C.G. conceived and executed experiments and wrote the paper; I.T.W., E.J. and Y-A.L. executed experiments.
Oxidative stress increases levels of endogenous amyloid-β peptides secreted from primary chick brain neurons
Article first published online: 1 AUG 2008
© 2008 The Authors. Journal compilation © Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2008
Volume 7, Issue 5, pages 771–775, October 2008
How to Cite
Goldsbury, C., Whiteman, I. T., Jeong, E. V. and Lim, Y.-A. (2008), Oxidative stress increases levels of endogenous amyloid-β peptides secreted from primary chick brain neurons. Aging Cell, 7: 771–775. doi: 10.1111/j.1474-9726.2008.00423.x
- Issue published online: 17 SEP 2008
- Article first published online: 1 AUG 2008
- Accepted for publication 16 July 2008
- Alzheimer's disease;
- amyloid-β peptide;
- oxidative stress
Oxidative damage is associated with Alzheimer's disease and mild cognitive impairment, but its relationship to the development of neuropathological lesions involving accumulation of amyloid-β (Aβ) peptides and hyperphosphorylated tau protein remains poorly understood. We show that inducing oxidative stress in primary chick brain neurons by exposure to sublethal doses of H2O2 increases levels of total secreted endogenous Aβ by 2.4-fold after 20 h. This occurs in the absence of changes to intracellular amyloid precursor protein or tau protein levels, while heat-shock protein 90 is elevated 2.5-fold. These results are consistent with the hypothesis that aging-associated oxidative stress contributes to increasing Aβ generation and up-regulation of molecular chaperones in Alzheimer's disease.