article · Journal of Experimental and Clinical Anatomy
Age-related neurodegenerative conditions such as Alzheimer's disease involve progressive neuronal decline and cognitive impairment. In laboratory research, combining aluminium chloride and D-galactose induces neurotoxicity and senescence, creating an animal model to study these mechanisms. An aqueous leaf extract of Ziziphus mauritiana was tested across two dosages in male Wistar rats subjected to this chemically induced cognitive dysfunction, comparing outcomes against the standard drug donepezil. Rats exposed to the neurotoxins displayed reduced cognitive performance in T-maze tests, elevated levels of the oxidative stress marker malondialdehyde, and neuronal degradation in brain tissue. Administration of the plant extract significantly improved cognitive alternation scores, lowered malondialdehyde concentrations, and helped restore brain cytoarchitecture. These results demonstrate that Ziziphus mauritiana leaf extract counteracts oxidative damage and preserves neuronal structure, indicating therapeutic potential for managing cognitive deficits associated with neurodegenerative conditions.
Neurodegenerative disorders such as Alzheimer's disease present a major health challenge linked to aging and cellular damage. Identifying natural compounds that protect neurons and sustain cognitive abilities offers alternative routes for treatment development. Demonstrating that an extract from Ziziphus mauritiana leaves reduces oxidative markers and repairs tissue damage in rodent models strengthens the evidence base for investigating botanical substances in neurodegenerative disease management.
This research represents early-stage preclinical work conducted exclusively in animal models. The findings could eventually interest pharmaceutical developers, nutraceutical manufacturers, or herbal medicine researchers seeking candidate compounds to combat neurodegeneration. However, practical application remains distant, requiring constituent compound isolation, pharmacokinetic evaluation, safety testing, and human clinical trials before any commercial or therapeutic product can be realised.
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Background and Aim: Neurodegenerative diseases are a group of disorders characterized by the progressive degeneration of neurons in the brain and spinal cord. Age-related cognitive dysfunctions, notably in conditions like Alzheimer’s disease (AD), are closely linked to neurotransmission abnormalities. Aluminium (Al) been the third most abundant metal that constitutes about 8% of the total earth crust has been known for its neurotoxic effects, while D-galactose (D-gal) a type of sugar that reacts with the free amines of amino acids in proteins induces senescence. The combination of AlCl3 and D-gal has been explored to induce neurotoxicity thus providing a model for studying the mechanism of AD. Ziziphus mauritiana (ZME) leaf extract a natural fruit rich in various nutrients and compounds including vitamin C, potassium and other minerals such as phosphorus, zinc and magnesium has enhanced cell proliferation and neuroblast diffentiation in dentate gyrus in middle-aged rodents. This study explores the therapeutic potential of ZME in rat models with cognitive dysfunction induced by Aluminium Chloride (AlCl3) and D-gal. Methodology: Thirty-five healthy male Wistar rats weighing between 150–200 g was administered with D-gal (60 mg/kg intraperitoneal) and AlCl3 (200 mg/kg orally). Subsequently, the rats in groups 4 and 5 received ZME (100 mg/kg and 50 mg/kg/day) while the positive control (donepezil) were treated with 1 mg/kg in addition to AlCl3 200 mg/kg and D-gal (60 mg/kg. Cognitive function was evaluated using the T-maze test. Oxidative stress biomarker; malondialdehyde (MDA), was measured, and brain histology was assessed to evaluate neuronal integrity. Results: The high dose (100 mg//kg) and low dose (50 mg/kg) of Ziziphus mauritiana showed a significant level of high percentage spontaneous alternation compared with the rats in the model group. Results of the current study indicated significant cognitive impairments and neuronal loss in rats exposed to AlCl3 and D-gal (model), accompanied by elevated MDA levels in the brain (p < 0.05). However, ZME treatment mitigated these cognitive deficits by reducing the MDA levels and restoring brain cytoarchitecture. Conclusion: The biochemical profiles of the ZME-treated rats suggested its therapeutic potential in treating AD-related cognitive impairments.
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DOI: 10.4314/jeca.v22i2.23
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