Background: Despite decades of research, neurodegenerative disorders like Parkinson’s disease remain a leading cause of disability worldwide, due to the insufficient reduction of disease burden by available medications. Recently the benefits of dietary supplements like co-enzyme Q10 (CQ10) in neurodegenerative diseases have been reported.
Aim: The protective effects of supplemental CQ10 and possible additive benefits of CQ10/levodopa-carbidopa (LD) in Chlorpromazine (CPZ)-induced Parkinsonism-like changes in mice were investigated.
Methods: Male mice were assigned to ten groups of 30 mice each. Groups are: Vehicle control (fed standard diet (SD), and given intraperitoneal (ip) plus oral saline), LD group (fed SD, and given ip saline plus oral LD), two groups fed CQ10-supplemented diet (at 60 and 120 mg/kg of feed), and given ip plus oral saline, CPZ group (fed SD, and given ip CPZ plus oral saline), CPZ/LD group (fed SD, and given ip CPZ plus oral LD), two groups fed CQ10-supplemented diet (at 60 and 120 mg/kg of feed) and given ip CPZ plus oral saline, and another two groups fed CQ10-supplemented diet (at 60 and 120 mg/kg of feed) and given ip CPZ plus oral LD. Total duration of study was 21 days, and treatments were administered daily. Body weight and food intake were measured weekly while, neurobehavioural and biochemical tests were assessed at the end of the experimental period.
Results: CQ10-supplementation was protective against CPZ-induced parkinsonism-like changes including, reduction in mortality, reversal of retardation of open-field behaviours and reduction of catalepsy, increase in dopamine levels and decreased oxidative stress. CQ10 also showed significant improvements in these parameters when co-administered with LD. CQ10 (in groups administered CPZ/CQ10 60 mg/kg of feed) showed greater benefit over LD on anxiety-related behaviours and also had additive benefits on working-memory.
Conclusion: Dietary CQ10-supplementation was associated with demonstrable benefits in CPZ-induced Parkinsonism-like changes in mice.