APE1/Ref-1 in Alzheimer's disease: an immunohistochemical study.

Abstract

The oxidative injury in Alzheimer's disease (AD), in which amyloid beta protein induces production of reactive oxygen species, may be cause of neurodegeneration. APE1/Ref-1 is a protein involved in DNA repair and in redox co-activating function over different transcription factors. We investigated by immunohistochemistry using a highly specific monoclonal antibody, the localization of APE1/Ref-1 in autoptic and bioptic AD brain tissues in comparison with brains with unrelated pathological or normal conditions. Reliable APE1/Ref-1 immunostaining was obtained in biopsies, but not in autoptic tissues. An increased nuclear expression of APE1/Ref-1 in AD cerebral cortex supports the view that the cellular adaptive response to the oxidative stress condition is involved in the pathogenesis of this disease.

• Authors: Gabriella Marcon, Gianluca Tell, Lorena Perrone, Rita Garbelli, Franco Quadrifoglio, Fabrizio Tagliavini, Giorgio Giaccone
• Journal: Neuroscience letters (Neurosci Lett) Vol. 466 Issue 3 Pg. 124-7 (Dec 11 2009) ISSN: 1872-7972 [Electronic] Ireland
• PMID: 19782121 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antibodies, Monoclonal
• APEX1 protein, human
• DNA-(Apurinic or Apyrimidinic Site) Lyase

Topics

• Aged
• Alzheimer Disease (metabolism)
• Antibodies, Monoclonal
• Autopsy
• Biopsy
• Brain (metabolism)
• DNA-(Apurinic or Apyrimidinic Site) Lyase (immunology, metabolism)
• Humans
• Immunohistochemistry
• Middle Aged