Phase 3 trials of solanezumab for mild-to-moderate Alzheimer's disease.
By R. Doody, Ronald G. Thomas, M. Farlow, T. Iwatsubo, Bruno Vellas, S. Joffe, K. Kieburtz, R. Raman, Xiaoying Sun, P. Aisen and 3 more. New England Journal of Medicine, 2014
1,548 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/d180387f40d92ffebf5a5c1df03c6ac6b5553169
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In Molecular Biology
- D. Selkoe
- Urmi Sengupta
- John Hardy
- A. Nilson
- R. Kayed
- David Watson
- Christopher M. Dobson
- Sokratis G. Papageorgiou
In Physiology
- D. Selkoe
- John Hardy
- R. Kayed
- Urmi Sengupta
- A. Nilson
- D. Holtzman
- David Watson
- Christopher M. Dobson
In Psychiatry and Mental health
Citations in the corpus
- Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease (2018, background): “In addition, various immunotherapies targeting Aβ in AD model mice were effective in decreasing Aβ deposition in the brains, but it did not lead to improvement of actual symptoms or accumulation of tau (Ostrowitzki et al., 2012; Giacobini and Gold, 2013; Doody et al., 2014; Salloway et al., 2014).”
- The amyloid hypothesis of Alzheimer's disease at 25 years (2016, background): “These brains were selected to have similar plaque densities, but the oligomer-specific ELISA revealed that the non-demented plaque-rich subjects had much lower oligomer-to-plaque ratios than the mildly demented plaque-rich patients (Esparza et al, 2013).”
- The Role of Amyloid-β Oligomers in Toxicity, Propagation, and Immunotherapy (2016, background): “Preferential binding of the monomer may explain why clinical trials failed to show improvement due to the fact that they used a lower dosage which may have been saturated by monomers (Goure et al., 2014; Doody et al., 2014).”