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PARK(ing) time–How park deficiency affects the biological clock in a Drosophila model of Parkinson's disease
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DOI：10.1002/1873-3468.70389.png)
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Abstract
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Sleep and circadian disruptions are early symptoms of Parkinson's disease (PD), which is one of the most common neurodegenerative disorders. However, PD has an idiopathic origin, and the factors accelerating the progression of symptoms are not fully understood. One genetic factor associated with PD is a mutation in the parkin gene, which impairs mitophagy and increases oxidative stress. In this research, we used Drosophila melanogaster as a model of PD, employing both a park1 mutant and cell-specific park silencing, and followed the progression of main clock disruption. Our data suggest that pacemaker neurons are sensitive to oxidative stress, and increased ROS levels disrupt daily changes in the morphology of their termini, affecting circadian network communication and sleep regulation.
Keywords:
circadian clock
Drosophila melanogaster
oxidative stress
Parkinson's disease
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