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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\n                    <jats:italic>Drosophila melanogaster<\/jats:italic>\n                    as a model of PD, employing both a\n                    <jats:italic>park<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>1<\/jats:italic>\n                    <\/jats:sup>\n                    mutant and cell\u2010specific\n                    <jats:italic>park<\/jats:italic>\n                    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.\n                  <\/jats:p>","DOI":"10.1002\/1873-3468.70389","type":"journal-article","created":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T11:06:14Z","timestamp":1781607974000},"page":"1992-2011","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>PARK<\/scp>\n                    (ing) time\u2013How\n                    <i>park<\/i>\n                    deficiency affects the biological clock in a\n                    <i>Drosophila<\/i>\n                    model of Parkinson's 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