IV Prostaglandin D₂
　　Eicosanoids are divided into two groups according to their mechanism of action: the conventional eicosanoids, e.g., prostaglandin D₂ (PGD₂) and PGE₂, the cyclopentenone-type PGs, e.g., PGJ₂ and PGA₂. PGD₂ and PGE₂ are further dehydrated to produce PGJ₂ and PGA₂, respectively. Once AA has been supplied, both isoforms of COX form PGG₂ and PGH₂ via identical enzymatic processes (Figure 3). Following these steps, PGH₂ can be metabolized by different enzyme pathways to a range of products with potent biological effects. The profile of products made by cells expressing
COX-1/COX-3 or COX-2 is therefore determined by the presence of different downstream enzymes. Eicosanoids modulate cellular function during a variety of physiologic and pathologic processes
　　In the frontal cortex of AD patients, the level of PGD₂ is elevated. Aβ increased PGD₂ transiently before neuronal apoptosis (Figure 4). Neuronal apoptosis was induced PGD₂ at high concentration (Figure 5). However, the toxicity of PGD₂ via its GTP-binding protein-coupled PGD₂ receptors does not occur. First, the PGD₂ receptor blocker did not inhibit PGD₂-induced neuronal cell death (Figure 5). Second, little mRNA of the PGD₂ receptor is observed in the rat and human cerebral cortex. Third, few binding sites of [³H]PGD₂were detected in the plasma membranes from rat cortices (Figure 6). Fourth, the LD₅₀ value (8.2 μM) of PGD₂ is much higher than the affinity for PGD₂ receptor (dissociation constant = 14 nM). Finally, PGD₂ required a latent time to exert toxicity.