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

G. Münch; J. Gasic-Milenkovic; T. Arendt

doi:10.1007/978-3-7091-0643-3_4

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

G. Münch
, J. Gasic-Milenkovic
, T. Arendt

Neuroimmunological Cell Biology Unit
Leipzig University

Research output: Contribution to journal › Article › peer-review

30 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	63-71
Number of pages	9
Journal	Journal of Neural Transmission, Supplement
Issue number	65
DOIs	https://doi.org/10.1007/978-3-7091-0643-3_4
Publication status	Published - 2003
Externally published	Yes

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AU - Arendt, T.

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AB - 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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DO - 10.1007/978-3-7091-0643-3_4

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JO - Journal of Neural Transmission, Supplement

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ER -

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

Abstract

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