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The aim of this study is to evaluate the neuroprotective role of farnesol against rotenone induced neurotoxicity in Drosophila melanogaster by survival rate study, negative geotaxis assay and estimation of in vivo antioxidant parameters. To induce neurotoxicity in flies, 500µmol of rotenone was used. After successful induction the flies were treated with 300 µmol and 600 µmol of farnesol for the duration of experimental period. The survival rate study was carried out to estimate the effect of farnesol on longevity of flies and negative geotaxis assay was carried out to determine the effect of farnesol on locomotor function of flies. The results indicated that 300 µmol and 600 µmol of farnesol extended the longevity and locomotor functions of the flies in a dose dependent manner. The in vivo antioxidant studies revealed that farnesol increased the activity of catalase and SOD and decreased lipid peroxidation. Based on the effect of farnesol on survival rate, longevity assay and antioxidant assay, we conclude that farnesol might possess significant neuroprotective property.

Oxidative stress-induced neuronal damage plays a significant role in pathogenesis of several neuro-degenerative disorders including Huntington’s disease. In Huntington’s disease, oxidative stress-induced neuronal damage is reported to be mediated by PGC-1α and microglial cells. This development led to various clinical trials that tested the efficacy of several exogenous antioxidants such as vitamin E, vitamin C, etc. to prevent the oxidative stress-induced cell damage in several neuro-degenerative disorders. But these randomized clinical trials did not find any significant beneficial effects of exogenous antioxidants in neuro-degenerative disorders. This forced scientists to search endogenous targets that would enhance the production of antioxidants. Nrf2 is one such ideal target that increases the transcription of genes involved in production of antioxidants. Nrf2 is a transcription factor that controls the expression of antioxidant genes that defend cells against oxidative stress. This chapter focuses on the role of oxidative stress in Huntington’s disease and explores the therapeutic benefits of Nrf2 activators.