PLoS ONE · 2013 · 14 citations · 63 references
Life SciencesNeurobiologyNeuroscienceDementiaMolecular NeuroscienceNeurodegenerationAlzheimer DiseaseCell-cycle CheckpointsCell-cycle DysregulationMitochondrial DysfunctionNeurodegenerative DiseasesNeurodegenerative DisordersCell Cycle Checkpoint DisruptionCell Cycle Checkpoint DysfunctionCell Cycle Checkpoint FailureCell-cycle Checkpoint RegulationDna Damage Checkpoint KinasesDna Damage Checkpoint SignalingDna Damage Response GenesDna Damage Response Pathways
Background: Increasing evidence suggests an association between neuronal cell cycle (CCL) events and the processes that underlie neurodegeneration in Alzheimer's disease (AD). Elevated levels of oxidative stress markers and mitochondrial dysfunction are also among early events in AD. Recent studies have reported the role of CCL checkpoint proteins and tumor suppressors, such as ATM and p53 in the control of glycolysis and oxidative metabolism in cancer, but their involvement in AD remains uncertain.
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