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Current treatments for Parkinson’s disease (PD) only alleviate symptoms doing little to inhibit the onset and progression of the disease, thus we must research the mechanism of Parkinson’s. Rotenone is a known inducer of parkinsonian conditions in rats; we use rotenone to induce parkinsonian cellular conditions in Dictyostelium discoideum. In our model we primarily focus on mitochondrial dynamics. We found that rotenone disrupts the actin and microtubule cytoskeleton but mitochondrial morphology remains intact. Rotenone stimulates mitochondrial velocity while inhibiting mitochondrial fusion, increases reactive oxygen species (ROS) but has no effect on ATP levels. Antioxidants have been shown to decrease some PD symptoms thus we added ascorbic acid to our rotenone treated cells. Ascorbic acid administration suggests that rotenone effects may be specific to the disruption of the cytoskeleton rather than the increase in ROS. Our results imply that D. discoideum may be a valid cellular PD model and that the rotenone induced velocity increase and loss of fusion could prevent mitochondria from effectively providing energy and other mitochondrial products in high demand areas. The combination of these defects in mitochondrial dynamics and increased ROS could result in degeneration of neurons in PD.
Chernivec et al. (Thu,) studied this question.