ArticleMolecular neurobiology2026
β-Cyclodextrin-Complexed 1,8-Cineole Attenuates Motor Deficits and Preserves Tyrosine Hydroxylase Immunoreactivity in a Reserpine-Induced Mouse Model of Parkinsonism.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic dysfunction and motor impairment. Natural compounds have emerged as promising candidates for neuroprotection and symptomatic relief in experimental models of PD. This study investigated the effects of β-cyclodextrin-complexed 1,8-cineole (CIN) in a reserpine (RES)-induced mouse model of parkinsonism. Male mice were treated with RES (0.1 mg/kg, s.c., every 48 h) and/or CIN (5 mg/kg, p.o., once daily) for 30 days. Behavioral assessments evaluated motor, sensorimotor, and locomotor function. Tyrosine hydroxylase (TH) and α-synuclein immunoreactivity were assessed by immunohistochemistry. Repeated RES administration induced progressive motor and sensorimotor impairments and reduced TH immunoreactivity in mesencephalic dopaminergic nuclei. CIN treatment significantly reduced catalepsy, vacuous chewing movements, and chin tremors and improved sensorimotor performance in the adhesive removal test. These behavioral effects were accompanied by preservation of TH immunoreactivity in the substantia nigra pars compacta (SNpc) and ventral tegmental area (VTA). However, CIN did not significantly alter hippocampal α-synuclein immunoreactivity. These findings indicate that β-cyclodextrin-complexed CIN attenuates motor and sensorimotor deficits and is associated with preservation of dopaminergic markers in a RES-induced mouse model of parkinsonism. These results support further investigation of CIN as a neuroactive compound in experimental models of PD.
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