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Abstract
DNA damage contributes to brain aging and neurodegenerative diseases. This research shows that HDAC1 modulates OGG1-initiated 8-oxoguanine (8-oxoG) repair in the brain. HDAC1-deficient mice exhibit age-associated DNA damage, cognitive impairment, and impaired OGG1 activity. HDAC1 deficiency leads to 8-oxoG accumulation at gene promoters, causing transcriptional repression. Similar effects are observed in a 5XFAD Alzheimer's disease mouse model. Pharmacological HDAC1 activation alleviates these effects, highlighting its therapeutic potential.
Publisher
NATURE COMMUNICATIONS
Published On
May 18, 2020
Authors
Ping-Chieh Pao, Debasis Patnaik, L. Ashley Watson, Fan Gao, Ling Pan, Jun Wang, Chinnakkaruppan Adaikkan, Jay Penney, Hugh P. Cam, Wen-Chin Huang, Lorena Pantano, Audrey Lee, Alexi Nott, Trongha X. Phan, Elizabeta Gjoneska, Sara Elmsaouri, Stephen J. Haggarty, Li-Huei Tsai
Tags
DNA damage
neurodegeneration
HDAC1
brain aging
cognitive impairment
OGG1
therapeutics

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