期刊
NUCLEIC ACIDS RESEARCH
卷 43, 期 2, 页码 943-959出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gku1356
关键词
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资金
- Intramural Research Program of the National Institutes of Health (NIH), National Institute on Aging [Z01-AG00735]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo-FAPESP [2013/11052-1]
- NIH Intramural Program
We explore the role of DNA damage processing in the progression of cognitive decline by creating a new mouse model. The new model is a cross of a common Alzheimer's disease (AD) mouse (3xTgAD), with a mouse that is heterozygous for the critical DNA base excision repair enzyme, DNA polymerase beta. A reduction of this enzyme causes neurodegeneration and aggravates the AD features of the 3xTgAD mouse, inducing neuronal dysfunction, cell death and impairing memory and synaptic plasticity. Transcriptional profiling revealed remarkable similarities in gene expression alterations in brain tissue of human AD patients and 3xTg/Pol beta(+/-) mice including abnormalities suggestive of impaired cellular bioenergetics. Our findings demonstrate that a modest decrement in base excision repair capacity can render the brain more vulnerable to AD-related molecular and cellular alterations.
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