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HDAC1 modulates OGG1-initiated oxidative DNA damage repair in the aging brain and Alzheimer's disease

Medicine and Health

HDAC1 modulates OGG1-initiated oxidative DNA damage repair in the aging brain and Alzheimer's disease

P. Pao, D. Patnaik, et al.

Exciting research by Ping-Chieh Pao and colleagues reveals how HDAC1 influences the brain's ability to repair DNA damage, which is crucial for combating aging and neurodegenerative diseases. Their findings show that enhancing HDAC1 activity could be a promising therapeutic approach to mitigate cognitive decline.

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Playback language: English
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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