• Open Access

Oxidative stress increases levels of endogenous amyloid-β peptides secreted from primary chick brain neurons

Authors

  • Claire Goldsbury,

    1. Brain and Mind Research Institute, University of Sydney, Camperdown, NSW 2050, Australia
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  • Ineka T. Whiteman,

    1. Brain and Mind Research Institute, University of Sydney, Camperdown, NSW 2050, Australia
    2. Discipline of Anatomy and Histology, Bosch Institute, School of Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia
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  • Erica V. Jeong,

    1. Brain and Mind Research Institute, University of Sydney, Camperdown, NSW 2050, Australia
    2. Discipline of Anatomy and Histology, Bosch Institute, School of Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia
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  • Yun-An Lim

    1. Brain and Mind Research Institute, University of Sydney, Camperdown, NSW 2050, Australia
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  • C.G. conceived and executed experiments and wrote the paper; I.T.W., E.J. and Y-A.L. executed experiments.


Claire Goldsbury, Brain and Mind Research Institute, University of Sydney, 100 Mallett St, Camperdown, NSW 2050, Australia. Tel.: +61 2 9351 0878; fax: +61 2 9351 0731; e-mail: cgoldsbury@usyd.edu.au

Summary

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.

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