The concentration of L-PGDS in CSF under normal conditions would be sufficient to prevent the aggregation or promote the disaggregation of Aβ, since the concentration of Aβ40 (981 ± 409 pM) and Aβ42 (73.6 ± 41.8 pM) in AD patients is much lower than that of L-PGDS [42]. This evidence concerns the gene PTGDS and Alzheimer disease.