The Japanese Mutant Aβ (ΔE22-Aβ1−39) Forms Fibrils Instantaneously, with Low-Thioflavin T Fluorescence: Seeding of Wild-Type Aβ1−40 into Atypical Fibrils by ΔE22-Aβ1−39-Reference-Cited by-同舟云学术

The Japanese Mutant Aβ (ΔE22-Aβ1−39) Forms Fibrils Instantaneously, with Low-Thioflavin T Fluorescence: Seeding of Wild-Type Aβ1−40 into Atypical Fibrils by ΔE22-Aβ1−39

Published:2011-02-24 Issue:12 Volume:50 Page:2026-2039
ISSN:0006-2960
Container-title:Biochemistry
language:en
Short-container-title:Biochemistry

Author:

Cloe Adam L.¹,Orgel Joseph P. R. O.²,Sachleben Joseph R.³,Tycko Robert⁴,Meredith Stephen C.¹⁵

Affiliation:

1. Department of Pathology, The University of Chicago, Chicago, Illinois 60637, United States

2. BioCAT and μCoSM, Pritzker Institute of Biomedical Science and Engineering, and CSRRI and Department of Biological Chemical and Physical Sciences, Illinois Institute of Technology, Chicago, Illinois 60616, United States

3. Biomolecular NMR Facility, Shared Research Facilities, The University of Chicago, Chicago, Illinois 60637, United States

4. Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-0520, United States

5. Department of Biochemistry and Molecular Biology, The University of Chicago, Chicago, Illinois 60637, United States

Publisher

American Chemical Society (ACS)

Subject

Biochemistry

Link

https://pubs.acs.org/doi/pdf/10.1021/bi1016217

Reference49 articles.

1. Mutation of the Alzheimer's Disease Amyloid Gene in Hereditary Cerebral Hemorrhage, Dutch Type

2. Amyloid β Protein Precursor Gene and Hereditary Cerebral Hemorrhage with Amyloidosis (Dutch)

3. Presenile Alzheimer dementia characterized by amyloid angiopathy and large amyloid core type senile plaques in the APP 692Ala→Gly mutation

4. The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Aβ protofibril formation

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