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阿尔茨海默型痴呆中与抗神经肽Y抗血清免疫反应的海马神经元和轴突改变的分布。

Distribution of altered hippocampal neurons and axons immunoreactive with antisera against neuropeptide Y in Alzheimer's-type dementia.

作者信息

Chan-Palay V, Lang W, Haesler U, Köhler C, Yasargil G

出版信息

J Comp Neurol. 1986 Jun 15;248(3):376-94. doi: 10.1002/cne.902480307.

Abstract

This paper provides detailed information on the distribution of neuropeptide tyrosine (neuropeptide Y; NPY) immunoreactive neurons and fibers in the hippocampal region of eight neuropathologically confirmed cases of Alzheimer's-type dementia (ATD) at postmortem. These neuronal networks are detected by a polyclonal antibody raised against the unconjugated peptide and controls were obtained by using liquid phase absorption immunocytochemistry. The description covers the subfields area dentata, CA3 and CA1, the subicular complex, and the entorhinal area. The hippocampal regions in which the NPY-i neuron networks are most severely affected are the hilus, CA1, the parasubiculum, and the entorhinal cortex. Less obvious reductions occurred in CA3, subiculum, and the presubiculum. Parallel semiquantitative estimates were made of the numbers of neuritic plaques and neurofibrillary tangles in the other hippocampus of the brains in every ATD case. The areas of heaviest pathological changes by these indices are CA1 and the entorhinal cortex. The subicular complex CA3 and the area dentata are less affected. These findings show that the areas with the most severe loss of NPY-i neurons and axons, CA1 and the entorhinal cortex, are the same as those areas most severely affected by the other indices of ATD. Thus NPY-i networks are involved in the ATD disease process. However, other NPY-i networks survive, in some subfields better than in others. The cumulative evidence suggests a population of hippocampal peptide neurons that are remarkably resistant in terminal neurological disease. These neurons have the capability to participate in the maintenance of minimal functioning circuits in target areas of the disease and as such hold significant links for our understanding of synaptic plasticity in disease.

摘要

本文提供了八例经神经病理学确诊的阿尔茨海默型痴呆(ATD)患者死后海马区神经肽酪氨酸(神经肽Y;NPY)免疫反应性神经元和纤维分布的详细信息。这些神经网络通过针对未结合肽产生的多克隆抗体进行检测,并采用液相吸收免疫细胞化学方法获得对照。描述涵盖齿状回、CA3和CA1亚区、海马下托复合体以及内嗅区。NPY免疫反应性神经元网络受影响最严重的海马区是齿状回门、CA1、副海马旁回和内嗅皮质。CA3、海马下托和前海马旁回的减少不太明显。对每例ATD患者大脑另一侧海马区的神经炎性斑块和神经原纤维缠结数量进行了平行的半定量评估。这些指标显示病理变化最严重的区域是CA1和内嗅皮质。海马下托复合体、CA3和齿状回受影响较小。这些发现表明,NPY免疫反应性神经元和轴突损失最严重的区域,即CA1和内嗅皮质,与受ATD其他指标影响最严重的区域相同。因此,NPY免疫反应性网络参与了ATD疾病进程。然而,其他NPY免疫反应性网络得以保留,在某些亚区比其他亚区保留得更好。累积证据表明,海马区存在一群在终末期神经疾病中具有显著抗性的肽能神经元。这些神经元有能力参与疾病靶区最小功能回路的维持,因此对于我们理解疾病中的突触可塑性具有重要联系。

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