@article{b4748e4a1599406a8f0147919a75aa04,
title = "Aggressive amyloidosis in mice expressing human amyloid peptides with the Arctic mutation",
abstract = "The Arctic mutation within the amyloid-β (Aβ) peptide causes Alzheimer disease. In vitro, Arctic-mutant Aβ forms (proto)fibrils more effectively than wild-type Aβ. We generated transgenic mouse lines expressing Arctic-mutant human amyloid precursor proteins (hAPP). Amyloid plaques formed faster and were more extensive in Arctic mice than in hAPP mice expressing wild-type Aβ, even though Arctic mice had lower Aβ1-42/1-40 ratios. Thus, the Arctic mutation is highly amyloidogenic in vivo.",
author = "Cheng, {Irene H.} and Palop, {Jorge J.} and Esposito, {Luke A.} and Nga Bien-Ly and Fengrong Yan and Lennart Mucke",
note = "Funding Information: We thank E. Koo for the CT15 antibody, P. Seubert for the 8E5 antibody, G.-Q. Yu and X. Wang for technical support, G. Howard and S. Ordway for editorial review, and D. McPherson and L. Manuntag for administrative assistance. This study was supported in part by United States Public Health Services grants AG11385, AG022074 and NS41787 to L.M. and National Institute on Aging-funded Training Grant T32 AG00278 (I.C.).",
year = "2004",
month = nov,
doi = "10.1038/nm1123",
language = "English",
volume = "10",
pages = "1190--1192",
journal = "Nature Medicine",
issn = "1078-8956",
publisher = "Nature Publishing Group",
number = "11",
}
