Abstract

AbstractBackgroundTo evaluate the antioxidant potential of Neem (Azadirachta indica) leaf supplement in attenuating Alzheimer’s disease (AD) pathology induced by aluminum neurotoxicity (Animal model of AD). Y‐ maze test, neuro‐morphology and astrocytic proliferation will be study in the fronto‐hippocampal and cerebellar cortices to elucidates the therapeutic role of neem leaf in AD pathology.MethodsTwenty (20) adult male Wistar rats were grouped (4 groups, n = 5); Control group (A), Aluminum treated group for 7 days (B), 200mg/kg body weight Neem leaf supplement for 7 days (C), and the AD model post‐treated with 200mg/kg Neem leaf supplement for 7 days (D). Study was done for 14 days via oral administration of study materials. Neurobehavioral test for memory and learning done using Y‐maze test. Excised brain was fixed in 10% formol calcium, processed for Cresyl fast violet (CFV) stain for Nissl (chromatophilic) bodies and astrocytes immunohistochemistry using glial fibrillary acidic protein (GFAP) monoclonal primary antibodies in biotinylated secondary antibodies. Behavioural test data were analyzed using ANOVA, post hoc test and significance set at p<0.05.ResultsAluminum treated group cortical area was characterized by necrosis, chromatolysis, neuropil vacuolations and astrocytes proliferation with impaired memory demonstrated by a reduction in the number of arm entries and spontaneous alternations as compared with the control and neem treated groups. However, these pathological changes were reversed by neem leaf supplementation seen in AD model neem leaf post‐treated group (D) showing an increased number of arm entries and spontaneous alternations, regeneration of neurons and a reduced reactive astrocytes (astro‐gliosis) proliferation.ConclusionNeem leaf supplement neuroprotective and repair role in AD pathological is proposed to be via ameliorating astrocytes mediated neuroinflammatory response via the neuron‐astrocytes interaction and antioxidant role during neuroinflammation induced by aluminum in the fronto‐hippocampal and cerebellar cortices

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