References |
---|---|---|---|---|
1-DHA-LPC 2-DHA-LPC |
adult mice | 1 mg/d (oral administration); 1 month |
-Increased the percentage of DHA and C20:4 in the plasma -Improved DHA level and C22:6/C20:4 ratio in all regions of the brain -LPC-DHA treatment remarkably improved memory and spatial learning -Increased molecular species of DHA-PC, DHA-PE in the plasma and BNDF level (brain derived neurotrophic factor) in all brain regions |
[14] |
sn-1 LPC-EPA | adult mice | 1 mg DHA per d or ∼40 mg/kg body weight | -Improved memory and cognition. -LPC-EPA in the brain increased from 0.03 to 4 μmol/g (>100-fold) -Little effect on free EPA -DHA was increased 2-fold by LPC-EPA but not by free EPA. -LPC-EPA also increased DHA concentration in the retina and improved brain-derived neurotrophic factors in the brain |
[15] |
Labelled LPC | adult squirrel monkeys | 1.36 μmol | -LPC in the plasma is taken up by the brain, metabolized in brain tissue and acts as a precursor of PC and choline | [96] |
LPC-DHA | APOE3- and APOE4-TR mice | 4 to 12 months | -LPC-DHA-enriched krill oil could increase DHA level in the brain -Improved memory relevant behaviour -LPC-DHA supplements could be preventive for some level of age-related neurodegeneration |
[16] |
LPC | adult mice | - | -Revealed the protection against LPC-induced demyelinating lesion and cognitive deficits -Could be a feasible and promising therapeutic treatment against demyelinating diseases |
[97] |
LPC-DHA | expectant mice | DHA-LPC (68.8 mg/mL, oral administration); 4 d | -Improved the DHA level in the brain | [98] |