The reason for the sn-1 specificity is unclear although loss of ApoE, a risk factor associated with AD, has been shown to alter the traffic of polyunsaturated lipids from astrocytes to neurons, biasing the composition of long-chain fatty acids in synaptosome PCs toward fully saturated (16:0) species in null-mutant mice (Igbavboa et al., 2002) (Figure 3B, Table S2). This evidence concerns the gene APOE and Alzheimer disease.