A study by Elharram et al. has demonstrated that, in an oxidative stress-dependent mouse model of age-related cognitive impairment with AD-like biochemical and structural pathologies with deletion of the aldehyde dehydrogenease 2 gene (Aldh2-/-), treatment with D-PUFAs for 18 weeks evoked an approximate 55% decrease of F2-isoprostanes (F2-IsoPs) and 20–25% decrease of prostaglandin F2α (PGF2α) in both the cortex and hippocampus, as compared to H-PUFA-treated Aldh2-/- mice for 18 weeks. Here, ALDH2 is linked to Alzheimer disease.