The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease
By J. Sevigny, P. Chiao, T. Bussiere, P. Weinreb, Leslie Williams, M. Maier, R. Dunstan, Stephen Salloway, Tianle Chen, Yan Ling and 18 more. Nature, 2016
2,711 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Pharmacology, Physiology
View Paper: https://www.semanticscholar.org/paper/0c6822c69e0552742f803798db47eed457f8badc
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In Cellular and Molecular Neuroscience
- J. Long
- Dennis W. Dickson
- Reisa A. Sperling
- John Q. Trojanowski
- Clifford R. Jack Jr.
- Peter T. Nelson
- William W. Seeley
- D. Holtzman
In Pharmacology
In Physiology
- J. Long
- D. Holtzman
- Clifford R. Jack Jr.
- John Hardy
- Dennis W. Dickson
- Reisa A. Sperling
- B. de Strooper
- Thomas Wisniewski
Citations in the corpus
- APP mouse models for Alzheimer's disease preclinical studies (2017, positive): “Plaque-bearing Tg2576 mice that were chronically treated with aducanumab experienced a dose-dependent reduction of cerebral A b levels by up to ~ 70% compared to vehicle (Sevigny et al , 2016).”
- Oxidative stress and the amyloid beta peptide in Alzheimer’s disease (2017, background): “And in parallel, antibody-based therapeutic strategies fighting against Aβ aggregates are now emerging and seem to be promising [216].”
- Alzheimer’s disease: experimental models and reality (2017, background): “1 3 drop-out rate due to the development of this side effect) [136, 145, 171].”
- Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report (2019, background): “This stratification will enable enrichment for subjects on the ADNC continuum (Sevigny et al., 2016) while excluding subjects likely to have high risk for LATE-NC (Botha et al., 2018).”
- Aging and aging-related diseases: from molecular mechanisms to interventions and treatments (2022, background): “The expression of Aβ is mainly reduced via immunotherapy or by inhibiting γ- and β-secretase.(503) The aggregation of phosphorylated tau proteins in neurons leads to neuronal damage and AD; therefore, it is considered another potential drug target for AD.”
- Two Randomized Phase 3 Studies of Aducanumab in Early Alzheimer’s Disease (2022, methodology): “In a prior phase 1b study (PRIME), aducanumab treatment resulted in dose- and time-dependent reduction in Aβ plaques, accompanied by slowed clinical decline (exploratory endpoint) (8).”
- Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019, positive): “Further, after one year of monthly infusions, participants receiving aducanumab had slower decline in CDR-sum of boxes and MMSE in a phase 1b trial (Sevigny et al., 2016).”