= Emerging. More than 5 years before clinical availability. (9.82%)
= Expected to be clinically available in 1 to 4 years. (12.95%)
= Clinically available now. (22.77%)
MSACL 2018 EU : Hanrieder

MSACL 2018 EU Abstract

Topic: Tissue Imaging

Podium Presentation in the Ether on Wednesday at 9:00 (Chair: Vladimir Frankevich)

Probing Amyloid Aggregation Dynamics in vivo, Using SILK Imaging (iSILK)

Jörg Hanrieder (Presenter)
University of Gothenburg

Presenter Bio(s): Jörg has been working with different modalities of imaging mass spectrometry over the last 10 years to understand biochemical processes underlying neurodegeneration.
He has a background in chemistry and molecular neuroscience (MSc 2005, University of Leipzig; PhD 2011, Uppsala University). Following a Postdoc on SIMS imaging at Chalmers University of Technology he joined the University of Gothenburg as Assistant Professor in Neurochemistry. He was promoted to Associate Professor in 2017. Since 2017, he is establishing a second group at University College London, where he holds an honorary appointment at the Institute of neurology. The work of his group concerns the development and advancement of chemical imaging tools for probing neurodegenerative disease pathology, specifically amyloid plaque pathology in Alzheimer’s disease.

Authors: Jörg Hanrieder(1,2), Wojciech Michno (1), Henrik Zetterberg (1,2), Kaj Blennow (1)
(1) University of Gothenburg, Sweden, (2) University College London, UK

Abstract

Although the importance of amyloid beta (Aβ) plaque deposition in Alzheimer’s disease (AD) has long been recognized, exactly how plaques develop over time and their neurotoxic potential is not clear. Recent advances in imaging technologies such as imaging mass spectrometry (IMS) greatly increase the resolution of such events and the advent of isotope labelling of proteins and high-resolution IMS opens up possibilities for measuring spatial protein turnover kinetics in tissue. The aim of this study is to take advantages of such advances by using IMS along with metabolic labeling to recently developed novel genetic mouse models of AD. The results show distinct rates of secretion and deposition for distinct Aβ peptides within different brain regions. These data allow us to understand the progression of plaque deposition from initial seeding through to later aggregation.


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