The most prevalent form of dementia, Alzheimer's disease (AD), is a neurological disorder that causes gradual memory loss. AD is characterized by amyloid-beta plaques, neurofibrillary tangles, and neuron loss. While preclinical and clinical trials are underway to reduce the generation and overall brain disease load, current treatment focuses on alleviating symptoms. Animal studies are essential for advancing our understanding of AD, identifying potential drug targets, and testing experimental therapies. An ideal animal model not only exhibits the same symptoms and pathological changes as a human disease but also follows the same sequence of pathological events. This review highlights the various inducing agents used to model AD in animals, such as streptozotocin, aluminium chloride, trimethyltin, lipopolysaccharide, scopolamine, and others, along with their underlying mechanisms. The outcomes of some studies that used such inducing agents to develop AD are discussed briefly. Among chemically induced models, streptozotocin and amyloid-beta are the most frequently used, while d-galactose, scopolamine, and aluminium-induced models are being used because they are non-invasive, reproducible, and compatible. However, none of the chemical/drug-induced models fully capture the scope of AD pathology and cognitive impairment. Overall, further research is necessary to establish the stability of the models in terms of consistency and reproducibility.
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Khan et al. (2024) studied this question.
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