**5. Conclusions**

The present study demonstrates that DIM exerts a neuroprotective action by producing BDNF and antioxidant enzymes through activation of the TrkB/Akt signal pathway in oxidative stress-exposed hippocampal neuronal cells. In addition, DIM ameliorates cognitive ability by maintaining the cholinergic system in scopolamine-exposed mice. These findings reveal a feature of the mechanism for the neuroprotective action of DIM against oxidative stress-induced apoptosis in neuronal cells. Such effects of DIM may provide further information for the application of DIM as a neuroprotective agent for the prevention and treatment of neurodegenerative diseases. In addition, this study may be helpful to establish new diagnostic and theranostic paradigms of neurodegenerative diseases, to explore a new biomarker of the diagnostic criteria of neurodegenerative diseases, and to develop innovative pharmacological protocols for the patients of neurodegenerative diseases. Further animal model studies may be required to confirm the feasibility of the use of DIM as a neuroprotective agent for specific neurodegenerative diseases.

**Author Contributions:** Conceptualization, M.R.K., B.D.L., and J.-M.Y.; methodology, M.R.K.; validation, S.Y.B. and F.Y.L.; formal analysis, B.D.L. and J.-M.Y.; investigation, B.D.L., S.Y.B., and F.Y.L.; data curation, M.R.K.; writing—original draft preparation, J.-M.Y.; writing—review and editing, D.-E.S. and M.R.K.; visualization, J.-M.Y.; supervision, M.R.K.; project administration, M.R.K.; funding acquisition, M.R.K. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2017R1D1A3B03027867).

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