Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.

Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. Research Abstract Details 

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Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. Abstract Text:

Irene H Cheng,Kimberly Scearce-Levie,Justin Legleiter,Jorge J Palop,Hilary Gerstein,Nga Bien-Ly,Jukka ,Sylvain ,Karen H Ashe,Paul J Muchowski,Lennart Mucke,

Many proteins suspected of causing neurodegenerative diseases exist in diverse assembly states. For most, it is unclear whether shifts from one state to another would be helpful or harmful. We used mutagenesis to change the assembly state of Alzheimer disease (AD)-associated amyloid-beta (Abeta) peptides. In vitro, the "Arctic" mutation (AbetaE22G) accelerated Abeta fibrillization but decreased the abundance of nonfibrillar Abeta assemblies, compared with wild-type Abeta. In human amyloid precursor protein (hAPP) transgenic mice carrying mutations adjacent to Abeta that increase Abeta production, addition of the Arctic mutation markedly enhanced the formation of neuritic amyloid plaques but reduced the relative abundance of a specific nonfibrillar Abeta assembly (Abeta*56). Mice overexpressing Arctic mutant or wild-type Abeta had similar behavioral and neuronal deficits when they were matched for Abeta*56 levels but had vastly different plaque loads. Thus, Abeta*56 is a likelier determinant of functional deficits in hAPP mice than fibrillar Abeta deposits. Therapeutic interventions that reduce Abeta fibrils at the cost of augmenting nonfibrillar Abeta assemblies could be harmful.

Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. Publishing Authors By Initials

IH Cheng,K Scearce-Levie,J Legleiter,JJ Palop,H Gerstein,N Bien-Ly,J ,S ,KH Ashe,PJ Muchowski,L Mucke,

For similar peptides: oligopeptides research abstracts see: peptides: oligopeptides research

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Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The Journal of biological chemistry

VOLUME: 282

Page Numbers: 23818-28

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 4

MONTH: 06

YEAR: 2007

Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. Information

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LANGUAGE: eng

NlmUniqueID: 2985121

Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. Keywords Mesh Terms:

KEYWORDS: Oligopeptides

MESH TERMS: etiology

Chemical & Substance for Abstract: Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. Information

Substance Name: Oligopeptides

Registry Number: 0

Grant and Affiliation Information for Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.

AFFILIATION: Gladstone Institute of Neurological Disease, San Francisco, California 94158, USA.

Country: United States

AGENCY: United States NCRR

GRANT: RR 18928-01

ACRONYM: RR

MEDLINETA: J Biol Chem

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