Attems Johannes, Jellinger Kurt A
Institute of Pathology, Otto Wagner Hospital, Baumgartner Hoehe 1, 1140 Vienna, Austria.
Acta Neuropathol. 2004 Feb;107(2):83-90. doi: 10.1007/s00401-003-0796-9. Epub 2003 Dec 4.
Data on the relationship between cerebral amyloid angiopathy (CAA) ("congophilic angiopathy") and Alzheimer's disease (AD) pathology are conflicting. In the present study, CAA and capillary CAA (CapCAA) ("dyshoric angiopathy") were examined in the frontal cortex of 100 human brains obtained at autopsy from both male and female, demented and non-demented patients (mean age +/- SD 84.3+/-9.3 years); 50 brains with high (mean 5.0) and 50 with low (mean 2.4) Braak stages. CAA was assessed according to the method of Olichney et al. [25]; CapCAA was grouped into four grades by counting the affected capillaries in 10 high power fields. General CAA was present in 61% (87.5% demented, 55.6% non-demented; 70% with high and 52% low Braak stages). CAA did not correlate with either clinical diagnosis of dementia or high-grade AD pathology; CapCAA showed a low correlation with dementia and a medium positive correlation with high Braak stages. The severity of both lesions did not correlate with clinical dementia; whereas that of CAA showed low correlation with CERAD, Braak, and NIA-Reagan-Institute criteria, the severity of CapCAA correlated significantly with all three AD criteria. The presence and severity of CAA and CapCAA showed only low correlation, suggesting a different pathogenesis of these types of lesion. Since CapCAA represents insoluble amyloid peptide (Abeta) deposits in and around capillaries, its correlation with neuritic AD pathology supports the concept of neuronal origin of Abeta via drainage from interstitial fluid from the central nervous system to capillary walls. Studies to answer the question whether CapCAA represents an epiphenomenon or an indicator of a pathogenic association between tau cytopathology and Abeta deposition in capillaries are in progress.
关于脑淀粉样血管病（CAA）（“嗜刚果红血管病”）与阿尔茨海默病（AD）病理之间关系的数据存在矛盾。在本研究中，对100例男女皆有、患有痴呆和未患痴呆的患者（平均年龄±标准差84.3±9.3岁）尸检获得的人脑额叶皮质进行了CAA和毛细血管CAA（CapCAA）（“发育异常性血管病”）检查；50例Braak分期高（平均5.0）的脑和50例Braak分期低（平均2.4）的脑。根据Olichney等人[25]的方法评估CAA；通过在10个高倍视野中计数受影响的毛细血管将CapCAA分为四个等级。61%存在一般性CAA（痴呆患者中为87.5%，非痴呆患者中为55.6%；Braak分期高的患者中为70%，分期低的患者中为52%）。CAA与痴呆的临床诊断或高级别AD病理均无相关性；CapCAA与痴呆呈低相关性，与高Braak分期呈中度正相关。两种病变的严重程度均与临床痴呆无关；而CAA的严重程度与CERAD、Braak和NIA-里根-研究所标准呈低相关性，CapCAA 的严重程度与所有三项AD标准均显著相关。CAA和CapCAA的存在及严重程度仅呈低相关性，提示这些类型病变的发病机制不同。由于CapCAA代表毛细血管内及周围的不溶性淀粉样肽（Aβ）沉积，其与神经炎性AD病理的相关性支持Aβ通过从中枢神经系统间质液引流至毛细血管壁而起源于神经元的概念。关于CapCAA是代表一种副现象还是tau细胞病理学与毛细血管中Aβ沉积之间致病关联指标的问题，相关研究正在进行中。
