Based on the above-mentioned observations, the aims of the present study were: (1) to assess for the first time the modulation of UCP2 in the brain of high-salt-fed SHRSP versus SHRSR, as well as in two SHRSR/SHRSP-STR1/QTL stroke congenic lines; (2) to explore the impact of PPARα and UCP2 expression modulation by BO and fenofibrate on the stroke susceptibility of high-salt-fed SHRSP; and (3) to explain part of the mechanisms underlying brain UCP2 downregulation upon JD in the stroke-prone strain. This evidence concerns the gene PPARA and stroke disorder.