Parkinson's disease is the second most common
neurodegenerative disease characterized by the loss of dopaminergic neurons in the brain.
Parkinson's disease has both familial and sporadic cases of origin governed differentially by genetic and/or environmental factors. Different epidemiological studies have proposed an association between the pathogenesis of
cancer and
Parkinson's disease; however, a precise correlation between these two illnesses could not be established yet. In this study, we examined the disease-modifying property of dmyc (a Drosophila homolog of human cmyc proto-oncogene) in the
paraquat-induced sporadic
Parkinson's disease model of Drosophila. We report for the first time that targeted upregulation of dMyc significantly restricts
paraquat-mediated neurotoxicity. We observed that
paraquat feeding reduces the cellular level of dMyc. We further noted that targeted upregulation of dMyc in
paraquat-exposed flies mitigates degeneration of dopaminergic neurons by reinstating the aberrantly activated JNK pathway, and this in turn improves the motor performance and survival rate of the flies. Our study provides the first evidence that improved cellular level of dMyc could efficiently minimize the neurotoxic effects of
paraquat, which could be beneficial in designing novel therapeutic strategies against
Parkinson's disease.