R
Rakez Kayed
Researcher at University of Texas Medical Branch
Publications - 194
Citations - 30060
Rakez Kayed is an academic researcher from University of Texas Medical Branch. The author has contributed to research in topics: Amyloid & Tauopathy. The author has an hindex of 60, co-authored 178 publications receiving 26252 citations. Previous affiliations of Rakez Kayed include University of California & University of Southern California.
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Journal ArticleDOI
Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis
Rakez Kayed,Elizabeth Head,Jennifer L. Thompson,Theresa M. McIntire,Saskia Milton,Carl W. Cotman,Charles G. Glabe +6 more
TL;DR: It is shown that all of the soluble oligomers tested display a common conformation-dependent structure that is unique to soluble oligomer regardless of sequence, suggesting they share a common mechanism of toxicity.
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Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles: Intracellular Aβ and Synaptic Dysfunction
Salvatore Oddo,Antonella Caccamo,Jason D. Shepherd,M. Paul Murphy,Todd E. Golde,Rakez Kayed,Raju Metherate,Mark P. Mattson,Yama Akbari,Frank M. LaFerla +9 more
TL;DR: The recapitulation of salient features of AD in these mice clarifies the relationships between Abeta, synaptic dysfunction, and tangles and provides a valuable model for evaluating potential AD therapeutics as the impact on both lesions can be assessed.
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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.
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Curcumin Inhibits Formation of Amyloid β Oligomers and Fibrils, Binds Plaques, and Reduces Amyloid in Vivo
Fusheng Yang,Giselle P. Lim,Giselle P. Lim,Aynun N. Begum,Aynun N. Begum,Oliver J. Ubeda,Oliver J. Ubeda,Mychica Simmons,Mychica Simmons,Surendra S. Ambegaokar,Surendra S. Ambegaokar,Pingping P. Chen,Pingping P. Chen,Rakez Kayed,Charles G. Glabe,Sally A. Frautschy,Sally A. Frautschy,Gregory M. Cole,Gregory M. Cole +18 more
TL;DR: It is suggested that low dose curcumin effectively disaggregates Aβ as well as prevents fibril and oligomer formation, supporting the rationale forCurcumin use in clinical trials preventing or treating AD.
Journal ArticleDOI
Calcium dysregulation and membrane disruption as a ubiquitous neurotoxic mechanism of soluble amyloid oligomers.
TL;DR: Observations that Aβ42 and other oligomers caused rapid cellular leakage of anionic fluorescent dyes point to a generalized increase in membrane permeability, which may provide a common mechanism for oligomer-mediated toxicity in many amyloidogenic diseases.