Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.
Neurosci Lett. 2009 Dec 11;466(3):124-7. doi: 10.1016/j.neulet.2009.09.039. Epub 2009 Sep 25.
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.
阿尔茨海默病（AD）中的氧化损伤，其中淀粉样β蛋白诱导活性氧的产生，可能是神经退行性变的原因。APE1/Ref-1 是一种参与 DNA 修复和不同转录因子的氧化还原共激活功能的蛋白质。我们使用高度特异性的单克隆抗体通过免疫组织化学研究了 APE1/Ref-1 在尸检和活检 AD 脑组织中的定位与无相关病理或正常条件的脑组织进行比较。在活检中获得了可靠的 APE1/Ref-1 免疫染色，但在尸检组织中未获得。AD 大脑皮层中 APE1/Ref-1 的核表达增加支持这样一种观点，即细胞对氧化应激条件的适应性反应参与了这种疾病的发病机制。
