Alzheimer disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory loss , and impaired daily functioning. With the aging population worldwide, the burden of AD has become a significant public health concern. Despite extensive research, there is currently no cure for AD, and available treatments offer only limited symptomatic relief . However, recent years have witnessed significant progress in the development of novel drugs targeting various aspects of AD pathogenesis. This abstract provides an overview of promising novel drugs that hold potential for the treatment od AD and highlights their mechanisms of action. One class of novel drugs focuses on reducing the accumulation of amyloid beta(Aβ) plaques, a hallmark feature of AD pathology. Monoclonal antibodies, such as aducanumab and lecanemab, have shown promise in clinical trails by selectively targeting and clearing Aβ plaques from the brain. Another approach involves inhibiting beta-secretase enzymes, responsible for the production of Aβ peptides. Solanezumab is thought to act as ‘’ amyloid beta sink’’ that is facilitating flux of amyloid beta from a central to peripheral compartment. crenezumab is highly homologous to solanezumab another monoclonal antibody targeting amyloid - β peptides. Keywords: Progressive neurodegenerative disorder, cognitive decline, impaired daily functioning, symptomatic relief, amyloid beta(Aβ) plaques, monoclonal antibodies, lecanemab, Aβ Peptides, Amyloid beta sink.