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Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
Published on: July 26, 2011
APE1/Ref-1 in Alzheimer's disease: an immunohistochemical study
Gabriella Marcon1, Gianluca Tell, Lorena Perrone
1Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. gmarcon@istituto-besta.it
Neuroscience Letters
|September 29, 2009
Summary
Oxidative stress in Alzheimer's disease (AD) may cause neurodegeneration. Researchers found increased APE1/Ref-1 protein in AD brain cells, suggesting a cellular response to oxidative stress is involved in AD.
Area of Science:
- Neuroscience
- Biochemistry
- Genetics
Background:
- Alzheimer's disease (AD) pathogenesis involves oxidative injury, where amyloid beta protein triggers reactive oxygen species production, leading to neurodegeneration.
- APE1/Ref-1 is a crucial protein with roles in DNA repair and redox co-activation of transcription factors.
Purpose of the Study:
- To investigate the localization of APE1/Ref-1 in Alzheimer's disease (AD) brain tissues.
- To compare APE1/Ref-1 expression in AD brains with normal or pathologically unrelated brain tissues.
Main Methods:
- Immunohistochemistry utilizing a highly specific monoclonal antibody.
- Analysis of autoptic and bioptic brain tissues from AD patients and control groups.
Main Results:
- Reliable APE1/Ref-1 immunostaining was successfully achieved in brain biopsies.
- Autoptic tissues did not yield reliable APE1/Ref-1 immunostaining.
- A notable increase in nuclear APE1/Ref-1 expression was observed in the cerebral cortex of AD brains.
Conclusions:
- The findings support the involvement of cellular adaptive responses to oxidative stress in Alzheimer's disease pathogenesis.
- Increased nuclear APE1/Ref-1 expression in AD cerebral cortex indicates its potential role in the disease process.
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