Johannes Levin, Simone Baiardi, Corinne Quadalti, Marcello Rossi, Angela Mammana, Jonathan Vöglein, Alexander Bernhardt, Richard J Perrin, Mathias Jucker, Oliver Preische, Anna Hofmann, Günter U Höglinger, Nigel J Cairns, Erin E Franklin, Patricio Chrem, Carlos Cruchaga, Sarah B Berman, Jasmeer P Chhatwal, Alisha Daniels, Gregory S Day, Natalie S Ryan, Alison M Goate, Brian A Gordon, Edward D Huey, Laura Ibanez, Celeste M Karch, Jae-Hong Lee, Jorge Llibre-Guerra, Francisco Lopera, Colin L Masters, John C Morris, James M Noble, Alan E Renton, Jee Hoon Roh, Matthew P Frosch, C Dirk Keene, Catriona McLean, Raquel Sanchez-Valle, Peter R Schofield, Charlene Supnet-Bell, Chengjie Xiong, Armin Giese, Oskar Hansson, Randall J Bateman, Eric McDade, Piero Parchi
INTRODUCTION: Amyloid beta and tau pathology are the hallmarks of sporadic Alzheimer's disease (AD) and autosomal dominant AD (ADAD). However, Lewy body pathology (LBP) is found in ≈ 50% of AD and ADAD brains. METHODS: Using an α-synuclein seed amplification assay (SAA) in cerebrospinal fluid (CSF) from asymptomatic (n = 26) and symptomatic (n = 27) ADAD mutation carriers, including 12 with known neuropathology, we investigated the timing of occurrence and prevalence of SAA positive reactivity in ADAD in vivo...
April 26, 2024: Alzheimer's & Dementia: the Journal of the Alzheimer's Association