DNA double strand breaks: A common theme in neurodegenerative diseases

Daniela Merlo, Cristiana Mollinari, Mauro Racaniello, Enrico Garaci, Alessio Cardinale

Research output: Contribution to journalReview articlepeer-review

Abstract

Accumulation of DNA damage and impairment of DNA repair systems are involved in the pathogenesis of different neurodegenerative diseases. Whenever DNA damage is too extensive, the DNA damage response pathway provides for triggering cellular senescence and/or apoptosis. However, whether the increased level of DNA damage in neurodegenerative disorders is a cause rather than the consequence of neurodegenerative events remains to be established. Among possible DNA lesions, DNA double strand breaks (DSBs) are rare events, nevertheless they are the most lethal form of DNA damage. In neurons, DSBs are particularly deleterious because of their reduced DNA repair capability as compared to proliferating cells. Here, we provide a description of DSB repair systems and describe human studies showing the presence of several types of DNA lesions in three major neurodegenerative diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD). Then, we analyze the role of DSB accumulation and deficiency of DSB repair systems in neurodegeneration by examining studies on animal models of neurodegenerative diseases.

Original languageEnglish
Pages (from-to)1208-1218
Number of pages11
JournalCurrent Alzheimer Research
Volume13
Issue number11
DOIs
Publication statusPublished - Nov 1 2016

Keywords

  • Alzheimer’s disease
  • DNA damage
  • DNA double strand breaks
  • DNA repair
  • Huntington’s disease
  • Neurodegenerative diseases
  • Parkinson’s disease

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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