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Effect of advanced glycation endproducts on cell cycle and their relevance for Alzheimer’s disease

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Advances in Research on Neurodegeneration

Part of the book series: Journal of Neural Transmission. Supplementa ((NEURAL SUPPL,volume 65))

Summary

In Alzheimer’s disease, neurons in affected regions re-enter the cell cycle, leave the G0 state and appear to be arrested at both the G1/S and G2/M phase with resulting cell death, predominantly by apoptosis. Further hallmarks of AD are crosslinked protein deposits (amyloid plaques and neurofibrillary tangles), which time-dependently become modified by “advanced glycation endproducts (AGEs)”. Since AGEs activate both mitogenic and redox-sensitive pathways, they might be involved both in cell cycle re-entry and arrest.

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Abbreviations

Aβ):

β-amyloid peptide

AD):

Alzheimer’s disease

AGEs):

advanced glycation endproducts

APP):

amyloid precursor protein

GSH):

reduced lutathione

MAP):

microtubuli associated protein tai

NFT):

neurofibrillary tangles

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© 2003 Springer-Verlag Wien

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Münch, G., Gasic-Milenkovic, J., Arendt, T. (2003). Effect of advanced glycation endproducts on cell cycle and their relevance for Alzheimer’s disease. In: Horowski, R., et al. Advances in Research on Neurodegeneration. Journal of Neural Transmission. Supplementa, vol 65. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0643-3_4

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  • DOI: https://doi.org/10.1007/978-3-7091-0643-3_4

  • Publisher Name: Springer, Vienna

  • Print ISBN: 978-3-211-83907-2

  • Online ISBN: 978-3-7091-0643-3

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