Background: Sporadic Alzheimer's disease (SAD) represents one of the major cognitive and memory deficits that is characterized by tau hyperphosphorylation and amyloid beta (Aβ) deposition in the brain. Both are considered AD hallmarks which are mediated through neuroinflammation, oxidative stress, and cholinergic circuit interruption. There are many genetic and chemical induced models of SAD. The most commonly used chemical models are Aβ, D-galactose, and streptozotocin (STZ) models due to their reproducibility of pathologic markers of AD, especially STZ model due to similarity between this model and the pathogenesis of AD in human. Many studies displayed that targeting several pathways apart from the traditional ones could delay the progression of SAD. Aim: This review aimed to highlight the most relevant key findings of different studies through targeting mainly wingless-related integration site (Wnt)/β-catenin and c-Jun N-terminal protein kinase (JNK) pathways against chemically- induced SAD in experimental animals. Conclusion: AD pathways are demonstrated with corresponding some of the recent treatments for those pathways as well as commonly used chemical models and their attributed benefits altogether with limitations.