This study was carried out to investigate the physiological processes through which lutein affects anxiety and depression behavior in Scopolamine-treated animal models. 30 male Wistar rats (105g-153g) were randomly assigned to six groups. Group 1: Negative Control, Group 2: Scopolamine only treated group, Group 3: Scopolamine + Lutein (20mg/kg), Group 4: Scopolamine + Lutein (40mg/kg), Group 5: Scopolamine + Lutein (60mg/kg), Group 6: Scopolamine + Imipramine (standard drug). scopolamine was administered intraperitoneally and lutein orally. The data was analyzed using one way ANOVA followed by Post hoc Fischer’s LSD. Multiple comparison values were considered significant at P<0.05 Results. The administration of Scopolamine led to decreased acetylcholinesterase (AChE) concentration in Group 2 (P < 0.0001) and Group 3 (P < 0.01) when compared to the control group. The combined use of lutein and imipramine preserved Acetylcholinesterase levels between Groups 4, 5 and 6 after brain treatment. Brain-derived neurotrophic factor (BDNF-α) experienced a significant decrease in Groups 2 and 3 (P < 0.0001) together with Group 4 (P < 0.001) whereas the levels in Groups 5 and 6 remained comparable to the control. Nitric oxide (NO) levels significantly increased in Group 2 (P < 0.01) but remained unchanged in Groups 3-6 compared to the control. The findings established that while scopolamine negatively affected AChE and BDNF-α levels, lutein and imipramine mitigated these effects. Scopolamine caused a decrease in neurotrophic factors (BDNF-α, AChE) and also increased the level of oxidative marker (NO) and depressive like behaviors. Lutein treatment, at moderate (40 mg/kg) and high (60 mg/kg) doses effectively normalized these biomarkers and augmented neurotrophic signaling.