Duyckaerts C, Bennecib M, Grignon Y, Piette F, Hauw J J
Laboratoire de Neuropathologie R. Escourolle, Hôpital de La Salpêtrière, Paris.
Bull Acad Natl Med. 1996 Oct;180(7):1703-14.
Neurofibrillary changes, labelled by antitau antibodies and deposits, labelled by anti-A beta antibodies, were counted in 6 cortical areas in 29 prospectively studied cases (Charles Foix Longitudinal Study). The intellectual status had been assessed by the Blessed test score; 10% of the cases were found to be normal (score > 27), 10 other percents were deeply demented (score < 2) and the other cases were regularly distributed over the intermediate values. Tau positive neurofibrillary changes were present in the hippocampus and in the parahippocampal gyrus even in intellectually normal cases. They were found in a primary sensory cortex (the visual cortex) only in the most severely affected cases. Associative cortices were spared in the normal cases and in the least demented patients. They were involved only at a critical value of the Blessed Test Score. A beta deposits involved more areas than the neurofibrillary pathology and their distribution was less systematically organized. Their density was poorly correlated with the intellectual status. Neuritic plaques, made of an amyloid core and of a crown of tau positive neurites, were present only in those areas that also contained neurofibrillary tangles. Our findings support the contention that neurofibrillary pathology, involving a set of short range, "feed-backward", cortico-cortical connections, is a close correlate of dementia. The role of A beta deposits remains unclear. Although poorly connected with dementia, they could be the remote initiator of the pathological cascade that leads to the neurofibrillary pathology, immediate cause of the cortical dysfunction.
在29例前瞻性研究病例（查尔斯·福瓦纵向研究）的6个皮质区域中，对用抗tau抗体标记的神经原纤维变化和用抗Aβ抗体标记的沉积物进行了计数。通过Blessed测试评分评估智力状态；发现10%的病例正常（评分>27），另外10%的病例严重痴呆（评分<2），其他病例均匀分布在中间值范围内。即使在智力正常的病例中，海马体和海马旁回也存在tau阳性神经原纤维变化。仅在受影响最严重的病例中，才在初级感觉皮质（视觉皮质）中发现这种变化。在正常病例和痴呆程度最轻的患者中，联合皮质未受影响。仅在Blessed测试评分达到临界值时，联合皮质才会受到影响。Aβ沉积物累及的区域比神经原纤维病变更多，且其分布缺乏系统性。其密度与智力状态的相关性较差。由淀粉样核心和tau阳性神经突冠组成的神经炎斑块仅存在于同时含有神经原纤维缠结的区域。我们的研究结果支持这样的观点，即涉及一组短程“反馈”皮质 - 皮质连接的神经原纤维病变与痴呆密切相关。Aβ沉积物的作用仍不清楚。尽管与痴呆的关联不大，但它们可能是导致神经原纤维病变（皮质功能障碍的直接原因）的病理级联反应的远程启动因素。
