Title page for etd-1103115-165537


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URN etd-1103115-165537
Author Yu-Ru Li
Author's Email Address linkin519@hotmail.com
Statistics This thesis had been viewed 5567 times. Download 4 times.
Department Biological Sciences
Year 2015
Semester 1
Degree Master
Type of Document
Language zh-TW.Big5 Chinese
Title To Explore β-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons
Date of Defense 2015-10-28
Page Count 56
Keyword
  • β-amyloid
  • Amyloid precursor protein
  • Alzheimer's disease
  • DNA repair
  • Neurotoxicity
  • Abstract Alzheimer's disease (AD) is one of the common form of age-related neurodegenerative diseases and the leading cause of senile dementia. In the beta-amyloid (Aβ) cascade hypothesis, the aggregation of Aβ is a crucial event that produces amounts of oxidative stress contributed to neurotoxicity. In this study, our hypothesis is that Aβ-peptide aggregation enhances oxidative stress which leads to DNA damage and contributes to neurotoxicity. Therefore, increasing DNA repair efficiency and DNA integrity could rescue neuronal cells from Aβ-induced neuronal death. To test our hypothesis, we utilized lentivirus transduction to overexpress Aβ in rat primary cortical neurons. Results of Western blotting and dihydroethidium (DHE) staining have shown that expression of Aβ reached the peak in the first three days as well as the production of reactive oxygen species (ROS), then both Aβ and ROS levels were decreasing in the following day four to day seven. The DNA damage marker, phosphor-histone 2A (γH2AX), demonstrated that neuronal DNA injury was correlated to both levels of Aβ and ROS. Glucagon-like peptide-1 (GLP-1) is a growth factor which has been proved to have neuroprotective properties. After GLP-1 treatment, the production of Aβ and ROS was reduced, but γH2AX was still remaining in 72 hours. GLP-1 has been proved the effects of decreasing Aβ, inflammation and the improvement of recognition, learning and memory in animal model from previous studies. Although we did not see GLP-1 significantly reducing γH2AX, GLP-1 is still a potential drug involving DNA repair. In Alzheimer’s disease, to elevate DNA repair capability is also a important field to investigate in the future.
    Advisory Committee
  • Steve Leu - chair
  • Wu, Kay L.H. - co-chair
  • Yang, Jenq-Lin - advisor
  • Chen Chun-Lin - advisor
  • Files
  • etd-1103115-165537.pdf
  • Indicate in-campus at 5 year and off-campus access at 5 year.
    Date of Submission 2016-01-11

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