Cognito-Motor and Neuro-Behavioural Modulatory Action of Lutein on BDNF-α Activities in Aluminium Chloride-Induced Memory Impaired Mice

Lutein enhances Cognito-motor and neuro-behavioural processes by modulating BDNF-α activity in a mouse model with memory impairment caused by aluminum chloride (AlCl3). Aluminium chloride neurotoxicity frequently leads to cognitive abnormalities similar to Alzheimer's. Neurotrophin variation of BDNF-α, plays key roles in synaptic plasticity, and cognitive functions. This study aims to evaluate the Cognito-motor and neuro-behavioural modulatory action of lutein on BDNF-α activities in AlCl3-induced memory-impaired mice. 30 adult Mice (30kg) were randomly divided into six groups and treated for three weeks: Group 1 (Negative Control), Group 2 (100mg/kg-AlCl3), Group 3 (100mg/kg-AlCl3 + 20mg/kg-Lutein), Group 4 (100mg/kg-AlCl3 + 40mg/kg-Lutein), Group 5 (100mg/kg-AlCl3 + 60mg/kg-Lutein), Group 6 (100mg/kg-AlCl3 + 5mg/kg-Donepezil). Neurobehavioral activities (Barnes, Y-maze, handgrip and Rotarod) were recorded and analyzed using ANOVA. Ethical approval for this research was obtained from the University of Port Harcourt ethics committee. In Barnes maze test, Group 2 and 3 showed significantly increased escape times (p<0.0001, p<0.05) compared to control for week 2 and 3. Hand grip test showed decreased in grip strength in Group 2 (p<0.0001), and reduced navigation time in Group 3 (p<0.05). Rotarod tests indicated reduced stability time and Y-maze test showed increase in inflexion ratio in Groups 2 and 3. In BDNF-α level, Group 2 and 3 had a significant reduction (p < 0.0001 and p < 0.001) respectively. Aluminum chloride intake reduced BDNF-α level, negatively impacting Cognito-motor performance. Lutein administration increased cognitive and behavioral performance through BDNF-α modulation. The group receiving both treatments showed a notable increase in BDNF-α level and cognitive performance. Hence, lutein significantly mitigates Aluminium Chloride-induced neurotoxicity and cogni-motor dysfunction in mice through antioxidant, anti-inflammatory, and neurotrophic mechanis