Enduring Elevations of Hippocampal Amyloid Precursor Protein and Iron Are Features of β-Amyloid Toxicity and Are Mediated by Tau-Reference-Cited by-同舟云学术

Enduring Elevations of Hippocampal Amyloid Precursor Protein and Iron Are Features of β-Amyloid Toxicity and Are Mediated by Tau

Published:2015-08-11 Issue:4 Volume:12 Page:862-873
ISSN:1933-7213
Container-title:Neurotherapeutics
language:en
Short-container-title:Neurotherapeutics

Author:

Li Xuling,Lei Peng^ORCID,Tuo Qingzhang,Ayton Scott,Li Qiao-Xin,Moon Steve,Volitakis Irene,Liu Rong,Masters Colin L.,Finkelstein David I.,Bush Ashley I.

Publisher

Springer Science and Business Media LLC

Subject

Pharmacology (medical),Neurology (clinical),Pharmacology

Link

http://link.springer.com/content/pdf/10.1007/s13311-015-0378-2.pdf

Reference47 articles.

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2. Rapoport M, Dawson HN, Binder LI, Vitek MP, Ferreira A. Tau is essential to beta-amyloid-induced neurotoxicity. Proc Natl Acad Sci U S A 2002;99:6364–6369.

3. Vossel KA, Zhang K, Brodbeck J, et al. Tau reduction prevents A{beta}-induced defects in axonal transport. Science 2010;330:198.

4. Shipton OA, Leitz JR, Dworzak J, et al. Tau protein is required for amyloid {beta}-induced impairment of hippocampal long-term potentiation. J Neurosci 2011;31:1688–1692.

5. Roberson ED, Scearce-Levie K, Palop JJ, et al. Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer’s disease mouse model. Science 2007;316:750–754.

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