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In eukaryotic cell nuclei, DNA is wrapped around and firmly associated with histone proteins, forming chromatin. When DNA is damaged, the chromatin structure needs to be loosened to allow repair enzymes to gain access to the damage. This requires modifying the histone proteins. These modifications, called epigenetic alterations, do not alter the base-pair sequence. Repair-associated epigenetic alterations are usually transient, removed when no longer needed for repair. However, some remain after repair. In the human brain, long-lasting novel epigenetic alterations appear to account for the persistence of addictions to such substances as alcohol, nicotine and cocaine. Certain neurodegenerative diseases are caused by inherited mutations in genes necessary for DNA repair. Deficient DNA repair in these diseases is associated with extensive epigenetic alterations that likely have a role in the disease phenotype. Persistent epigenetic alterations due to DNA repair processes, both histone modifications and methylations of DNA, can also have positive consequences. Stimulation of brain activity (e.g. learning and memory formation) is often accompanied by the generation of DNA damage in neuronal DNA, followed by repair associated with persistent epigenetic alterations. In particular, recent research has shown the need for non-homologous end joining and base excision repair in memory formation.

The Role of DNA Repair and the Epigenetic Markers Left after Repair in Neurologic Functions, Including Memory and Learning