Developmental and Neuroprotective Effects of α-Terpineol in MPTP-Induced Parkinsonism in Zebrafish Larvae

Parkinson's disease (PD) is caused by dopaminergic neurodegeneration and α-synuclein aggregation. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), used to replicate PD symptoms, disrupts erythropoiesis, leading to anemia, potentially contributing to dopaminergic neurotoxin-induced developmental toxicity and further investigation into novel therapeutic approaches for reversing PD pathology is strongly advocated. The monoterpene α-terpineol (α-TPN) exhibits several pharmacological effects, including neuroprotection. This study aims to investigate the developmental and neuroprotective roles of α-TPN in a PD model of zebrafish embryos induced by MPTP. Our findings suggest that α-TPN significantly guards early developmental processes, as evidenced by improved survival rates, enhanced hatching rates, stabilized heart rate and amelioration of phenotypic abnormalities. In addition, α-TPN shows strong neuroprotective effects by enhancing locomotor function and improving acetylcholinesterase (AChE) activity in MPTP larvae. Moreover, α-TPN markedly reduces oxidative stress by lowering intracellular reactive oxygen species (ROS), lipid accumulation and apoptotic signatures. Collectively our findings highlight the dual role of α-TPN in promoting healthy development and protecting MPTP toxicity, emphasizing its potential as a therapeutic candidate for PD and related neurodegenerative disorders.