Hydrolysis of TGRLs by LpL present in the circulation results in the release of lipolysis products, including TGRL remnant particles, mono-, di- and tri-acylglycerols, phospholipids and NEFAs. Lipolysis products may influence the inflammatory environment of the brain through two pathways: (i) direct injury to brain microvascular endothelial cells or astrocytes, or (ii) indirect injury to glial cells and neurons through cascades that begin with damaged endothelial cells. In addition, apoE4 associated with TGRL undergoes a conformational change to a more linear species in the presence of TGRL lipolysis products. This conformational change may influence the binding of apoE4 to brain microvascular endothelial cells. Negative effects to the endothelial cells due to the altered apoE4 conformation may disrupt the barrier function of the cerebrovasculature and allow TGRL lipolysis products to access the brain parenchyma, causing damage to neurons and glial cells.