Ceruloplasmin immunoreactivity in neurodegenerative disorders

Ceruloplasmin immunoreactivity in neurodegenerative disorders
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DOI:
10.1080/10715760100300651
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发表时间:
2001-01-01
影响因子:
3.3
通讯作者:
LeWitt, PA
LeWitt, PA
中科院分区:
生物学3区
文献类型:
--
作者:
Loeffler, DA;Sima, AAF;LeWitt, PA

文献摘要

被引文献

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血浆铜蓝蛋白(CP)是一种分子量为132 kd的铜蛋白,它与转铁蛋白一起提供了血清中大部分的抗氧化能力。遗传性CP缺乏症患者基底神经节铁沉积和脂质过氧化增加表明CP也可能在大脑中起抗氧化作用。本研究比较了正常对照组和神经退行性疾病(阿尔茨海默病[AD]、帕金森病[PD]、进行性核上性麻痹[PSP]和亨廷顿病[HD])受试者脑标本中的CP免疫反应性(每组n = 5)。在海马(CAI、下托和海马旁回)、顶叶皮质、额叶皮质、黑质和尾状核中测定神经元CP染色的相对强度和每25倍显微镜视野中CP染色神经元的数量。CP在所有标本的神经元和星形胶质细胞中均检测到,在AD脑的老年斑和偶尔的神经元缠结中也检测到。神经元CP染色强度在大多数AD脑区域中倾向于增加,但仅在海马的CAI区域中与对照相比具有统计学显著性(p = 0.016)。来自其他神经退行性疾病的脑标本中的神经元CP染色显示与对照相比轻微但不显著的增加。CP染色的神经元的数量每个字段之间没有不同的各种神经退行性疾病和控制。这些结果表明,AD脑中存在神经元CP含量的适度增加,并且本研究中的其他神经退行性疾病中神经元CP的升高较少。虽然CP在外周组织中既作为急性期蛋白又作为抗氧化剂发挥作用,但它是否在大脑中发挥作用仍有待确定。
Ceruloplasmin (CP) is a 132 kd cuproprotein which, together with transferrin, provides the majority of anti-oxidant capacity in serum. Increased iron deposition and lipid peroxidation in the basal ganglia of subjects with hereditary CP deficiency suggest that CP may serve as an anti-oxidant in the brain as well. The present study compared CP immunoreactivity in brain specimens from normal controls and subjects with neurodegenerative disorders (Alzheimer's disease [AD], Parkinson's disease [PD], progressive supranuclear palsy [PSP], and Huntington's disease [HD]) (n = 5 per group). The relative intensity of neuronal CP staining and the numbers of CP-stained neurons per 25x microscope field were determined in hippocampus (CAI, subiculum, and parahippocampal gyrus), parietal cortex, frontal cortex, substantia nigra, and caudate. CP was detected in both neurons and astrocytes in all specimens, and in senile plaques and occasional neurofibrillary tangles in AD brain. Neuronal CP staining intensity tended to increase in most AD brain regions, but was statistically significant vs controls only in the CAI region of hippocampus (p = .016). Neuronal CP staining in brain specimens from other neurodegenerative disorders showed a slight but nonsignificant increase vs controls. The numbers of CP-stained neurons per field did not differ between the various neurodegenerative disorders and controls. These results suggest that a modest increase in neuronal CP content is present in the AD brain, and lesser elevations in neuronal CP occur in the other neurodegenerative disorders in this study. Though CP functions as both an acute phase protein and an anti-oxidant in peripheral tissues, whether it does so in the brain remains to be determined.