, Volume 10, Issue 4, pp 817–830

Chromatin Modifications Associated with DNA Double-strand Breaks Repair as Potential Targets for Neurological Diseases


DOI: 10.1007/s13311-013-0210-9

Cite this article as:
Brochier, C. & Langley, B. Neurotherapeutics (2013) 10: 817. doi:10.1007/s13311-013-0210-9


The integrity of the genome is continuously challenged by both endogenous and exogenous DNA damaging agents. Neurons, due to their post-mitotic state, high metabolism, and longevity are particularly prone to the accumulation of DNA lesions. Indeed, DNA damage has been suggested as a major contributor to both age-associated neurodegenerative diseases and acute neurological injury. The DNA damage response is a key factor in maintaining genome integrity. It relies on highly dynamic posttranslational modifications of the chromatin and DNA repair proteins to allow signaling, access, and repair of the lesion. Drugs that modulate the activity of the enzymes responsible for these modifications have emerged as attractive therapeutic compounds to treat neurodegeneration. In this review, we discuss the role of DNA double-strand breaks and abnormal chromatin modification patterns in a range of neurodegenerative conditions, and the chromatin modifiers that might ameliorate them. Finally, we suggest that understanding the epigenetic modifications specific to neuronal DNA repair is crucial for the development of efficient neurotherapeutic strategies.


Neurodegeneration DNA damage DNA repair Chromatin modification Epigenetics 

Supplementary material

13311_2013_210_MOESM1_ESM.pdf (1.2 mb)
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Copyright information

© The American Society for Experimental NeuroTherapeutics, Inc. 2013

Authors and Affiliations

  1. 1.The Burke Medical Research InstituteWhite PlainsUSA
  2. 2.Department of Neurology and NeuroscienceWeill Medical College of Cornell UniversityNew YorkUSA

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