与阿尔茨海默病中淀粉样斑块形成相关的进行性神经元损伤。
Progressive neuronal injury associated with amyloid plaque formation in Alzheimer disease.
作者信息
Sheng J G, Zhou X Q, Mrak R E, Griffin W S
机构信息
Department of Geriatrics, University of Arkansas for Medical Sciences, Little Rock 72205, USA.
出版信息
J Neuropathol Exp Neurol. 1998 Jul;57(7):714-7. doi: 10.1097/00005072-199807000-00008.
Neuronal injury associated with amyloid plaque progression in Alzheimer disease was examined using TUNEL combined with beta-amyloid immunolabeling. There was a progressive increase in the frequency of TUNEL-positive neurons associated with plaque types representing a hypothesized sequence of plaque evolution, from 20% of neurons not associated with plaques to 40%, 70-80%, and 100% of neurons in diffuse, neuritic, and dense-core non-neuritic plaques, respectively. The total number of neurons associated with end-stage, dense-core, non-neuritic plaques declined by 70% (per unit plaque area) compared with neuritic plaque forms. This decline, together with the fact that virtually all of those remaining were TUNEL-positive, suggests that neuronal cell damage increases as plaques evolve from diffuse to more complex forms and that eventually all plaque-associated neurons are lost. This novel demonstration of neurotoxicity associated with amyloid plaque formation and progression suggests that plaque-associated neuronal injury is a major cause of neuronal loss in Alzheimer disease.
使用TUNEL法结合β-淀粉样蛋白免疫标记，研究了阿尔茨海默病中与淀粉样斑块进展相关的神经元损伤。与代表斑块进化假设序列的斑块类型相关的TUNEL阳性神经元频率逐渐增加，从不与斑块相关的神经元中的20%，分别增加到弥漫性、神经炎样和致密核心非神经炎样斑块中神经元的40%、70 - 80%和100%。与晚期致密核心非神经炎样斑块相关的神经元总数（每单位斑块面积）与神经炎样斑块形式相比减少了70%。这种减少，再加上几乎所有剩余神经元均为TUNEL阳性这一事实，表明随着斑块从弥漫性发展为更复杂的形式，神经元细胞损伤增加，最终所有与斑块相关的神经元都会丢失。这种与淀粉样斑块形成和进展相关的神经毒性的新证明表明，与斑块相关的神经元损伤是阿尔茨海默病中神经元丢失的主要原因。
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