Qin Weiping, Ho Lap, Wang Jun, Peskind Elaine, Pasinetti Giulio Maria
Department of Psychiatry, Mount Sinai School of Medicine, New York, New York, USA.
PLoS One. 2009;4(1):e4183. doi: 10.1371/journal.pone.0004183. Epub 2009 Jan 13.
Alzheimer's disease (AD) is the most common cause of dementia among older people. At present, there is no cure for the disease and as of now there are no early diagnostic tests for AD. There is an urgency to develop a novel promising biomarker for early diagnosis of AD. Using surface-enhanced laser desorption ionization-mass spectrometry SELDI-(MS) proteomic technology, we identified and purified a novel 11.7-kDa metal- binding protein biomarker whose content is increased in the cerebrospinal fluid (CSF) and in the brain of AD dementia subjects as a function of clinical dementia. Following purification and protein-sequence analysis, we identified and classified this biomarker as S100A7, a protein known to be involved in immune responses. Using an adenoviral-S100A7 expression system, we continued to examine the potential role of S100A7 in AD amyloid neuropathology in in vitro model of AD. We found that the expression of exogenous S100A7 in primary cortico-hippocampal neuron cultures derived from Tg2576 transgenic embryos inhibits the generation of beta-amyloid (Abeta)(1-42) and Abeta(1-40) peptides, coincidental with a selective promotion of "non- amyloidogenic" alpha-secretase activity via promotion of ADAM (a disintegrin and metalloproteinase)-10. Finally, a selective expression of human S100A7 in the brain of transgenic mice results in significant promotion of alpha-secretase activity. Our study for the first time suggests that S100A7 may be a novel biomarker of AD dementia and supports the hypothesis that promotion of S100A7 expression in the brain may selectively promote alpha-secretase activity in the brain of AD precluding the generation of amyloidogenic peptides. If in the future we find that S1000A7 protein content in CSF is sensitive to drug intervention experimentally and eventually in the clinical setting, S100A7 might be developed as novel surrogate index (biomarker) of therapeutic efficacy in the characterization of novel drug agents for the treatment of AD.
阿尔茨海默病(AD)是老年人痴呆最常见的病因。目前,该病无法治愈,且尚无针对AD的早期诊断检测方法。迫切需要开发一种有前景的新型生物标志物用于AD的早期诊断。利用表面增强激光解吸电离飞行时间质谱(SELDI-MS)蛋白质组学技术,我们鉴定并纯化了一种新型的11.7 kDa金属结合蛋白生物标志物,其在AD痴呆患者的脑脊液(CSF)和大脑中的含量随临床痴呆程度增加。经过纯化和蛋白质序列分析,我们将该生物标志物鉴定并归类为S100A7,一种已知参与免疫反应的蛋白质。使用腺病毒-S100A7表达系统,我们继续在AD体外模型中研究S100A7在AD淀粉样神经病理学中的潜在作用。我们发现,源自Tg2576转基因胚胎的原代皮质-海马神经元培养物中外源性S100A7的表达可抑制β-淀粉样蛋白(Aβ)(1-42)和Aβ(1-40)肽的生成,同时通过促进ADAM(一种解整合素和金属蛋白酶)-10选择性地促进“非淀粉样生成性”α-分泌酶活性。最后,人S100A7在转基因小鼠大脑中的选择性表达导致α-分泌酶活性显著增强。我们的研究首次表明S100A7可能是AD痴呆的一种新型生物标志物,并支持以下假说:促进大脑中S100A7的表达可能选择性地促进AD大脑中的α-分泌酶活性,从而阻止淀粉样生成肽的产生。如果未来我们发现CSF中S100A7蛋白含量在实验中以及最终在临床环境中对药物干预敏感,那么S100A7可能会被开发为治疗AD新型药物疗效表征的新型替代指标(生物标志物)。