Background: Alzheimer’s disease (AD) therapeutic interventions has a lot of limitations and the progression of the disease is alarming globally. There is a need to discover new and natural products such as neem plant with potential antioxidant properties and document their therapeutic mechanism of neuroprotection through which natural products averts memory impairments by evaluating behavioral changes and neuroarchitecural changes in the PFC and hippocampus.
Methods: The twenty (20) healthy adult male Wistar rats used, were grouped as (n=5) groups A-D viz group A: control, B; AD-model C; oral 200mg/kg neem leaf supplement, and D: 200mg/kg neem leaf supplement treated AD model. Neuro-behavioral changes in memory was studied using Y-maze and open field test for object recognition. The brain samples were carefully removed for fixation in 10% formol calcium ready for tissue processing and staining using Haematoxylin and Eosin (H and E) stain, histochemical stain for Nissil bodies using Cresyl Fast Violent (CFV) stain and immuno-histochemical stain using Glial Fibrillary Acidic Protein (GFAP) for astrocytes. Data analysis was done using ANOVA and test for statistical significance set at p<0.05.
Results: Results show that neem leaf supplement reversed the declined spontaneous alternation behaviour, familiar object recognition time, recognition index while increasing novel object recognition and discriminatory index at p<0.05 in the AD model treated with neem leaf when compared with the AD model. These behavioral changes in neem leaf supplement correlates with histomorphological changes in the PFC and CA1 of the hippocampus having the presence of neurons with neurites, lack chromatolysis and reduced proliferation of reactive astrocytes a neuroinflammatory response to neurodegeneration perturbing neural circuit as seen in the AD model.
Conclusion: Neem leaf supplement improves memory by inhibiting progressive proliferation of astrocytes, while boosting immune response for tissue repair that protect against loss of neurons and improve neuron function and connection in the prefrontal cortex and CA1 hippocampal region for memory consolidation
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