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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 Drosophila melanogaster 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-expressing fruit flies. Our findings extend genipin's protective profile in Drosophila melanogaster and highlight sleep regulation as an additional phenotype responsive to α‑synuclein-targeted interventions.
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