LAUSR

DNA double-strand breaks (DSBs) are common events that were recognized as one of the most toxic lesions in eu-karyotic cells. DSBs are widely involved in many physiological processes such as V(D)J recombination, meiotic recombina-tion, DNA replication and transcription. Deregulation of DSBs has been reported in multiple diseases in human beings, such as the neurodegenerative diseases, with which the underlying mechanisms are needed to be illustrated. Here, we reviewed the recent insights into the dysfunction of DSB formation and repair, contributing to the pathogenesis of neurodegenerative dis-orders including Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD) and ataxia tel-angiectasia (A-T).