Recent studies have shown that Kallikrein-related peptidases (KLKs) play crucial roles in the pathological progression of Alzheimer's disease (AD). This review systematically summarizes the latest research advances in AD-related KLKs (KLK1, KLK6, KLK7, KLK8, and KLK10). Studies have revealed that KLK6 affects amyloid-β (Aβ) generation by inhibiting α-secretase and enhancing γ-secretase activity; KLK7, as an Aβ-degrading enzyme secreted by astrocytes, shows accelerated Aβ deposition in AD model mice when deficient; KLK8 influences the PI3K/Akt/GSK-3β signaling pathway, leading to decreased Akt phosphorylation and increased GSK-3β expression, thereby promoting Tau protein hyperphosphorylation, with significantly higher expression levels observed in female AD patients compared to males. Furthermore, KLKs impair blood-brain barrier function through mechanisms including extracellular matrix protein cleavage and reduction of endothelial cell inflammation. Meanwhile, KLK6 and KLK8 exhibit significantly elevated expression levels in the cerebrospinal fluid and blood of AD patients, suggesting their potential value as biomarkers. A deeper understanding of KLKs' mechanisms in AD will provide new insights into the early diagnosis and treatment of the disease.