Progress in the Study of the Pathogenesis of AD and Its Treatment Based on Lecanemab

Alzheimer's disease (AD), the world's premier neurodegenerative disease, has long lacked effective disease-modifying therapies for its core pathological mechanisms - -amyloid (A) deposition and tau protein tangles. In recent years, research breakthroughs have focused on anti-A monoclonal antibodies, among which Lecanemab has become the first disease-modifying drug fully approved by the FDA by targeting soluble A protofibrils, with a significant delay in cognitive decline of 27% (CDR-SB) and a manageable risk of ARIA (11.6%) in Phase III. However, the lack of dynamic monitoring technology, the uncertainty of long-term safety, and the cost-effectiveness paradox remain unresolved. This paper systematically analyses Lecanemab's mechanism of action (selective removal of protofibrils), clinical evidence (dose-response and safety in phase II/III trials), and integrate a biomarker (p-tau217) driven stratification strategy with the ARIA risk management framework. It was found that precision interventions for toxic A subtypes can reshape treatment regimens, but need to be combined with tau-targeted therapies to enhance late-stage efficacy. This review provides three major references for precision therapy in AD: establishing the stratification value of early biomarkers, optimising risk-benefit assessment models, and revealing pathways for combination therapy potentiation. In the future, plasma protofibril detection technology needs to be developed, APOE genotype-oriented ARIA prediction algorithms need to be established, and low-cost delivery systems need to be explored to enhance accessibility.