The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease

@article{Sevigny2016TheAA,
  title={The antibody aducanumab reduces A$\beta$ plaques in Alzheimer’s disease},
  author={Jeff Sevigny and Ping Chiao and Thierry Bussiere and Paul H Weinreb and Leslie Williams and Marcel Maier and Robert W. Dunstan and Stephen P. Salloway and Tianle Chen and Yan Ling and John O’Gorman and Fang Qian and Mahin F. Arastu and Mingwei Li and Sowmya Chollate and Melanie S. Brennan and Omar Quintero-Monzon and Robert H. Scannevin and H. Moore Arnold and Thomas M. Engber and Kenneth J. Rhodes and Jim Ferrero and Yaming Hang and Alvydas Mikulskis and Jan Grimm and Christoph Hock and Roger M. Nitsch and Alfred W. Sandrock},
  journal={Nature},
  year={2016},
  volume={537},
  pages={50-56}
}
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… 
Aducanumab reduces Aβ plaques in Alzheimer's disease
  • D. Vaillancourt
  • Medicine
    Movement disorders : official journal of the Movement Disorder Society
  • 2016
TLDR
Evidence is provided that aducanumab penetrates the brain and decreases amyloid plaques in patients with AD during a 54-week period, and the importance of having an imaging marker in Parkinson’s disease that can be used to assess a potential therapy is shown.
Alzheimer disease: Anti-Aβ antibody treatment shows promise in Alzheimer disease
  • I. Fyfe
  • Medicine
    Nature Reviews Neurology
  • 2016
TLDR
A robust time-dependent and dose-dependent reduction in amyloid burden is found and is probably the key reason for the hint of clinical efficacy on the exploratory cognitive endpoints, says Sandrock.
Drug candidates in clinical trials for Alzheimer’s disease
TLDR
The findings from recent clinical trials are systemically reviewed to provide a comprehensive review of novel therapeutic compounds in the treatment and prevention of AD.
Alzheimer's disease: Recent treatment strategies.
Alzheimer’s disease: the controversial approval of Aducanumab
TLDR
Treatment with Aducanumab at the highest dose resulted in a 23% reduction in clinical decline compared to placebo, as determined by the Clinical Dementia Rating scale Sum of Boxes, a composite measure with cognitive and functional components that was set as the primary efficacy endpoint.
Immune modulations and immunotherapies for Alzheimer’s disease: a comprehensive review
TLDR
Here, a comprehensively review immune-based therapeutic approaches toward AD, including monoclonal antibodies and vaccines, and highlights the capacity of modulating the neuroimmune interactions and targeting neuroinflammation as a promising opportunity for finding optimal treatments for AD.
Alzheimer's disease: Attack on amyloid-β protein
TLDR
Interim results from a clinical trial of monthly infusions of aducanumab in subjects with prodromal or mild Alzheimer's disease support further development of aduecanumab as an Aβ-removing therapy.
Amyloid β oligomers (AβOs) in Alzheimer’s disease
TLDR
Increased A β42/oligomer ratio in the CSF of AD/MCI patients indicated that the presence of soluble AβOs in CSF may be linked to lowering of natively measured monomeric Aβ42 by epitopes masking, and hence, concentrations of A βOs in theCSF are postulated to as useful AD biomarkers.
BACE inhibitors in clinical development for the treatment of Alzheimer’s disease
TLDR
A comprehensive review of BACE inhibitors for AD treatment is provided, focusing on the most advanced compounds in Phase III RCTs, and indicates that blocking the formation of nascent Aβ is not useful in AD.
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