Abstract/Journal Article

DZNE-2020-00728

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Invited.20: Prion-like aspects of Alzheimer pathology

Jucker, M. (First author)DZNE*

2013

Abstract: Many neurodegenerative disorders are characterized by a predictable temporal progression of specific aggregated proteins in thebrain. The hallmark proteopathy is Alzheimer disease in whichAbeta is deposited in brain. Abeta-amyloidosis can be exogenously induced by the application of Abeta-containing brainextracts (Meyer-Lühmann et al., Science 2006; Eisele et al.,Science 2010). The amyloid-inducing agent is likely Abeta itself,although in a conformation generated most effectively in the living brain. Once induced, Abeta lesions spread within and amongbrain regions. The induced amyloid is dependent on the natureof the Abeta seed and of the host, an observation reminiscent of prion strains. Recently, the concept of prion-like induction ofpathogenic proteins has been expanded to include intracellularlesions (Jucker and Walker, Ann Neurol 2011). Nevertheless, theclinical implications of these observations are not yet clear. Ourfinding that the Abeta-inducing agent is partly soluble (Langeret al., J Neurosci 2011) intensifies the search for protein seeds inbodily fluids that may have diagnostic value and be a novel targetfor early therapeutic intervention.

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Contributing Institute(s):

1. Cell Biology of Neurological Diseases (AG Jucker)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2013

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