Potent amyloidogenicity and pathogenicity of Aβ43-Reference-Cited by-同舟云学术

Potent amyloidogenicity and pathogenicity of Aβ43

Published:2011-07-03 Issue:8 Volume:14 Page:1023-1032
ISSN:1097-6256
Container-title:Nature Neuroscience
language:en
Short-container-title:Nat Neurosci

Author:

Saito Takashi,Suemoto Takahiro,Brouwers Nathalie,Sleegers Kristel,Funamoto Satoru,Mihira Naomi,Matsuba Yukio,Yamada Kazuyuki,Nilsson Per,Takano Jiro,Nishimura Masaki,Iwata Nobuhisa,Van Broeckhoven Christine,Ihara Yasuo,Saido Takaomi C

Publisher

Springer Science and Business Media LLC

Subject

General Neuroscience

Link

http://www.nature.com/articles/nn.2858.pdf

Reference50 articles.

1. Blennow, K., de Leon, M.J. & Zetterberg, H. Alzheimer's disease. Lancet 368, 387–403 (2006).

2. Miravalle, L. et al. Amino-terminally truncated Aβ peptide species are the main component of cotton wool plaques. Biochemistry 44, 10810–10821 (2005).

3. Van Vickle, G.D. et al. TgCRND8 amyloid precursor protein transgenic mice exhibit an altered γ-secretase processing and an aggressive, additive amyloid pathology subject to immunotherapeutic modulation. Biochemistry 46, 10317–10327 (2007).

4. Iizuka, T. et al. Amyloid β-protein ending at Thr43 is a minor component of some diffuse plaques in the Alzheimer's disease brain, but is not found in cerebrovascular amyloid. Brain Res. 702, 275–278 (1995).

5. Parvathy, S. et al. Correlation between Aßx-40-, Aßx-42- and Aßx-43-containing amyloid plaques and cognitive decline. Arch. Neurol. 58, 2025–2032 (2001).

Cited by 256 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. Production of a heterozygous exon skipping model of common marmosets using gene-editing technology;Lab Animal;2024-08-30

2. The dopaminergic system promotes neprilysin-mediated degradation of amyloid-β in the brain;Science Signaling;2024-08-06

3. Oligomer Formation by Physiologically Relevant C-Terminal Isoforms of Amyloid β-Protein;Biomolecules;2024-06-28

4. Rodent Models of Alzheimer’s Disease: Past Misconceptions and Future Prospects;International Journal of Molecular Sciences;2024-06-05

5. The presenilin 1 mutation P436S causes familial Alzheimer's disease with elevated Aβ43 and atypical clinical manifestations;Alzheimer's & Dementia;2024-06-02