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From: TSS ()
In Reply to:
Alzheimer’s may 'seed' itself like mad cow disease posted by TSS on September 21, 2006 at 11:46 am:
b-Amyloidogenesis Is Governed by Agent and Host Melanie Meyer-Luehmann,1* Janaky Coomaraswamy,1* Tristan Bolmont,1,2* Stephan Kaeser,1 Claudia Schaefer,1 Ellen Kilger,1 Anton Neuenschwander,3 Dorothee Abramowski,3 Peter Frey,3 Anneliese L. Jaton,3 Jean-Marie Vigouret,3 Paolo Paganetti,3 Dominic M. Walsh,4 Paul M. Mathews,5 Jorge Ghiso,6 Matthias Staufenbiel,3 Lary C. Walker,7† Mathias Jucker1,2† 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-b (Ab)– containing brain extracts from humans with Alzheimer’s disease or b-amyloid precursor protein (APP) transgenic mice induced cerebral b-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 Ab immunodepletion, protein denaturation, or by Ab 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 Ab strains with varying biological activities reminiscent of prion strains. snip... There is currently no evidence that bamyloidosis (and in particular AD) is transmissible in the same sense as are prion diseases, which can be transmitted to wild-type hosts via diverse routes of varying efficiency and involve systemic cellular mechanisms of prion uptake and distribution (7, 32). However, an understanding of the mechanisms involved in the instigation and propagation of abnormal Ab assemblies in vivo could shed light on the origins of idiopathic Alzheimer_s disease. .............END http://www.sciencemag.org/cgi/content/abstract/313/5794/1781 tss
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