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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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
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