The authors propose a novel mechanism, termed Activity‐DEPendent Transpositon (ADEPT), in which epigenetic drift and the preferential use of homologous‐directed repair allows transposable elements to hijack activity‐induced double‐strand breaks in aged neurons, contributing to neurodegenerative disease.[Image: see text]
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| http://dx.doi.org/10.15252/embr.201643797 | DOI Listing |
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Activity-DEPendent Transposition.
EMBO Rep
March 2017
Institute for Cell and Neurobiology, Charité Universitätsmedizin Berlin, Berlin, Germany.
The authors propose a novel mechanism, termed Activity‐DEPendent Transpositon (ADEPT), in which epigenetic drift and the preferential use of homologous‐directed repair allows transposable elements to hijack activity‐induced double‐strand breaks in aged neurons, contributing to neurodegenerative disease.[Image: see text]
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