Chandrasekaran K, Hatanpää K, Brady D R, Stoll J, Rapoport S I
Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA.
Brain Res. 1998 Jun 15;796(1-2):13-9. doi: 10.1016/s0006-8993(98)00248-0.
Messenger RNA (mRNA) for cytochrome oxidase subunit II (COX II) was localized by in situ hybridization in the entorhinal cortex and hippocampal formation of postmortem brain tissue from normal human subjects and from patients with Alzheimer disease (AD). In the control entorhinal cortex, COX II mRNA was detected mainly in neuronal cell bodies of layers II and IV. In control hippocampal formation, highest levels were localized in neuronal cell bodies of the dentate gyrus and the CA3 and CA1 regions, neurons that are involved in the major input and output pathways of the hippocampal formation. In AD brain, COX II mRNA was markedly reduced in the entorhinal cortex and the hippocampal formation compared with control brain. In the AD hippocampal formation, reductions were in regions severely affected by AD pathology as well as in regions that were relatively spared. These results are consistent with the hypothesis that reduced mitochondrial energy metabolism reflects loss of neuronal connections in AD.
通过原位杂交技术，在正常人类受试者以及阿尔茨海默病（AD）患者死后的脑组织内，对细胞色素氧化酶亚基II（COX II）的信使核糖核酸（mRNA）进行了定位。在对照的内嗅皮质中，COX II mRNA主要在第II层和第IV层的神经元细胞体中检测到。在对照的海马结构中，最高水平定位于齿状回以及CA3和CA1区的神经元细胞体，这些神经元参与海马结构的主要输入和输出通路。与对照脑相比，AD脑内嗅皮质和海马结构中的COX II mRNA明显减少。在AD海马结构中，受AD病理严重影响的区域以及相对未受影响的区域均出现减少。这些结果与线粒体能量代谢降低反映AD中神经元连接丧失这一假说相符。
