p66Shc activation promotes increased oxidative phosphorylation and renders CNS cells more vulnerable to amyloid beta toxicity-Reference-Cited by-同舟云学术

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p66Shc activation promotes increased oxidative phosphorylation and renders CNS cells more vulnerable to amyloid beta toxicity

Published:2018-11-20 Issue:1 Volume:8 Page:
ISSN:2045-2322
Container-title:Scientific Reports
language:en
Short-container-title:Sci Rep

Author:

Lone Asad,Harris Richard A.,Singh Olivia,Betts Dean H.,Cumming Robert C.

Funder

Canada Foundation for Innovation

Gouvernement du Canada | Natural Sciences and Engineering Research Council of Canada

Publisher

Springer Science and Business Media LLC

Subject

Multidisciplinary

Link

http://www.nature.com/articles/s41598-018-35114-y.pdf

Reference117 articles.

1. Mosconi, L., Pupi, A. & De Leon, M. J. Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer’s disease. Ann N. Y. Acad Sci. 1147, 180–95 (2008).

2. Nistor, M. et al. Alpha-and beta-secretase activity as a function of age and beta-amyloid in Down syndrome and normal brain. Neurobiol Aging. 28, 1493–1506 (2007).

3. Pedersen, J. T. & Sigurdsson, E. M. Tau immunotherapy for Alzheimer’s disease. Trends Mol Med. 21, 394–402 (2015).

4. Masters, C. L. et al. Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proc Natl Acad Sci. 82, 4245–4249 (1985).

5. Morris, J. C. et al. Cerebral amyloid deposition and diffuse plaques in “normal” aging: Evidence for presymptomatic and very mild Alzheimer’s disease. Neurol. 46, 707–719 (1996).

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