Abstract
Drosophila melanogaster has been established as a reliable in vivo model for studying human diseases. However, the varied designs of such studies and the different origins of the strains have significantly contributed to metabolic and molecular differences between strains. Parkinson's disease (PD) is a neurodegenerative disorder involving the loss of dopaminergic neurons, leading to various motor and non-motor symptoms including but not limited to bradykinesia, postural instability, cognitive decline, and gut dysbiosis. Chronic exposure to toxins such as rotenone can induce neuronal cell death. We have developed a sporadic PD model by direct feeding of rotenone-supplemented food to Drosophila melanogaster wild-type strains, which has previously been shown to cause neuronal cell death and used to mimic PD in Drosophila. Upon exposure to rotenone in two wild-type strains (Oregon-R and Canton-S) , differences in their climbing ability and lifespan were monitored. We found that the degree of motor defects upon rotenone exposure is higher in Oregon-R compared to age-matched Canton-S flies. We also observed that the Canton-S flies (rotenone-fed and non-rotenone-fed) exhibited a lower survival percentage than Oregon-R flies. However, the climbing defects in Canton-S flies are not as pronounced as in Oregon-R flies. The mechanism(s) involved in such differential effects in different wild-type Drosophila strains are yet to be explored and may provide a perspective on differential symptoms of PD patients belonging to different demographics.
