Since OEA was identified as a pro-longevity compound whose levels were dysregulated in AD plasma and CSF samples [3, 4], we first evaluated whether this is associated with altered expression of PPARα and its activity in aging mouse brains and postmortem AD brain samples, using its downstream target cytochrome P450 family 4 subfamily A (CYP4A) as a readout. Here, PPARA is linked to Alzheimer disease.