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除非存在β-淀粉样蛋白沉积,否则在其他神经退行性疾病中不会发现与老年斑特征性相关的阿尔茨海默病样营养不良性神经突。

Alzheimer's disease-like dystrophic neurites characteristically associated with senile plaques are not found within other neurodegenerative diseases unless amyloid beta-protein deposition is present.

作者信息

Benzing W C, Mufson E J, Armstrong D M

机构信息

FIDIA-Georgetown Institute for the Neurosciences, Georgetown University, Washington, DC 20007.

出版信息

Brain Res. 1993 Mar 19;606(1):10-8. doi: 10.1016/0006-8993(93)91563-8.

Abstract

Swollen, bulbous-shaped (dystrophic) neurites are a common pathologic feature of Alzheimer's disease (AD) and represent one of the most abundant neuritic abnormalities within the brains of patients with this disease. In the present study, we sought to determine whether the dystrophic neurites which are observed in association with senile plaques are unique to AD or whether they are characteristic of a more generalized process of neuritic and/or neuronal degeneration which can be observed in other neurodegenerative diseases. To accomplish this, we examined post-mortem brain material from patients with AD, Parkinson's disease (PD), Parkinson's disease with associated AD, Parkinson's disease with dementia yet without AD pathology, Huntington's disease (HD), Pick's disease and normal age-matched controls (NC). Using a battery of antibodies to amyloid beta-protein (A beta P), paired-helical filaments (PHF), tyrosine hydroxylase, substance P, neurotensin, and somatostatin we found that immunolabeled dystrophic neurites of the type characteristically observed in AD, were seen only in cases and in brain regions where A beta P deposition was present. More specifically, brain areas known to display severe afferent and/or local degenerative changes such as the caudate and putamen in all three PD groups, the caudate in the HD cases, and the temporal cortex in the HD and Pick's cases were conspicuously free of these swollen neurites unless A beta P deposition was also present.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

肿胀的、球根状(营养不良性)神经突是阿尔茨海默病(AD)的常见病理特征,也是该病患者大脑中最丰富的神经突异常之一。在本研究中,我们试图确定与老年斑相关的营养不良性神经突是否为AD所特有,或者它们是否是在其他神经退行性疾病中也能观察到的更普遍的神经突和/或神经元变性过程的特征。为了实现这一目标,我们检查了AD患者、帕金森病(PD)患者、合并AD的帕金森病患者、有痴呆但无AD病理的帕金森病患者、亨廷顿病(HD)患者、皮克病患者以及年龄匹配的正常对照(NC)的尸检脑材料。使用一系列针对淀粉样β蛋白(AβP)、双螺旋丝(PHF)、酪氨酸羟化酶、P物质、神经降压素和生长抑素的抗体,我们发现,在AD中典型观察到的那种免疫标记的营养不良性神经突,仅在存在AβP沉积的病例和脑区中出现。更具体地说,已知显示严重传入和/或局部退行性变化的脑区,如所有三个PD组中的尾状核和壳核、HD病例中的尾状核以及HD和皮克病病例中的颞叶皮质,除非也存在AβP沉积,否则明显没有这些肿胀的神经突。(摘要截断于250字)

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