Passive immunotherapy for Alzheimer's disease (AD) has shown promising results in targeting key pathological features such as amyloid-β (Aβ), tau, and neuroinflammation. Monoclonal antibodies (mAbs) targeting Aβ, such as lecanemab and donanemab, have demonstrated significant efficacy in reducing amyloid plaques and slowing cognitive decline in phase III clinical trials. Lecanemab, approved by the FDA in 2023, significantly reduced cognitive decline and amyloid levels in AD patients. Donanemab also showed substantial amyloid clearance and cognitive benefits in phase III trials. However, these therapies are associated with side effects like ARIA (Amyloid-Related Imaging Abnormalities), which can lead to severe neurological complications. Anti-Aβ mAbs, including aducanumab and gantenerumab, have shown variable efficacy, with aducanumab being conditionally approved by the FDA. The effectiveness of these mAbs is influenced by factors such as the epitope targeted, dose, and patient genetic background (e.g., ApoE ε4 allele). In addition to Aβ, tau-targeting mAbs have been developed to address the neurofibrillary tangles (NFTs) associated with AD. Several mAbs, including gosuranemab, tilavonemab, and semorinemab, have been tested in clinical trials, but most have failed to show significant clinical benefits. However, semorinemab showed some promise in slowing cognitive decline in moderate AD patients. Other tau-targeting mAbs, such as BIIB076, PNT001, and JNJ-63733657, are in various stages of clinical development, with some showing potential in reducing tau pathology. The effectiveness of these mAbs is influenced by their ability to target specific tau epitopes and their capacity to prevent tau aggregation and spread. Despite these advancements, challenges remain in improving the safety and efficacy of passive immunotherapy for AD, particularly in reducing side effects like ARIA and enhancing the ability of mAbs to cross the blood-brain barrier. Ongoing research aims to develop more effective and safer mAbs by modifying antibody structures and improving delivery methods.Passive immunotherapy for Alzheimer's disease (AD) has shown promising results in targeting key pathological features such as amyloid-β (Aβ), tau, and neuroinflammation. Monoclonal antibodies (mAbs) targeting Aβ, such as lecanemab and donanemab, have demonstrated significant efficacy in reducing amyloid plaques and slowing cognitive decline in phase III clinical trials. Lecanemab, approved by the FDA in 2023, significantly reduced cognitive decline and amyloid levels in AD patients. Donanemab also showed substantial amyloid clearance and cognitive benefits in phase III trials. However, these therapies are associated with side effects like ARIA (Amyloid-Related Imaging Abnormalities), which can lead to severe neurological complications. Anti-Aβ mAbs, including aducanumab and gantenerumab, have shown variable efficacy, with aducanumab being conditionally approved by the FDA. The effectiveness of these mAbs is influenced by factors such as the epitope targeted, dose, and patient genetic background (e.g., ApoE ε4 allele). In addition to Aβ, tau-targeting mAbs have been developed to address the neurofibrillary tangles (NFTs) associated with AD. Several mAbs, including gosuranemab, tilavonemab, and semorinemab, have been tested in clinical trials, but most have failed to show significant clinical benefits. However, semorinemab showed some promise in slowing cognitive decline in moderate AD patients. Other tau-targeting mAbs, such as BIIB076, PNT001, and JNJ-63733657, are in various stages of clinical development, with some showing potential in reducing tau pathology. The effectiveness of these mAbs is influenced by their ability to target specific tau epitopes and their capacity to prevent tau aggregation and spread. Despite these advancements, challenges remain in improving the safety and efficacy of passive immunotherapy for AD, particularly in reducing side effects like ARIA and enhancing the ability of mAbs to cross the blood-brain barrier. Ongoing research aims to develop more effective and safer mAbs by modifying antibody structures and improving delivery methods.