| Literature DB >> 34155411 |
Stephen Salloway1, Martin Farlow2, Eric McDade3, David B Clifford3, Guoqiao Wang3, Jorge J Llibre-Guerra3, Janice M Hitchcock4, Susan L Mills3, Anna M Santacruz3, Andrew J Aschenbrenner3, Jason Hassenstab3, Tammie L S Benzinger3, Brian A Gordon3, Anne M Fagan3, Kelley A Coalier3, Carlos Cruchaga3, Alison A Goate5, Richard J Perrin3, Chengjie Xiong3, Yan Li3, John C Morris3, B Joy Snider3, Catherine Mummery6, G Mustafa Surti1, Didier Hannequin7, David Wallon7, Sarah B Berman8, James J Lah9, Ivonne Z Jimenez-Velazquez10, Erik D Roberson11, Christopher H van Dyck12, Lawrence S Honig13, Raquel Sánchez-Valle14, William S Brooks15, Serge Gauthier16, Douglas R Galasko17, Colin L Masters18, Jared R Brosch2, Ging-Yuek Robin Hsiung19, Suman Jayadev20, Maité Formaglio21, Mario Masellis22, Roger Clarnette23, Jérémie Pariente24, Bruno Dubois25, Florence Pasquier26, Clifford R Jack27, Robert Koeppe28, Peter J Snyder29, Paul S Aisen30, Ronald G Thomas17, Scott M Berry31, Barbara A Wendelberger31, Scott W Andersen32, Karen C Holdridge32, Mark A Mintun32, Roy Yaari32, John R Sims32, Monika Baudler33, Paul Delmar33, Rachelle S Doody33, Paulo Fontoura33, Caroline Giacobino33, Geoffrey A Kerchner33, Randall J Bateman34.
Abstract
Dominantly inherited Alzheimer's disease (DIAD) causes predictable biological changes decades before the onset of clinical symptoms, enabling testing of interventions in the asymptomatic and symptomatic stages to delay or slow disease progression. We conducted a randomized, placebo-controlled, multi-arm trial of gantenerumab or solanezumab in participants with DIAD across asymptomatic and symptomatic disease stages. Mutation carriers were assigned 3:1 to either drug or placebo and received treatment for 4-7 years. The primary outcome was a cognitive end point; secondary outcomes included clinical, cognitive, imaging and fluid biomarker measures. Fifty-two participants carrying a mutation were assigned to receive gantenerumab, 52 solanezumab and 40 placebo. Both drugs engaged their Aβ targets but neither demonstrated a beneficial effect on cognitive measures compared to controls. The solanezumab-treated group showed a greater cognitive decline on some measures and did not show benefits on downstream biomarkers. Gantenerumab significantly reduced amyloid plaques, cerebrospinal fluid total tau, and phospho-tau181 and attenuated increases of neurofilament light chain. Amyloid-related imaging abnormalities edema was observed in 19.2% (3 out of 11 were mildly symptomatic) of the gantenerumab group, 2.5% of the placebo group and 0% of the solanezumab group. Gantenerumab and solanezumab did not slow cognitive decline in symptomatic DIAD. The asymptomatic groups showed no cognitive decline; symptomatic participants had declined before reaching the target doses.Entities:
Mesh:
Substances:
Year: 2021 PMID: 34155411 PMCID: PMC8988051 DOI: 10.1038/s41591-021-01369-8
Source DB: PubMed Journal: Nat Med ISSN: 1078-8956 Impact factor: 87.241