| A metabolomic study of the CRND8 transgenic mouse model of Alzheimer's disease. | |
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MedLine Citation:
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PMID: 20398713 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Alzheimer's disease is the most common neurodegenerative disease of the central nervous system characterized by a progressive loss in memory and deterioration of cognitive functions. In this study the transgenic mouse TgCRND8, which encodes a mutant form of the amyloid precursor protein 695 with both the Swedish and Indiana mutations and develops extracellular amyloid beta-peptide deposits as early as 2-3 months, was investigated. Extract from eight brain regions (cortex, frontal cortex, cerebellum, hippocampus, olfactory bulb, pons, midbrain and striatum) were studied using (1)H NMR spectroscopy. Analysis of the NMR spectra discriminated control from APP695 tissues in hippocampus, cortex, frontal cortex, midbrain and cerebellum, with hippocampal and cortical region being most affected. The analysis of the corresponding loading plots for these brain regions indicated a decrease in N-acetyl-L-aspartate, glutamate, glutamine, taurine (exception hippocampus), gamma-amino butyric acid, choline and phosphocholine (combined resonances), creatine, phosphocreatine and succinate in hippocampus, cortex, frontal cortex (exception gamma-amino butyric acid) and midbrain of affected animals. An increase in lactate, aspartate, glycine (except in midbrain) and other amino acids including alanine (exception frontal cortex), leucine, iso-leucine, valine and water soluble free fatty acids (0.8-0.9 and 1.2-1.3 ppm) were observed in the TgCRND8 mice. Our findings demonstrate that the perturbations in metabolism are more widespread and include the cerebellum and midbrain. Furthermore, metabolic perturbations are associated with a wide range of metabolites which could improve the diagnosis and monitoring of the progression of Alzheimer's disease. |
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Authors:
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Reza M Salek; Jing Xia; Amy Innes; Brian C Sweatman; Robert Adalbert; Suzanne Randle; Eileen McGowan; Piers C Emson; Julian L Griffin |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-04-14 |
Journal Detail:
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Title: Neurochemistry international Volume: 56 ISSN: 1872-9754 ISO Abbreviation: Neurochem. Int. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-05-18 Completed Date: 2010-11-29 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8006959 Medline TA: Neurochem Int Country: England |
Other Details:
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Languages: eng Pagination: 937-47 Citation Subset: IM |
Copyright Information:
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2010 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Biochemistry, The Hopkins Building, Tennis Court Road, University of Cambridge, Cambridge CB21QW, UK. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Alzheimer Disease
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diagnosis,
metabolism*,
pathology* Animals Biological Markers / metabolism Brain / metabolism, pathology Disease Models, Animal* Female Humans Male Metabolome / genetics Metabolomics / methods* Mice Mice, Transgenic |
| Grant Support | |
ID/Acronym/Agency:
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R01AG020216-01A2/AG/NIA NIH HHS; R21 DK070288-01/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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