Journal
SCIENCE
Volume 313, Issue 5794, Pages 1781-1784Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1131864
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- NCRR NIH HHS [RR-00165] Funding Source: Medline
- NINDS NIH HHS [NS45357] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
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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 (A beta)-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 A beta immunodepletion, protein denaturation, or by A beta 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 A beta strains with varying biological activities reminiscent of prion strains.
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