Preclinical Alzheimer disease: brain oxidative stress, Abeta peptide and proteomics.
Preclinical Alzheimer disease: brain oxidative stress, Abeta peptide and proteomics.
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DOI：
10.1016/j.nbd.2010.04.011
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发表时间：
2010-08
影响因子：
6.1
通讯作者：
Butterfield DA
中科院分区：
文献类型：
--
作者：
Aluise CD;Robinson RA;Beckett TL;Murphy MP;Cai J;Pierce WM;Markesbery WR;Butterfield DA
阿尔茨海默病（Alzheimer disease，AD）是一种神经退行性疾病，其临床特征为进行性记忆丧失和随后的痴呆，神经病理学特征为老年斑、神经元缠结和突触丧失。有趣的是，一小部分具有正常生前心理测量分数的个体符合AD的神经病理学标准（称为“临床前”AD（PCAD））。在这项研究中，PCAD和对照组的顶下小叶（IPL）进行了比较，氧化应激标记物的免疫化学，淀粉样β-肽的ELISA，和蛋白质组学的蛋白质表达差异的鉴定。我们观察到对照组和PCAD受试者之间高度不溶性单体Aβ42显著增加，但寡聚体Aβ和氧化应激测量值无显著差异。表达蛋白质组学鉴定了其在PCAD中的趋势指示细胞保护的蛋白质，这可能与先前显示PCAD中没有细胞损失的研究相关。我们的分析可能揭示了在一段时间内保护神经变性的过程，模拟PCAD的临床表型。
Alzheimer disease (AD) is a neurodegenerative disorder characterized clinically by progressive memory loss and subsequent dementia and neuropathologically by senile plaques, neurofibrillary tangles, and synapse loss. Interestingly, a small percentage of individuals with normal antemortem psychometric scores meet the neuropathological criteria for AD (termed `preclinical' AD (PCAD)). In this study, inferior parietal lobule (IPL) from PCAD and control subjects were compared for oxidative stress markers by immunochemistry, amyloid beta-peptide by ELISA, and identification of protein expression differences by proteomics. We observed a significant increase in highly insoluble monomeric Aβ42, but no significant differences in oligomeric Aβ nor in oxidative stress measurements between controls and PCAD subjects. Expression proteomics identified proteins whose trends in PCAD are indicative of cellular protection, possibly correlating with previous studies showing no cell loss in PCAD. Our analyses may reveal processes involved in a period of protection from neurodegeneration that mimic the clinical phenotype of PCAD.
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影响因子：
2
作者：
Howlett, D. R.;Bowler, K.;Richardson, J. C.
通讯作者：
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影响因子：
82.9
作者：
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影响因子：
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DOI：
10.1073/pnas.0705738104
发表时间：
2007-08-28
影响因子：
11.1
作者：
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通讯作者：
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影响因子：
3.1
作者：
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