We observed a significant enhancement in glycerophospholipid abundance in neuronal EVs (NEVs, marked as L1CAM) compared to multi-origin EVs (marked as Tetraspanin-EVs) in control samples (p = 0.023), as well as in the lysophospholipids pool between astrocytic EVs (AEVs, marked as GLAST) and multi-origin EVs in both AD and control samples (p = 0.021 and p = 0.005, respectively). This evidence concerns the gene SLC1A3 and Alzheimer disease.