TY - JOUR
T1 - Effect of advanced glycation endproducts on cell cycle and their relevance for Alzheimer's disease
AU - Münch, G.
AU - Gasic-Milenkovic, J.
AU - Arendt, T.
PY - 2003
Y1 - 2003
N2 - 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.
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.
UR - http://www.scopus.com/inward/record.url?scp=0141906286&partnerID=8YFLogxK
U2 - 10.1007/978-3-7091-0643-3_4
DO - 10.1007/978-3-7091-0643-3_4
M3 - Article
C2 - 12946049
AN - SCOPUS:0141906286
SN - 0303-6995
SP - 63
EP - 71
JO - Journal of Neural Transmission, Supplement
JF - Journal of Neural Transmission, Supplement
IS - 65
ER -