Satou T, Cummings B J, Cotman C W
Institute for Brain Aging and Dementia, University of California, Irvine 92717-4550, USA.
Brain Res. 1995 Oct 30;697(1-2):35-43. doi: 10.1016/0006-8993(95)00748-f.
Bcl-2 protein has been suggested to be one of the proteins preventing apoptosis in a variety of cell types. Recently, apoptosis has been suggested to have an important role in the pathogenesis of Alzheimer's disease (AD). We have utilized Bcl-2 immunohistochemical methods to examine Bcl-2 in the hippocampus and entorhinal cortex of AD patients ranging in clinical and neuropathological severity from mild to severe and compared these results to those obtained from age-matched controls. Immunoreactivity for Bcl-2 was predominantly found within neurons. Bcl-2 immunostaining within AD tissue was increased relative to controls in most neurons of the entorhinal cortex, subiculum, CA1, CA2, CA3, hilus and dentate gyrus. Relative Bcl-2 staining increased in parallel with increasing disease severity. However, neurons exhibiting immunoreactivity for markers of neurofibrillary tangle formation (AT8 and PHF-1) showed reduced Bcl-2 staining, suggesting that Bcl-2 may be down regulated in these degenerating neurons. Bcl-2 immunoreactivity within astrocytes and the vasculature was also increased in AD. These results suggest that Bcl-2 protein may have a role in compensation responses to AD pathology, perhaps affording to the remaining neurons a margin of protection from apoptosis.
Bcl-2蛋白被认为是多种细胞类型中阻止细胞凋亡的蛋白之一。最近，细胞凋亡被认为在阿尔茨海默病（AD）的发病机制中起重要作用。我们利用Bcl-2免疫组化方法检测了临床和神经病理学严重程度从轻度到重度的AD患者海马体和内嗅皮质中的Bcl-2，并将这些结果与年龄匹配的对照组的结果进行了比较。Bcl-2的免疫反应主要在神经元内发现。在AD组织中，内嗅皮质、海马下托、CA1、CA2、CA3、齿状回门和齿状回的大多数神经元中，相对于对照组，Bcl-2免疫染色增加。相对Bcl-2染色随着疾病严重程度的增加而平行增加。然而，对神经原纤维缠结形成标记物（AT8和PHF-1）表现出免疫反应的神经元显示Bcl-2染色减少，这表明在这些退化的神经元中Bcl-2可能被下调。AD中星形胶质细胞和脉管系统内的Bcl-2免疫反应性也增加。这些结果表明，Bcl-2蛋白可能在对AD病理学的代偿反应中起作用，也许为剩余的神经元提供一定程度的保护以免于凋亡。
