期刊
JOURNAL OF PROTEOME RESEARCH
卷 13, 期 5, 页码 2649-2658出版社
AMER CHEMICAL SOC
DOI: 10.1021/pr5000895
关键词
Alzheimer's disease; amnestic mild cognitive impairment; metabolomics; plasma; biomarkers
资金
- National Basic Research Development Program of China [2010CB945200, 2011CB504104]
- National Natural Science Foundation of China [81171027, 81200842, 91332107]
- National Twelfth Five-Year Plan for Science and Technology Support [2012BAI10B03]
- Shanghai Key Project of Basic Science Research [09DZ1950400]
- Program for Outstanding Medical Academic Leader [LJ 06003]
Previous studies have demonstrated altered metabolites in samples of Alzheimer's disease (AD) patients. However, the sample size from many of them is relatively small and the metabolites are relatively limited. Here we applied a comprehensive platform using ultraperformance liquid chromatography-time-of-flight mass spectrometry and gas chromatography-time-of-flight mass spectrometry to analyze plasma samples from AD patients, amnestic mild cognitive impairment (aMCI) patients, and normal controls. A biomarker panel consisting of six plasma metabolites (arachidonic acid, N,N-dimethylglycine, thymine, glutamine, glutamic acid, and cytidine) was identified to discriminate AD patients from normal control. Another panel of five plasma metabolites (thymine, arachidonic acid, 2-aminoadipic acid, N,N-dimethylglycine, and 5,8-tetradecadienoic acid) was able to differentiate aMCI patients from control subjects. Both biomarker panels had good agreements with clinical diagnosis. The 2 panels of metabolite markers were all involved in fatty acid metabolism, one-carbon metabolism, amino acid metabolism, and nucleic acid metabolism. Additionally, no altered metabolites were found among the patients at different stages, as well as among those on anticholinesterase medication and those without anticholinesterase medication. These findings provide a comprehensive global plasma metabolite profiling and may contribute to making early diagnosis as well as understanding the pathogenic mechanism of AD and aMCI.
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