**5. Conclusions**

This study concludes that Aβ (25–35) caused diminished ERα levels, which mediated estrogen actions to disrupt normal cell cycle regulation and thus potentiates cell death. S-equol might act as a putative neuroprotective agent against Aβ (25–35) cytotoxicity, and its neuroprotective role might be, at least in part, attributed to its estrogenic potency. The observed putative neuroprotective effects of equol were associated with sustaining ERα levels and cell survival in our cell models. Furthermore, the molecular mechanism underlying this putative neuroprotection of S-equol is shown to involve the suppression of cell cycle reentry which might be synergized with ERα-involved activation of ERK 1/2 along with the prevented activation of cyclin D1.

**Author Contributions:** Conceptualization, M.-C.T., S.-H.L., K.H., and C.-I.L.; methodology, S.-H.L., K.H., and C.-I.L.; software, S.-H.L. and K.H.; validation, M.-C.T., S-H.L., K.H., and C.-I.L.; formal analysis, S.-H.L. and K.H.; resources, M.-C.T. and S-H.L.; data curation, S.-H.L., K.H., and C.-I.L.; writing—original draft preparation, review, and editing, C.-I.L.; supervision, M.-C.T. and S.-H.L.; project administration, M.-C.T. and C.-I.L.; funding acquisition, M.-C.T.

**Funding:** This study was funded by the Research Program of Taoyuan General Hospital, Taiwan; grant number PTH10542.

**Conflicts of Interest:** The authors declare that there is no conflict of interest regarding the publication of this paper.
