Abstract
<jats:p> Parkinson′s disease is predominantly characterized by dopaminergic neurodegeneration linked to toxic aggregation of α–synuclein. Genipin, a bioactive iridoid, was previously shown to improve the motility and survival deficits caused by pan-neuronal expression of native α-synuclein in a transgenic <jats:italic>Drosophila melanogaster</jats:italic> model system. We show that expression of α–synuclein causes sleep deficits and that genipin treatment rescued these sleep deficits, increasing total sleep and consolidating nighttime sleep relative to untreated α–synuclein—xpressing fruit flies. Our findings extend genipin′ss protective profile in <jats:italic>Drosophila melanogaster</jats:italic> and highlight sleep regulation as an additional phenotype responsive to α–synuclein—targeted interventions. </jats:p>