**5. Conclusions**

This study demonstrated that SBE possesses antioxidant and neuroprotective effects against a β-amyloid induced memory loss model. Amyloid beta generates oxidative stress as an early event in AD and causes tau phosphorylation, mitochondria dysfunction and ROS generation. Consecutively, it leads to apoptosis and neurodegeneration. SBE treatment ameliorates memory deficits and improves learning and memory function. SBE also exhibited remarkable neuroprotective effects against Aβ 1–42 induced neurotoxicity via the apoptosis pathway (Figure 8). This study offers SBE at a dose of 100 mg/kg which suggests the possibility of development as a health functional food for the improvement of learning and memory impairment.

**Figure 8.** The proposed mechanism by which SBE ameliorates learning and memory in mice following an injection of amyloid-β 1–42 (Aβ 1–42).

**Author Contributions:** H.J.L. conducted the experiments and participated in the interpretation and writing of the manuscript. D.Y.L. and H.L.K. performed the data analysis and quality control assessment respectively. S.H.Y. planned and led the project, and contributed the data review, editing and manuscript finalization. All authors have read and agreed to the published version of the manuscript.

**Funding:** This study was carried out with the support of the 'Cooperative Research Program for Agriculture Science and Technology Development (Project no. PJ013215012020)' Rural Development Administration, Republic of Korea.

**Conflicts of Interest:** The authors declare no conflict of interest in this study.
