Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1772, Issue 4, Pages 409-412Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbadis.2006.10.016
Keywords
Alzheimer's disease; beta-amyloid; DNA polymerase-beta; APE-1; cell cycle; DNA replication; apoptosis
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The mechanism whereby a reactivation of cell cycle in neurons causes cell death is beginning to be identified. In cellular models of Alzheimer's disease, activation of a non-canonical pathway of DNA replication contributes to neuronal death. This pathway involves the repair enzyme DNA polymerase-beta, which is highly expressed in neurons of the Alzheimer's brain at early stages of the disease. Loading of DNA polymerase-beta into the replication forks generates a death signal, which involves the turner suppressor p53. The increasing knowledge of the main actors of the unscheduled DNA replication in neurons will pave the way for novel therapeutic interventions in Alzheimer's disease and other neurodegenerative disorders. (c) 2006 Elsevier B.V. All rights reserved.
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