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阿尔茨海默病患者脑脊液中的β淀粉样蛋白(Aβ)肽模式:一种新型羧基末端延长Aβ肽的证据。

The amyloid-beta (Abeta) peptide pattern in cerebrospinal fluid in Alzheimer's disease: evidence of a novel carboxyterminally elongated Abeta peptide.

作者信息

Lewczuk Piotr, Esselmann Hermann, Meyer Markus, Wollscheid Volker, Neumann Manuela, Otto Markus, Maler Juan Manuel, Rüther Eckart, Kornhuber Johannes, Wiltfang Jens

机构信息

Department of Psychiatry and Psychotherapy, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany.

Department of Psychiatry, University of Goettingen, von-Siebold-Str. 5, 37075 Goettingen, Germany.

出版信息

Rapid Commun Mass Spectrom. 2003;17(12):1291-1296. doi: 10.1002/rcm.1048.

DOI:10.1002/rcm.1048
PMID:12811752
Abstract

The patterns of amyloid beta (Abeta) peptides in human cerebrospinal fluid (CSF) and brain homogenates were studied by surface-enhanced laser desorption/ionization (SELDI) time-of-flight (TOF) mass spectrometry, and the results were compared with those obtained by Abeta-SDS-PAGE/immunoblot. Apart from the peptides known in the literature to occur in the CSF, we postulate the existence of a novel, previously not described peptide, either Abeta1-45 or Abeta2-46. This peptide was observed exclusively in a pool of samples originating from patients with AD, i.e. CSF and postmortem brain homogenates, but not in either the pooled CSF samples nor the pooled brain homogenates of the non-demented controls. Similarly to our previous results, Abeta1-42 was decreased in the CSF in AD. Expectedly, brain homogenates of the control subjects did not show the presence of Abeta peptides. Compared with Abeta-SDS-PAGE/immunoblot, SELDI-TOF enabled more precise analysis of Abeta peptides in the human material. We conclude that SELDI-TOF offers a promising tool for dementia expression pattern profiling using a minute amount of a biological sample.

摘要

通过表面增强激光解吸/电离(SELDI)飞行时间(TOF)质谱法研究了人脑脊液(CSF)和脑匀浆中β-淀粉样蛋白(Aβ)肽的模式,并将结果与通过Aβ-SDS-PAGE/免疫印迹法获得的结果进行了比较。除了文献中已知存在于脑脊液中的肽外,我们推测存在一种新的、以前未描述的肽,即Aβ1-45或Aβ2-46。这种肽仅在源自阿尔茨海默病患者的一组样本中观察到,即脑脊液和死后脑匀浆,但在非痴呆对照组的合并脑脊液样本或合并脑匀浆中均未观察到。与我们之前的结果相似,AD患者脑脊液中的Aβ1-42减少。不出所料,对照受试者的脑匀浆中未显示Aβ肽的存在。与Aβ-SDS-PAGE/免疫印迹法相比,SELDI-TOF能够更精确地分析人体材料中的Aβ肽。我们得出结论,SELDI-TOF为使用微量生物样本进行痴呆表达模式分析提供了一种有前景的工具。

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