Aim: Several reports have shown environmental neuron toxins such as aluminium to accumulate in the brain, potentially triggering neurodegenerative disorders. Adansonia digitata (Baobab) has been reported to possess beneficial properties. This study, assessed the neuroprotective properties of aqueous fruit pulp extract of Adansonia digitata (AEAD) on aluminum chloride (AlCl3) – induced memory dysfunctions and hippocampal changes in Wistar rats. The neuroprotective effects of AEAD were assessed with the Morris water maze for learning and memory, oxidative stress biomarkers glutathione (GSH), superoxide dismutase (SOD), and Malondialdehyde (MDA), and histopathological changes on the hippocampal CA3 region using histological techniques. Materials and Methods: Thirty male Wistar rats (110 and 150 g) were divided into six groups at random (n=5). The Control group, the animals in Group 1 received 2 ml/ kg distilled water. Group 2 received 100 mg/kg of AlCl3. Ascorbic acid at a dose of 595 mg/kg was given to Group 3. 100 mg/kg AlCl3 and different concentrations of the AEAD (500 mg/kg and 1500 mg/kg, respectively) were given to groups 4 and 5. Group 6 received 595 mg/kg of ascorbic acid and 100 mg/kg of AlCl3. Results: The latency time spent to locate the escape platform in the Morris water maze test was observed with remarkable (P<0.05) improvement in the AEAD treatments compared with the AlCl3- treated group. There was a notable increase in MDA levels and a reduction in SOD and GSH activities in the AlCl3-treated group in relation to the AEAD-treated groups. Histopathological examination of the CA3 hippocampal region treated with AlCl3 revealed neurodegenerative changes, whereas, administration of AEAD ameliorated AlCl3-induced neuronal damages in rats at doses 500mg/kg and 1500mg/kg when compared with the AlCl3-treated group. Conclusion: Aqueous fruit pulp extract of Adansonia digitata demonstrated a possible neuroprotection against aluminium chloride-induced memory deficit and CA3 hippocampal neurotoxicity.

Aim: Lack of sleep has been linked in studies to increased beta-amyloid levels, oxidative stress, and memory impairments. Furthermore, sleep is known to help clear toxins that accumulate in the brain. This study investigated the restorative potentials of recovery sleep on total sleep deprivationinduced memory impairment, oxidative stress, stress response and changes in beta amyloid plaques in the hippocampus of adult male Wistar rats. Materials and Methods: Twenty-four male Wistar rats weighing between 150 and 200 g were divided into four groups. Group I remained in their home cages, while Groups II, III, and IV underwent sleep deprivation for 5 days. Groups III and IV then had recovery periods of 7 and 21 days, respectively. Spatial learning and memory was measured using the Novel Object Recognition test. The rats were euthanized with ketamine, oxidative stress was analyzed using hippocampal tissue homogenate and beta-amyloid plaques in the CA1 and CA3 regions using Congo red stain. Results: Comparing the sleep-deprived group to the sleep-recovered group, the discrimination ratio increased significantly (p < 0.0001). Sleep recovery also decreased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and malonaldehyde (MDA) and corticosterone (p < 0.01). Additionally, extracellular amyloid-beta expression in the CA1 and CA3 regions of the sleep recovery groups was significantly reduced (p < 0.0001 and p < 0.01). Conclusion: Recovery sleep was found to improve memory and decrease beta amyloid expression and oxidative stress in the CA1 and CA3 areas of the hippocampus.