Ludwig-Maximilians-Universität, Chair of Metabolic Biochemistry

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Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and host

Science. 2006 Sep 22;313(5794):1781-4.

Authors/Editors: meyer-luehmann M
Coomaraswamy J
Bolmont T
Kaeser S
Schaefer C
Kilger E
Neuenschwander A
Abramowski D
Frey P
Jaton AL
Vigouret JM
Paganetti P
Walsh DM
Mathews PM
Ghiso J
Staufenbiel M
Walker LC
Jucker M
Publication Date: 2006
Type of Publication: Journal Article
Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but little is known about the initiation of this process in vivo. Intracerebral injection of dilute, amyloid-beta (Abeta)-containing brain extracts from humans with Alzheimer's disease or beta-amyloid precursor protein (APP) transgenic mice induced cerebral beta-amyloidosis and associated pathology in APP transgenic mice in a time- and concentration-dependent manner. The seeding activity of brain extracts was reduced or abolished by Abeta immunodepletion, protein denaturation, or by Abeta immunization of the host. The phenotype of the exogenously induced amyloidosis depended on both the host and the source of the agent, suggesting the existence of polymorphic Abeta strains with varying biological activities reminiscent of prion strains.

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