Buée L, Hof P R, Delacourte A
INSERM U422, Lille, France.
Ann N Y Acad Sci. 1997 Sep 26;826:7-24. doi: 10.1111/j.1749-6632.1997.tb48457.x.
Vasculopathy in Alzheimer's disease (AD) may represent an important pathogenetic factor of this disorder. In the present study, microvasculature was studied by immunohistochemistry using a monoclonal antibody against a vascular heparan sulfate proteoglycan. Vascular changes were consistently observed in AD and included decrease in vascular density, presence of atrophic and coiling vessels, and glomerular loop formations. The laminar and regional distribution of these vascular alterations was correlated with the presence of neurofibrillary tangles. However, vascular changes may also follow neuronal loss. Vascular density may be related to a decrease in brain metabolism. Furthermore, one of the main features of AD is the presence of amyloid deposits within brain parenchyma and blood vessel walls. It is not yet clear whether amyloid components are derived from the blood or the central nervous system. Because AD is clearly heterogeneous, based on clinical and genetic data, evidence for either a brain or peripheral origin is discussed. Microvasculature was also analyzed in other neurodegenerative disorders devoid of amyloid deposits including amyotrophic lateral sclerosis/parkinsonism-dementia complex of Guam and Pick's disease. In conclusion, if vasculopathy in neurodegenerative disorders is not directly involved in pathogenesis, it may act synergistically with other pathogenetic mechanisms including genetic and environmental factors. This aspect of pathology is particularly interesting in view of its accessibility to therapeutic interventions.
阿尔茨海默病（AD）中的血管病变可能是该疾病的一个重要致病因素。在本研究中，使用针对血管硫酸乙酰肝素蛋白聚糖的单克隆抗体，通过免疫组织化学研究了微血管系统。在AD中始终观察到血管变化，包括血管密度降低、萎缩和盘绕血管的存在以及肾小球环形成。这些血管改变的层状和区域分布与神经原纤维缠结的存在相关。然而，血管变化也可能继发于神经元丢失。血管密度可能与脑代谢降低有关。此外，AD的主要特征之一是脑实质和血管壁内存在淀粉样沉积物。目前尚不清楚淀粉样成分是来自血液还是中枢神经系统。由于基于临床和遗传数据，AD明显具有异质性，因此讨论了其源于脑或外周的证据。还对其他不含淀粉样沉积物的神经退行性疾病进行了微血管系统分析，包括关岛肌萎缩侧索硬化/帕金森病-痴呆综合征和匹克病。总之，如果神经退行性疾病中的血管病变不直接参与发病机制，它可能与包括遗传和环境因素在内的其他致病机制协同作用。鉴于其对治疗干预的可及性，病理学的这一方面特别有趣。
