Zekry Dina, Duyckaerts Charles, Belmin Joël, Geoffre Caroline, Moulias Robert, Hauw Jean-Jacques
Laboratoire de Neuropathologie Raymond Escourolle, Hôpital de la Salpêtrière, INSERM U 106 and 360, Association Claude Bernard, Pierre et Marie Curie University, 47 Bd de l'Hôpital, 75013 Paris, France.
Acta Neuropathol. 2003 Oct;106(4):367-73. doi: 10.1007/s00401-003-0738-6. Epub 2003 Jul 29.
Abeta peptide deposits are observed in brain cortical and leptomeningeal microvessels in a few families, in patients with Alzheimer's disease and in cognitively normal elderly subjects. These deposits, which cause Abeta amyloid angiopathy, are usually associated with other lesions induced by Abeta peptide and tau pathologies. To investigate the consequences of cerebral amyloid angiopathy on arterial morphology and search for correlations with the degree of cognitive impairment, we carried out a prospective clinicopathological and morphometric study in 29 institutionalized elderly patients cognitively normal or affected with sporadic dementia associated with Alzheimer-type lesions, cerebral infarcts or both. We measured the external and internal diameters of arteries 40-120 microm wide, containing moderate or severe Abeta deposits, and of unaffected arteries in the temporal and frontal lobes. We found no differences in the mean external diameters. In contrast, the mean internal diameters of vessels with moderate Abeta deposits were smaller than those of unaffected vessels. Conversely, the internal diameters of severely affected vessels were larger than those of unaffected vessels. This suggests that arterial walls become thicker during the early stages of amyloid angiopathy, and the diameter of the lumen decreases, whereas during advanced stages, the walls become thinner and the lumen becomes larger. In addition, we assessed the overall severity of amyloid angiopathy. This showed that thinner arterial walls and the severity of amyloid angiopathy were correlated to dementia. In a multivariate model that integrates the other macroscopic and microscopic lesions that may be implied in the mechanism of cognitive impairment, the severity of amyloid angiopathy per se explained 10% of the variability in the cognitive impairment.
在一些家族、阿尔茨海默病患者以及认知功能正常的老年受试者的大脑皮质和软脑膜微血管中观察到β淀粉样蛋白沉积。这些沉积物会导致β淀粉样血管病，通常与β淀粉样肽和tau病理引发的其他病变相关。为了研究脑淀粉样血管病对动脉形态的影响，并寻找与认知障碍程度的相关性，我们对29名认知功能正常或患有与阿尔茨海默型病变、脑梗死或两者相关的散发性痴呆的老年住院患者进行了一项前瞻性临床病理和形态学研究。我们测量了颞叶和额叶中宽度为40 - 120微米、含有中度或重度β淀粉样蛋白沉积的动脉以及未受影响动脉的外径和内径。我们发现平均外径没有差异。相比之下，有中度β淀粉样蛋白沉积的血管的平均内径小于未受影响血管的内径。相反，严重受影响血管的内径大于未受影响血管的内径。这表明在淀粉样血管病的早期阶段动脉壁会变厚，管腔直径减小，而在晚期阶段，壁会变薄，管腔会变大。此外，我们评估了淀粉样血管病的总体严重程度。结果显示动脉壁变薄和淀粉样血管病的严重程度与痴呆相关。在一个整合了可能参与认知障碍机制的其他宏观和微观病变的多变量模型中，淀粉样血管病本身的严重程度解释了认知障碍变异性的10%。
