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Objective <p>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&#xa0;mg/kg), group III AlCl₃ + OLN (0.5&#xa0;mg/kg), group IV AlCl₃ + OLN (1.0&#xa0;mg/kg), and group V AlCl₃ + Donepezil (1&#xa0;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.</p> Results <p>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 AlCl<sub>3</sub> 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月1日

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  • Lawrence D. Adedayo,
  • Timothy O. Emmanuel,
  • Akinolu E. Adeleke,
  • Saminu Samaila,
  • Gideon O. Ayilara,
  • Olubayode Bamidele,
  • Gideon B. Ojo,
  • Nimedia G. Aitokhuehi,
  • Ovayoza O. Mosugu,
  • Iliya Ezekiel,
  • Ejike D. Eze

摘要

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.