Objectives: Cuprizone is a neurotoxicant used in modeling demyelinating disorders. This study explored the effects of Moringa oleifera (MO) on oxidative, histomorphological and behavioural changes in cuprizone-damaged cerebellum. Methods: Twenty adult female Wistar rats were grouped into 4, each group having five animals. Group A received 1 ml of normal saline (Control); group B received 0.4% cuprizone; group C received 15.6 mg/kgBW Moringa oleifera leaf extract; group D received 0.4% cuprizone and 15.6 mg/kgBW Moringa oleifera, orally for 5 weeks. The animals were assessed for exploratory and locomotor activities, while the cerebellum was processed for histology and assayed for nitric oxide (NO), catalase (CAT) and superoxide dismutase (SOD) activities. Results: Cuprizone treatment caused weight reduction, disruption of Purkinje cell layer, cellular degeneration, reduction in NO, CAT and SOD activities. However, these changes were ameliorated when co-administered with MO. Conclusion: The anti-oxidative property of Moringa oleifera is responsible for its ameliorative effect in cuprizone neurotoxicity.

Background: Recent evidences suggest that cerebellar degeneration may be associated with the development of Alzheimer's disease (AD). However, previous reports were mainly observational, lacking substantial characterization of cellular and molecular cerebellar features during AD progression. Purpose: This study is aimed at characterizing the cerebellum in rat models of AD and assessing the corresponding neuroprotective mechanisms of Garcinia biflavonoid complex (GBc). Methods: Male Wistar rats were grouped and treated alone or in combination with PBS (ad libitum)/day, corn oil (CO; 2 mL/kgBw/day), GBc (200 mg/kgBw/day), sodium azide (NaN₃) (15 mg/kgBw/day) and aluminium chloride (AlCl₃) (100 mg/kgBw/day). Groups A and B received PBS and CO, respectively; C received GBc; D received NaN₃; E received AlCl₃; F received NaN₃ then GBc subsequently; G received AlCl₃ then GBc subsequently; H received NaN₃ and GBc simultaneously while I received AlCl₃ and GBc simultaneously. Following treatments, cerebellar cortices were processed for histology, immunohistochemistry and colorimetric assays. Results: Our data revealed that cryptic granule neurons and pyknotic Purkinje cell bodies (characterized by short dendritic/axonal processes) correspond to indistinctly demarcated cerebellar layers in rats treated with AlCl₃ and NaN₃. These correlates, with observed hypertrophic astrogliosis, increased the neurofilament deposition, depleted the antioxidant system-shown by expressed superoxide dismutase and glutathione peroxidase, and cerebellar glucose bioenergetics dysfunction-exhibited in assayed lactate dehydrogenase and glucose-6-phosphate dehydrogenase. We further showed that GBc reverses cerebellar degeneration through modulation of neurochemical signaling pathways and stressor molecules that underlie AD pathogenesis. Conclusion: Cellular, molecular and metabolic neurodegeneration within the cerebellum is associated with AlCl₃ and NaN₃-induced AD while GBc significantly inhibits corresponding neurotoxicity and is more efficacious when pre-administered.

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