Achyrocline satureoides aqueous extract (ASAE) protective effects were evaluated on dopaminergic neurodegeneration induced by reserpine in Caenorhabditis elegans (C. elegans). Strain BY200 was cultured following standard procedure. The worms (L1 stage) were exposed to the treatments, ASAE (10 or 25 mg/ml) or no for 24 hours, followed by the induction of dopaminergic damage (reserpine, 60 µM, positive control; PC) or no (negative control; NC). Worm’s images (n=20) were captured using a fluorescence microscope and quantified using the ImageJ software. The locomotor behavior (body bends) of the worms was evaluated in the presence or absence of food (OP50). Analyzes were performed using one-way ANOVA and Tukey's test. Worms treated only with reserpine exhibited a significant reduction in fluorescence emitted by dopaminergic CEP neurons (3.84±0.12, p ≤ 0.001 vs. NC). ASAE at 25 mg/ml (6.41±1,2, p ≤ 0.001 vs. PC), but not at 10 mg/ml (3.68±0.25, ns p > 0.05 vs. PC), protected against reserpine induced neurodegeneration. When locomotor behavior was evaluated, the NC (0.97±0.5) group showed a different behavior than the PC (0.06 ± 0.17, p ≤ 0.001 vs. NC). The groups pretreated with ASAE (10 and 25 mg/ml) maintained similar behavior to the NC group when exposed to reserpine. Reserpine depleted the dopamine level via vesicular monoamine transporter 2 (VMAT2) blocking, causing dopaminergic neurodegeneration and motor deficits in C. elegans. Our findings showed that ASAE preserves the locomotion rate/food-sensing behavior, and attenuates dopaminergic neuron degeneration, suggesting a potential application in Parkinson's disease.