Ask any question about EPFL courses, lectures, exercises, research, news, etc. or try the example questions below.
DISCLAIMER: The Graph Chatbot is not programmed to provide explicit or categorical answers to your questions. Rather, it transforms your questions into API requests that are distributed across the various IT services officially administered by EPFL. Its purpose is solely to collect and recommend relevant references to content that you can explore to help you answer your questions.
beta-Amyloid (A beta) plaque formation is the major pathological hallmark of Alzheimer's disease (AD) and constitutes a potentially critical, early inducer driving AD pathogenesis as it precedes other pathological events and cognitive symptoms by decades. It is therefore critical to understand how A beta pathology is initiated and where and when distinct A beta species aggregate. Here, we used metabolic isotope labeling in APP(NL-G-F) knock-in mice together with mass spectrometry imaging to monitor the earliest seeds of A beta deposition through ongoing plaque development. This allowed visualizing A beta aggregation dynamics within single plaques across different brain regions. We show that formation of structurally distinct plaques is associated with differential A beta peptide deposition. Specifically, A beta 1-42 is forming an initial core structure followed by radial outgrowth and late secretion and deposition of A beta 1-38. These data describe a detailed picture of the earliest events of precipitating amyloid pathology at scales not previously possible.
Thomas Rizzo, Ahmed Ben Faleh, Stephan Warnke, Ali H Abikhodr