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Alzheimer's disease (AD) is an intricate neurodegenerative disorder characterized by the accumulation of misfolded proteins, including beta-amyloid (Aβ) and tau, leading to cognitive decline. Despite decades of research, the precise mechanisms underlying its onset and progression remain elusive. Cathepsins are a family of lysosomal enzymes that play vital roles in cellular processes, including protein degradation and regulation of immune responses. Emerging evidence suggests that cathepsins may be involved in AD pathogenesis. Cathepsins can influence the activation of microglia and astrocytes, the resident immune cells in the brain. However, cathepsin dysfunction may lead to the accumulation of misfolded proteins, notably Aβ and tau. In addition, dysregulated cathepsin activity may induce an exaggerated immune response, promoting chronic inflammation and neuronal dysfunction in patients with AD. By unraveling the classification, functions, and roles of cathepsins in AD's pathogenesis, this review sheds light on their intricate involvement in this devastating disease. Targeting cathepsin activity could be a promising and novel approach for mitigating the pathological processes that contribute to AD, providing new avenues for its treatment and prevention.