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Metabolites 2017, 7(2), 28;

Metabolomic Profiling of Bile Acids in Clinical and Experimental Samples of Alzheimer’s Disease

Advanced Asset Technology Centre, Institute for Global Food Security, Queen's University Belfast, Belfast BT9 5AG, UK
Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queen’s University Belfast, Belfast BT12 6BA, UK
Dementia Research Group, Institute of Clinical Neurosciences, School of Clinical Sciences, University of Bristol, Bristol BS10 5NB, UK
Division of Biomedical and Life Sciences, Lancaster University, Lancaster LA1 4YG, UK
Biomedical Sciences Research Institute, Ulster University, Clinical Translational Research and Innovation Centre C-TRIC, Derry/Londonderry BT47 6SB, UK
Beaumont Research Institute, Beaumont Health, Royal Oak, MI 48073, USA
Author to whom correspondence should be addressed.
Academic Editor: Peter Meikle
Received: 2 May 2017 / Revised: 11 June 2017 / Accepted: 14 June 2017 / Published: 17 June 2017
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Certain endogenous bile acids have been proposed as potential therapies for ameliorating Alzheimer’s disease (AD) but their role, if any, in the pathophysiology of this disease is not currently known. Given recent evidence of bile acids having protective and anti-inflammatory effects on the brain, it is important to establish how AD affects levels of endogenous bile acids. Using LC-MS/MS, this study profiled 22 bile acids in brain extracts and blood plasma from AD patients (n = 10) and age-matched control subjects (n = 10). In addition, we also profiled brain/plasma samples from APP/PS1 and WT mice (aged 6 and 12 months). In human plasma, we detected significantly lower cholic acid (CA, p = 0.03) in AD patients than age-matched control subjects. In APP/PS1 mouse plasma we detected higher CA (p = 0.05, 6 months) and lower hyodeoxycholic acid (p = 0.04, 12 months) than WT. In human brain with AD pathology (Braak stages V-VI) taurocholic acid (TCA) were significantly lower (p = 0.01) than age-matched control subjects. In APP/PS1 mice we detected higher brain lithocholic acid (p = 0.05) and lower tauromuricholic acid (TMCA; p = 0.05, 6 months). TMCA was also decreased (p = 0.002) in 12-month-old APP/PS1 mice along with 5 other acids: CA (p = 0.02), β-muricholic acid (p = 0.02), Ω-muricholic acid (p = 0.05), TCA (p = 0.04), and tauroursodeoxycholic acid (p = 0.02). The levels of bile acids are clearly disturbed during the development of AD pathology and, since some bile acids are being proposed as potential AD therapeutics, we demonstrate a method that can be used to support work to advance bile acid therapeutics. View Full-Text
Keywords: bile acids; metabolomics; Alzheimer’s disease; metabolites bile acids; metabolomics; Alzheimer’s disease; metabolites

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Pan, X.; Elliott, C.T.; McGuinness, B.; Passmore, P.; Kehoe, P.G.; Hölscher, C.; McClean, P.L.; Graham, S.F.; Green, B.D. Metabolomic Profiling of Bile Acids in Clinical and Experimental Samples of Alzheimer’s Disease. Metabolites 2017, 7, 28.

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