The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease

Jeff Sevigny, Ping Chiao, Thierry Bussière, Paul H. Weinreb, Leslie Williams, Marcel Maier, Robert Dunstan, Stephen Salloway, Tianle Chen, Yan Ling, John O’Gorman, Fang Qian, Mahin Arastu, Mingwei Li, Sowmya Chollate, Melanie S. Brennan, Omar Quintero-Monzon, Robert H. Scannevin, H. Moore Arnold, Thomas Engber, Kenneth Rhodes, James Ferrero, Yaming Hang, Alvydas Mikulskis, Jan Grimm, Christoph Hock, Roger M. Nitsch and Alfred Sandrock ()
Additional contact information
Jeff Sevigny: Biogen
Ping Chiao: Biogen
Thierry Bussière: Biogen
Paul H. Weinreb: Biogen
Leslie Williams: Biogen
Marcel Maier: Neurimmune
Robert Dunstan: Biogen
Stephen Salloway: Butler Hospital, Providence
Tianle Chen: Biogen
Yan Ling: Biogen
John O’Gorman: Biogen
Fang Qian: Biogen
Mahin Arastu: Biogen
Mingwei Li: Biogen
Sowmya Chollate: Biogen
Melanie S. Brennan: Biogen
Omar Quintero-Monzon: Biogen
Robert H. Scannevin: Biogen
H. Moore Arnold: Biogen
Thomas Engber: Biogen
Kenneth Rhodes: Biogen
James Ferrero: Biogen
Yaming Hang: Biogen
Alvydas Mikulskis: Biogen
Jan Grimm: Neurimmune
Christoph Hock: Neurimmune
Roger M. Nitsch: Neurimmune
Alfred Sandrock: Biogen

Nature, 2016, vol. 537, issue 7618, 50-56

Abstract: Abstract Alzheimer’s disease (AD) is characterized by deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles in the brain, accompanied by synaptic dysfunction and neurodegeneration. Antibody-based immunotherapy against Aβ to trigger its clearance or mitigate its neurotoxicity has so far been unsuccessful. Here we report the generation of aducanumab, a human monoclonal antibody that selectively targets aggregated Aβ. In a transgenic mouse model of AD, aducanumab is shown to enter the brain, bind parenchymal Aβ, and reduce soluble and insoluble Aβ in a dose-dependent manner. In patients with prodromal or mild AD, one year of monthly intravenous infusions of aducanumab reduces brain Aβ in a dose- and time-dependent manner. This is accompanied by a slowing of clinical decline measured by Clinical Dementia Rating—Sum of Boxes and Mini Mental State Examination scores. The main safety and tolerability findings are amyloid-related imaging abnormalities. These results justify further development of aducanumab for the treatment of AD. Should the slowing of clinical decline be confirmed in ongoing phase 3 clinical trials, it would provide compelling support for the amyloid hypothesis.

Date: 2016
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DOI: 10.1038/nature19323

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