In our present study, the results indicated that the levels of UCP4 and UCP5 mRNA were significantly increased in SAMP8 model mice relative to SAMR1 controls (Figures 2(e)–2(h)), suggesting that compensatory increases in UCP gene expression may be utilized as a cytoprotective mechanism to compensate for the increased level of oxidative stress in an early-stage of AD pathogenesis. Here, SLC25A27 is linked to Alzheimer disease.