Background Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by motor impairment, degeneration of nigrostriatal dopaminergic neurons, and pathological α-synuclein accumulation. Current therapies mainly provide symptomatic relief, while disease-modifying treatments remain limited. This study investigated the neuroprotective effects of a traditional medicine formulation composed of Calculus Bovis, Fel Ursi, and Moschus (BUM) in experimental models of PD. Methods The efficacy of BUM pharmacopuncture solution was evaluated in an MPTP-induced C57BL/6N mouse model and MPP⁺-induced Caenorhabditis elegans models. Motor function in mice was assessed using the rota-rod, pole, and grip strength tests. Nigrostriatal dopaminergic integrity was examined by tyrosine hydroxylase (TH) immunostaining in the substantia nigra pars compacta and striatum. In C. elegans , dopaminergic neurodegeneration and α-synuclein accumulation were assessed using BZ555 and NL5901 transgenic strains, respectively. Results BUM significantly improved motor performance in MPTP-treated mice, as evidenced by increased rota-rod latency, reduced pole descent time, and enhanced grip strength. BUM also preserved TH-positive dopaminergic neurons in the substantia nigra and dopaminergic fibers in the striatum. The magnitude of these effects was comparable to that of levodopa. In C. elegans , BUM significantly protected dopaminergic neurons against MPP⁺-induced degeneration and reduced α-synuclein-associated fluorescence. Conclusions BUM alleviates motor dysfunction, mitigates nigrostriatal dopaminergic neurodegeneration, and reduces α-synuclein accumulation across both vertebrate and invertebrate models of PD. These findings suggest that the BUM multicomponent formulation exerts multitargeted protective effects against PD-related pathology, providing a strong rationale for further mechanistic and translational investigations in neurodegenerative disease research.
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Baek et al. (2026) studied this question.
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