Amelioration of Alzheimer’s disease by neuroprotective effect of sulforaphane in animal model

Abstract

Pathophysiological evidences of AD have indicated that aggregation of Aβ is one of the principal causes of neuronal dysfunction, largely by way of inducing oxidative stresses such as free radical formation. We hypothesized that the known antioxidative attribute of SFN could be harnessed in Alzheimer’s treatment. SFN is an indirect, potent antioxidant derived from broccoli that has previously been found to stimulate the Nrf2-ARE pathway and facilitate several other cytoprotective mechanisms. In this study, administration of SFN ameliorated cognitive function of Aβ-induced AD acute mouse models in Y-maze and passive avoidance behavior tests. Interestingly, we found that the therapeutic effect of SFN did not involve inhibition of Aβ aggregation. While the exact mechanism of interaction of SFN in AD has not yet been ascertained, our results suggest that SFN can aid in cognitive impairment and may protect the brain from amyloidogenic damages.

Abbreviations: Aβ, amyloid-β; AD, Alzheimer’s disease; PBS, phosphate buffered saline; DMSO, dimethyl sulfoxide; ROS, reactive oxygen species; SFN, sulforaphane; DMEM, Dulbecco’s modified eagle medium; FBS, fetal bovine serum; ICR, imprinting control region; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; DW, deionized water; ThT, thioflavin T; PA, passive avoidance; ARE, antioxidant response element.

• Acute AD animal model
• Alzheimer’s disease
• amyloid-β
• cell viability assay
• passive avoidance test
• reactive oxygen species
• sulforaphane
• Y-maze test

Acknowledgements

A special thank you to Dr Jeiwon Cho and Medifron (Korea) for the animal test training. We also appreciate Dr Jun-Seok Lee and Young-Hwa Yoo for the Y-maze analysis program and Dr Changjoon Justin Lee for providing the PA instrument.

Declaration of interest: This work was supported by the Korea Institute of Science and Technology (2V02950 and 2E22310).