K
Karen H. Ashe
Researcher at University of Minnesota
Publications - 23
Citations - 5942
Karen H. Ashe is an academic researcher from University of Minnesota. The author has contributed to research in topics: Amyloid beta & Amyloid precursor protein. The author has an hindex of 11, co-authored 23 publications receiving 5709 citations. Previous affiliations of Karen H. Ashe include Veterans Health Administration.
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Journal ArticleDOI
A specific amyloid-|[beta]| protein assembly in the brain impairs memory
Sylvain Lesné,Ming Teng Koh,Linda Kotilinek,Rakez Kayed,Charles G. Glabe,Austin J. Yang,Michela Gallagher,Karen H. Ashe +7 more
TL;DR: It is found that memory deficits in middle-aged Tg2576 mice are caused by the extracellular accumulation of a 56-kDa soluble amyloid-β assembly, which is proposed to be Aβ*56 (Aβ star 56), which may contribute to cognitive deficits associated with Alzheimer's disease.
Journal ArticleDOI
Natural oligomers of the amyloid-|[beta]| protein specifically disrupt cognitive function
James P. Cleary,Dominic M. Walsh,Dominic M. Walsh,J. Hofmeister,Ganesh M. Shankar,Michael A. Kuskowski,Michael A. Kuskowski,Dennis J. Selkoe,Karen H. Ashe,Karen H. Ashe +9 more
TL;DR: The biochemical isolation of discrete amyloid-β moieties with pathophysiological properties sets the stage for a new approach to studying the molecular mechanisms of cognitive impairment in Alzheimer disease and related neurodegenerative disorders.
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The Relationship between Aβ and Memory in the Tg2576 Mouse Model of Alzheimer's Disease
Marcus A. Westerman,Deirdre Cooper-Blacketer,Ami Mariash,Linda Kotilinek,Takeshi Kawarabayashi,Linda H. Younkin,George A. Carlson,Steven G. Younkin,Karen H. Ashe +8 more
TL;DR: It is suggested that A βinsol is a surrogate marker for small assemblies of Aβ that disrupt cognition and occur as intermediates during Aβinsol formation, and they are the first descriptive in vivo data supporting their role in impairing memory.
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Evidence for glial-mediated inflammation in aged APPSW transgenic mice
W. C. Benzing,J. R. Wujek,E. K. Ward,D. Shaffer,Karen H. Ashe,Samuel Younkin,Kurt R. Brunden +6 more
TL;DR: Findings provide evidence that Tg2576 mice exhibit features of the inflammatory pathology seen in AD and suggest that these mice are a useful animal model for studying the role inflammation may play in this disease.
Journal ArticleDOI
Learning and Memory in Transgenic Mice Modeling Alzheimer's Disease
TL;DR: Future studies in composite transgenic mice developing amyloid plaques, neurofibrillary tangles, and other AD pathology may allow for the determination of the relative contribution of A Beta and non-A Beta components to dementia.