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.