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Updated: Jun 17, 2026

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress
Published on: May 7, 2014
Review: cell cycle aberrations and neurodegeneration
D J Bonda1, V P Bajić, B Spremo-Potparevic
1Departments of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Alzheimer disease (AD) involves abnormal cell cycle re-entry, a key factor in its development. Our hypothesis suggests that cell cycle alterations combined with oxidative stress drive neurodegeneration in AD.
Area of Science:
- Cellular Biology
- Neuroscience
- Pathology
Background:
- The cell cycle is a fundamental cellular process crucial for cell integrity.
- Aberrations in cell cycle regulation are implicated in neurodegenerative diseases like Alzheimer disease (AD).
- Abnormal cell cycle re-entry is observed early in AD pathogenesis, preceding other disease hallmarks.
Purpose of the Study:
- To review evidence linking cell cycle mechanisms to Alzheimer disease.
- To propose a 'Two-Hit Hypothesis' for AD pathogenesis.
- To explore new therapeutic opportunities based on cell cycle and oxidative stress interactions.
Main Methods:
- Review of existing scientific literature on cell cycle regulation in AD.
- Analysis of the interplay between cell cycle alterations and oxidative stress.
- Synthesis of evidence to support the 'Two-Hit Hypothesis'.
Main Results:
- Cell cycle re-entry is a significant early event in Alzheimer disease.
- The combination of cell cycle alterations and oxidative stress is proposed as a key driver of neurodegeneration.
- This interaction can trigger a cascade of events leading to AD pathology.
Conclusions:
- Cell cycle dysregulation is a critical factor in Alzheimer disease etiology.
- The 'Two-Hit Hypothesis' provides a framework for understanding AD pathogenesis.
- Targeting the interaction between cell cycle and oxidative stress may offer novel therapeutic strategies for AD.
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