Journal
CELL REPORTS
Volume 11, Issue 11, Pages 1760-1771Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.05.021
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Funding
- National Institute for Neurological Diseases and Stroke [NS33249]
- Robert A. and Renee E. Belfer Family Foundation
- NIH intramural research program
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The accumulation of amyloid-beta (Ab) as amyloid fibrils and toxic oligomers is an important step in the development of Alzheimer's disease (AD). However, there are numerous potentially toxic oligomers and little is known about their neurological effects when generated in the living brain. Here we show that Ab oligomers can be assigned to one of at least two classes (type 1 and type 2) based on their temporal, spatial, and structural relationships to amyloid fibrils. The type 2 oligomers are related to amyloid fibrils and represent the majority of oligomers generated in vivo, but they remain confined to the vicinity of amyloid plaques and do not impair cognition at levels relevant to AD. Type 1 oligomers are unrelated to amyloid fibrils and may have greater potential to cause global neural dysfunction in AD because they are dispersed. These results refine our understanding of the pathogenicity of Ab oligomers in vivo.
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