Pathological relationships between microglial cell activity and tau and amyloid β protein in patients with !Alzheimer's disease
Pathological relationships between microglial cell activity and tau and amyloid β protein in patients with !Alzheimer's disease
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DOI：
10.1016/s0304-3940(02)00888-1
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发表时间：
2002-10-18
影响因子：
2.5
通讯作者：
Mann, DMA
中科院分区：
文献类型：
--
作者：
Hayes, A;Thaker, U;Mann, DMA
通过对72例病理证实的阿尔茨海默病（AD）患者的额叶皮质铁蛋白免疫染色切片的图像分析，估计了小胶质细胞激活的程度（小胶质细胞负荷），并与病理性tau和淀粉样β蛋白（Abeta）的数量相关，因为在同一病例的相邻切片中，Abeta（40）和Abeta（42）负荷。小胶质细胞负荷与β(40)或β(42)负荷均不相关，但与病理性tau负荷显著相关。小胶质细胞负荷与发病年龄或病程无关。由于小胶质细胞的存在早于AD患者大脑皮层中病理性tau蛋白的存在，神经细胞的神经原纤维损伤可能源于小胶质细胞释放的促炎分子和其他潜在的神经毒性分子。(C) 2002爱思唯尔科学爱尔兰有限公司版权所有。
The extent of microglial cell activation (microglial cell load) was estimated by image analysis of ferritin-immunostained sections of frontal cortex from 72 patients with pathologically confirmed Alzheimer's disease (AD), and correlated with the amount of pathological tau and annyloid beta protein (Abeta), as both Abeta(40) and Abeta(42) load, in adjacent sections of the same cases. Microglial cell load did not correlate with either Abeta(40) or Abeta(42) load but was significantly correlated with pathological tau load. Microglial cell load was unrelated to age at onset of disease or duration of illness. It is possible that because the presence of microglial cells predates that of pathological tau proteins within the cerebral cortex in AD, neurofibrillary damage to nerve cells may stem from the release of proinflammatory and other potentially neurotoxic molecules from microglial cells. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.