Alzheimer’s disease (AD) is a progressive neurodegenerative disorder more prevalent among the elderly population. AD is characterised clinically by a progressive decline in cognitive functions and pathologically by the presence of neurofibrillary tangles (NFTs), deposition of beta-amyloid (Aβ) plaque and synaptic dysfunction in the brain. Centella asiatica (CA) is a valuable herb being used widely in African, Ayurvedic, and Chinese traditional medicine to reverse cognitive impairment and to enhance cognitive functions. This study aimed to evaluate the effectiveness of CA in preventing d-galactose/aluminium chloride (d-gal/AlCl3) induced AD-like pathologies and the underlying mechanisms of action were further investigated for the first time. Results showed that co-administration of CA to d-gal/AlCl3 induced AD-like rat models significantly increased the levels of protein phosphatase 2 (PP2A) and decreased the levels of glycogen synthase kinase-3 beta (GSK-3β). It was further observed that, CA increased the expression of mRNA of Bcl-2, while there was minimal effect on the expression of caspase 3 mRNA. The results also showed that, CA prevented morphological aberrations in the connus ammonis 3 (CA 3) sub-region of the rat’s hippocampus. The results clearly demonstrated for the first time that CA could alleviate d-gal/AlCl3 induced AD-like pathologies in rats via inhibition of hyperphosphorylated tau (P-tau) bio-synthetic proteins, anti-apoptosis and maintenance of cytoarchitecture.
Alzheimer's disease (AD) is the most frequent and multifactorial form of dementia, characterised by multiple cognitive impairments and personality changes. Different methods including chemicals have been used to induce AD-like symptoms in rodent in order to screen many therapeutic drugs for a variety of cognitive dysfunctions. Articles from reliable databases such as Google Scholar, Science Direct, PubMed, Scopus, and Ovid were searched and retrieved with the following descriptors: 'Alzheimer's Disease' , Cognitive impairments' , Neurotoxins that induce AD' , Alzheimerogenic chemicals' , excitotoxins' , Amyloid beta' , neurofibrillary tangles. A number of chemicals have been studied to develop an animal model of AD on the basis of their mechanism of action for cognitive dysfunctions. Some of such chemicals are Heavy metals, Scopolamine, Ethanol, Colchicine, Streptozotocin, Lipopolysaccharide, and Okadaic acid among others, with a view to understanding the pathogenesis of this devastating disease. The purpose of this review is to put forward some AD pathophysiology including AD causative theories and also highlight some Alzheimerogenic chemicals for the purpose of enriching our existing knowledge. It is worth mentioning that not all the biochemical, histopathological, cognitive and behavioural abnormalities can be recapitulated. Nonetheless, experimental models of AD produced by chemicals offer insights to unravelling the pathogenesis of the disease.
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