| Summary: | The majority of dementia is caused by Alzheimer’s disease (AD) that manifests in the familial and sporadic forms. The latter accounts for the most of the cases and is a complex multi-factorial disorder with no cure. Despite the vast growth of animal models, both the transgenic and non-transgenic therapeutic findings for AD seem ambiguous. Streptozotocin (STZ) administration is the most accepted sporadic rodent AD model due to its ability to mimic the sporadic variety in humans. Current literature lacks the information on the underlying mechanism of STZ with the formation of the neuropathological hallmarks of AD. Thus, this study focused on developing a comprehensive review on the mechanism of STZ in inducing diabetogenic effects, insulin signaling dysfunction, neuroinflammation, oxidative stress, cerebral amyloid angiopathy, and cholinergic deficit in AD rodent models. Also, we discussed the considerations that should be made when designing the AD rodent model. © 2022 Informa UK Limited, trading as Taylor & Francis Group.
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