Indeed, based on the evidence to date, reductions in free proresolving oxylipins characterized in AD could not be attributed to their synthetic enzymes (12/15-LOX, 5-LOX, and sEH), as these enzymes were shown to increase (rather than decrease) in both rodent models of AD (23, 34) and in human AD postmortem brain (17, 18). This evidence concerns the gene ALOX5 and Alzheimer disease.