The role of DNA double-strand break repair defects in the pathogenesis of neurodegenerative diseases

Abstract

DNA double-strand break repair (DSBR) plays an important role in maintaining genome stability and cell survival. DSBR are predominately accomplished by two pathways: Homologous Recombination (HR) and Non-homologous End Joining (NHEJ), and both pathways are essential for the maintenance of physiological functions in neurons. Dysregulation of DSBR has been reported to be involved in multiple neurodegenerative diseases. Therefore, a deeper understanding of mechanisms in the DSBR will provide further insights into the pathogenesis of distinct neurodegenerative disease and help to develop effective therapeutics for these diseases. In this review, we provide a comprehensive overview of the common DSBR pathways, and summarize the latest involvement of DSBR in the pathogenic mechanisms of several common neurodegenerative diseases.

Keywords

• dna double-strand break repair
• homologous recombination
• non-homologous end joining
• neurodegenerative diseases