C
Christopher B. Eckman
Researcher at Mayo Clinic
Publications - 85
Citations - 17750
Christopher B. Eckman is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Amyloid precursor protein & P3 peptide. The author has an hindex of 52, co-authored 85 publications receiving 16908 citations. Previous affiliations of Christopher B. Eckman include Jacksonville College & University of Alabama.
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Journal ArticleDOI
Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease.
D. Scheuner,Christopher B. Eckman,Christopher B. Eckman,Malene Jensen,X. Song,Martin Citron,Nobuhiro Suzuki,Thomas D. Bird,John Hardy,Mike Hutton,Walter A. Kukull,Eric Larson,Ephrat Levy-Lahad,Matti Viitanen,Elaine R. Peskind,Parvoneh Poorkaj,Gerard D. Schellenberg,Rudolph E. Tanzi,Wilma Wasco,Lars Lannfelt,Dennis J. Selkoe,Steven G. Younkin +21 more
TL;DR: The findings indicate that the FAD–linked mutations may all cause Alzheimer's disease by increasing the extracellular concentration of Aβ42(43), thereby fostering cerebral deposition of this highly amyloidogenic peptide.
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Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo
David R. Borchelt,Gopal Thinakaran,Christopher B. Eckman,Christopher B. Eckman,Michael K. Lee,Frances Davenport,Tamara Ratovitsky,Cristian Mihail Prada,Grace Kim,Sophia Seekins,Debra Yager,Hilda H. Slunt,Rong Wang,Mary Seeger,Allan I. Levey,Sam Gandy,Neal G. Copeland,Nancy A. Jenkins,Donald L. Price,Steven G. Younkin,Steven G. Younkin,Sangram S. Sisodia +21 more
TL;DR: These studies provide compelling support for the view that one mechanism by which these mutant PS1 cause AD is by increasing the extracellular concentration of Abeta peptides terminating at 42(43), species that foster Abeta deposition.
Journal ArticleDOI
An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants
Nobuhiro Suzuki,Tobun T. Cheung,Xiao Dan Cai,Asano Odaka,Laszlo Otvos,Christopher B. Eckman,Todd E. Golde,Steven G. Younkin +7 more
TL;DR: Human neuroblastoma cells transfected with constructs expressing wild-type beta APP or the beta APP717 mutants linked to familial Alzheimer's disease were compared and it was demonstrated that the 4-kilodalton A beta released from wild- type beta APP is primarily but not exclusively A beta 1-40.
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Insulin-degrading enzyme regulates the levels of insulin, amyloid β-protein, and the β-amyloid precursor protein intracellular domain in vivo
Wesley Farris,Stefan Mansourian,Yang Chang,Loren Lindsley,Elizabeth A. Eckman,Matthew P. Frosch,Christopher B. Eckman,Rudolph E. Tanzi,Dennis J. Selkoe,Suzanne Y. Guénette +9 more
TL;DR: In vivo findings suggest that IDE hypofunction may underlie or contribute to some forms of AD and DM2 and provide a mechanism for the recently recognized association among hyperinsulinemia, diabetes, and AD.
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The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Abeta protofibril formation.
Camilla Nilsberth,Anita Westlind-Danielsson,Anita Westlind-Danielsson,Christopher B. Eckman,Margaret M. Condron,Karin Axelman,Charlotte Forsell,Charlotte Stenh,Johan Luthman,David B. Teplow,Steven G. Younkin,Jan Näslund,Lars Lannfelt +12 more
TL;DR: The finding of increased protofibril formation and decreased Aβ plasma levels in the Arctic AD may reflect an alternative pathogenic mechanism for AD involving rapid Aβ protofibil formation leading to accelerated buildup of insoluble Aβ intra- and/or extracellularly.