Genipin Alleviates Sleep Deficiencies Caused by α-Synuclein Toxicity in a Drosophila melanogaster Model of Parkinsons Disease

Abstract

Parkinsons disease is predominantly characterized by dopaminergic neurodegeneration linked to toxic aggregation of -synuclein. Genipin, a bioactive iridoid, was previously shown to improve the motility and survival deficits caused by pan-neuronal expression of native -synuclein in a transgenic Drosophila melanogaster model system. We show that expression of -synuclein causes sleep deficits and that genipin treatment rescued these sleep deficits, increasing total sleep and consolidating nighttime sleep relative to untreated -synuclein-expressing fruit flies. Our findings extend genipins protective profile in Drosophila melanogaster and highlight sleep regulation as an additional phenotype responsive to -synuclein-targeted interventions.