Shimohama S, Narita M, Matsushima H, Kimura J, Kameyama M, Hagiwara M, Hidaka H, Taniguchi T
Department of Neurology, Faculty of Medicine, Kyoto University, Japan.
Neurology. 1993 Jul;43(7):1407-13. doi: 10.1212/wnl.43.7.1407.
We assessed the amount of protein kinase C (PKC) in samples from postmortem normal human and Alzheimer's disease (AD) brains by a two-site enzyme immunoassay that quantitatively identified types alpha, beta, and gamma isozymes. In the normal human brain matter, type beta was the main type present, the majority of each isozyme of PKC being present in the membranous fraction of the brain tissues. In AD brains, the amount of type beta PKC was significantly reduced in the membranous fraction of the temporal cortical tissues. The amounts of types alpha and gamma in the membranous fraction and types alpha, beta, and gamma in the cytosolic fraction in AD brains were lower than in the control brains, but the difference was not significant. There was also a significant decrease in the levels of PKC in the membranous fraction of AD brains, as measured by radioactive phorbol ester binding. These results suggest that the type beta PKC isozyme is mainly present in the human temporal cortex and that reduced levels of type beta PKC in the membranous fraction may reflect a biochemical deficit related specifically to the pathogenesis of AD.
我们通过一种能定量鉴定α、β和γ同工酶类型的双位点酶免疫测定法，评估了来自死后正常人脑和阿尔茨海默病（AD）脑样本中的蛋白激酶C（PKC）含量。在正常人类脑组织中，β型是主要存在的类型，PKC的每种同工酶大部分存在于脑组织的膜部分。在AD脑中，颞叶皮质组织膜部分的β型PKC含量显著降低。AD脑的膜部分中α和γ型以及胞质部分中α、β和γ型的含量低于对照脑，但差异不显著。通过放射性佛波酯结合测定，AD脑膜部分的PKC水平也显著降低。这些结果表明，β型PKC同工酶主要存在于人类颞叶皮质中，膜部分β型PKC水平的降低可能反映了与AD发病机制相关的特定生化缺陷。
