Objective. To study the effects of the adamantane derivative hemantane on the bioelectrical activity of mouse brain structures at the early and late (advanced) stages of an experimental model of Parkinson’s disease (PD). Materials and methods. PD was modeled experimentally in C57BL/6J mice using 30 males weighing 25–32 g given systemic (i.p.) proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) using two regimens corresponding to different clinical stages of the disease: four doses of MPTP at doses of 12 and 20 mg/kg with intervals of 2 h. Results. The early and late clinical stages of the experimental model of PD showed EEG desynchronization, increases in wave amplitude, and increases in the power spectrum in the δ and β frequency ranges at the late symptomatic stage of experimental PD, along with a decrease in bioelectrical activity in the 4–12 Hz range in the brain structures of mice (sensorimotor cortex, substantia nigra, and caudate nucleus). Prior use of hemantane at a dose of 20 mg/kg at both the early and late clinical stages of PD prevented excessive increases in the amplitudes of all wave groups, normalized θ activity in the 4–12 Hz range, and reduced pathological slowing and dysregulated activity in the δ and β wave ranges, these effects being dominant in the substantia nigra of the brain. Conclusions. The effects of hemantane were more marked at the initial clinical stage of the experiment model of PD than at the late (advanced) stage.