Basic Science and Pathogenesis.

Background: Lead, a pervasive and toxic environmental pollutant, of particular concern is its impact as a trigger for neurodegenerative diseases. Phoenix dactylifera (date palm), has garnered attention due to its pharmacological properties: antioxidant and anti-inflammatory, attributed to its rich flavonoid content. This assessed the therapeutic potentials of n-butanol fraction of P. dactylifera (BFPD) on the behavioral and histomorphology of hippocampus lead acetate (PbA)-induced neurotoxicity in Wistar rats.

Method: Forty-two rats were categorized into seven groups (n = 7). Two experimental phases were employed: Toxicity-phase, and Treatment-phase. Toxicity-phase: all rats received PbA (120 mg/kg), for 14 days, except group one (control); Treatment-phase: group II (sacrificed), group III (Natural recovery), while groups (IV-VII) received (500 mg/kg, 750 mg/kg and 1000 mg/kg) n-BFPD and (100 mg/kg) vitamin C (as reference antioxidant). Treatment was via oral route, which lasted for 28 days. Therapeutic properties of n-BFPD were assessed using Neurobehavioral assessment: Morris water maze performance and Novel object recognition test for (spatial memory, learning, and cognition); Oxidative stress biomarkers were assay using Malondialdehyde [MDA], and Superoxide dismutase [SOD], and microscopic hippocampus examination (CA1 and CA3) using histological and histochemical staining techniques and quantification of Nissl substance stain intensity using a computer running image analysis software (imageJ).

Result: PbA-treated group revealed neurodegenerative changes as remarkable (p<0.05) memory, learning and cognition impairment, elevation MDA levels and decrease in antioxidant enzymes (SOD), and cytoarchitectural distortions evidenced by necrotic nuclei, vacuolation and pyknosis, compared to the control. However, treatment with n-BFPD revealed cognitive improvement in memory and learning; decreased MDA levels and increased SOD activities. Mild distortion-to-relatively normal neuronal cytoarchitecture relative to the control was also observed with n-BFPD treatment.

Conclusion: n-BFPD possesses potential therapeutic properties against PbA-induced neurobehavioural and cognitive deficit and pathological changes which are indicator of neurodegenerative diseases. Keyword: cytoarchitecture, cognition, neurodegeneration.