Scheltens P, Barkhof F, Leys D, Wolters E C, Ravid R, Kamphorst W
Department of Neurology, Academisch Ziekenhuis VU, Amsterdam, The Netherlands.
Neurology. 1995 May;45(5):883-8. doi: 10.1212/wnl.45.5.883.
We investigated the histopathologic correlates of white matter changes in Alzheimer's disease (AD) patients (n = 6) and controls (n = 9) using postmortem MRI. White matter changes were rated on a 0 to 3 scale in 51 regions. Histopathologically, we subjectively rated the loss of myelinated axons in the deep and periventricular white matter, denudation of the ventricular ependyma, gliosis, width of the perivascular spaces, and leptomeningeal congophilic angiopathy; we measured structural changes in the walls of the blood vessels in the white matter in micrometers. The AD brains displayed significantly more white matter hyperintensities on MRI than controls. Histopathologically, the denudation of the ventricular ependyma and the gliosis were significantly more severe in AD than in controls, and there was a trend toward more loss of myelinated axons in the deep white matter in the AD brains (p = 0.07). The MRI abnormalities correlated with the loss of myelinated axons in the deep white matter (r' = 0.37; p < 0.01) and with the denudation of the ventricular lining (r' = 0.54; p < 0.01). We could not find any evidence for arteriolosclerosis, but the mean thickness of the adventitia of the arteries of the deep white matter in AD almost doubled the value in control brains (p = 0.0009). We conclude that white matter abnormalities in AD patients and controls consist of loss of myelinated axons, probably caused by arterial changes and breakdown of the ventricular lining. Since imaging/histopathologic correlation was similar in AD patients and controls, these changes probably represent some form of accelerated aging.
我们使用尸检MRI研究了阿尔茨海默病（AD）患者（n = 6）和对照组（n = 9）白质变化的组织病理学相关性。在51个区域对白质变化进行了0至3级评分。组织病理学上，我们主观评估了深部和脑室周围白质中髓鞘轴突的丢失、脑室室管膜剥脱、胶质增生、血管周围间隙宽度以及软脑膜嗜刚果红血管病；我们测量了白质中血管壁以微米为单位的结构变化。AD患者的大脑在MRI上显示出比对照组明显更多的白质高信号。组织病理学上，AD患者的脑室室管膜剥脱和胶质增生比对照组明显更严重，并且AD大脑深部白质中髓鞘轴突的丢失有增加的趋势（p = 0.07）。MRI异常与深部白质中髓鞘轴突的丢失相关（r' = 0.37；p < 0.01），也与脑室衬里的剥脱相关（r' = 0.54；p < 0.01）。我们未发现任何小动脉硬化的证据，但AD患者深部白质动脉外膜的平均厚度几乎是对照大脑中该值的两倍（p = 0.0009）。我们得出结论，AD患者和对照组的白质异常包括髓鞘轴突的丢失，可能是由动脉变化和脑室衬里破坏引起的。由于AD患者和对照组的成像/组织病理学相关性相似，这些变化可能代表某种形式的加速衰老。
