@misc{oai:kawasakigakuen.repo.nii.ac.jp:00000335,
 author = {Masatoshi TAKEDA and Sara YASUTAKE and Aoi AHIZUKA and Kenji OKA and Tomohiro OHGOMORI and Misa NAKAMURA},
 month = {Dec},
 note = {Understanding of the molecular pathology of Alzheimer's disease has been advanced, and amyloid β (Aβ) protein deposited in the core of amyloid plaques and phosphorylated tau protein constituting neurofibrillary tangles have been identified as the hallmark of Alzheimer's disease pathology. The development of disease-modifying drug has been focused on the amyloid cascade hypothesis, but neither the β-secretase inhibitors, γ-secretase inhibitors, nor γ-secretase modifiers have been successful. In 1999, administration of Aβ to transgenic mice as model animals for Alzheimer's disease was reported to significantly reduce amyloid deposition in the brain, which was the beginning of immunotherapy for Alzheimer's disease, but the antibody against amyloid (AN1792) clinical trial was discontinued due to the occurrence of aseptic meningoencephalitis in 2002. Recently, antibody therapy has been increasing year by year. Since the development of the first antibody therapeutic in 1986, 40 items in the oncology field and about the same number of monoclonal therapeutics in the non-cancer area have been approved as of 2020. In 2021, aducanumab has been approved by the FDA as an antibody therapeutic for early-stage Alzheimer's disease, albeit conditionally. In this paper, development status of monoclonal therapeutic agents for Alzheimer's disease will be reviewed, including aducanumab (Biogen), lecanemab (Biogen, Eisai), solanezumab (Eli Lily), crenezumab (Genentech), donanemab (Eli Lily), and gantenezumab (Hoffman-La Roche)., Review Article},
 title = {Development of monoclonal antibody therapy against Alzheimer’s disease},
 year = {2021}
}