Modulation of brain-kidney crosstalk by olanzapine in aluminum chloride-induced memory impairment: a preclinical investigation.

Abstract

Objective: The study investigated the impact of OLN on cognitive function, oxidative stress, neuroinflammation, and renal functions in a mouse model of aluminum chloride (AlCl₃) induced memory impairment. Twenty-five male mice were divided into five groups: group 1 (control) distilled water (10 mL/kg), group II AlCl₃ (100 mg/kg), group III AlCl₃ + OLN (0.5 mg/kg), group IV AlCl₃ + OLN (1.0 mg/kg), and group V AlCl₃ + Donepezil (1 mg/kg). Treatments were administered orally for seven days. Cognitive performance was assessed via Y-maze and open field test. Post-sacrifice, brain and kidney tissues were harvested and analysed for the levels of malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), tumour necrosis factor-alpha (TNF-α), nitrites, urea, and total protein, alongside histological examination of the hippocampus and prefrontal cortex.

Results: AlCl₃ significantly impaired cognitive and locomotor performance, elevated MDA, TNF-α, nitrite, urea levels, and reduced GSH, CAT, SOD and total protein. Histological studies showed that AlCl₃ caused neuronal loss in the hippocampus and prefrontal cortex. Findings of the study showed that OLN attenuated behavioural and biochemical changes in a dose-dependent manner, and at a higher dose preserved the neurons and enhanced memory and reduces neuroinflammation with effects to comparable to donepezil.