Plasma metabolic profiling of Alzheimer's disease by liquid chromatography/mass spectrometry

Li, Naijing; Liu, Wentao; Li, Wei; Li, Shengqi; Chen, Xiaohui; Bi, Kaishun; He, Ping

doi:10.1016/j.clinbiochem.2010.04.072

Cited by 116 publications

(85 citation statements)

References 27 publications

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“…Signals were preliminarily filtered by P < 0.05 and up-/downregulation factor (lower than −30% or higher than +30%) and manually processed to eliminate spurious peaks. The accurate mass list was searched against the METLIN web-based algorithm (50,51) (52), and, whenever possible, accurate MS/MS data, following the indications on MS/MS fragmentation patterns available in the literature (53)(54)(55)(56). The lipid species annotated are reported in SI Appendix, Table S1 (positive ion mode) and SI Appendix, Table S2 (negative ion mode).…”

Section: Methodsmentioning

confidence: 99%

Endogenous N -acyl taurines regulate skin wound healing

Sasso

Pontis

Armirotti

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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The intracellular serine amidase, fatty acid amide hydrolase (FAAH), degrades a heterogeneous family of lipid-derived bioactive molecules that include amides of long-chain fatty acids with taurine [N-acyl-taurines (NATs)]. The physiological functions of the NATs are unknown. Here we show that genetic or pharmacological disruption of FAAH activity accelerates skin wound healing in mice and stimulates motogenesis of human keratinocytes and differentiation of human fibroblasts in primary cultures. Using untargeted and targeted lipidomics strategies, we identify two longchain saturated NATs-N-tetracosanoyl-taurine [NAT(24:0)] and N-eicosanoyl-taurine [NAT(20:0)]-as primary substrates for FAAH in mouse skin, and show that the levels of these substances sharply decrease at the margins of a freshly inflicted wound to increase again as healing begins. Additionally, we demonstrate that local administration of synthetic NATs accelerates wound closure in mice and stimulates repair-associated responses in primary cultures of human keratinocytes and fibroblasts, through a mechanism that involves tyrosine phosphorylation of the epidermal growth factor receptor and an increase in intracellular calcium levels, under the permissive control of transient receptor potential vanilloid-1 receptors. The results point to FAAH-regulated NAT signaling as an unprecedented lipid-based mechanism of woundhealing control in mammalian skin, which might be targeted for chronic wound therapy.FAAH | N-acyl taurines | FAEs | fibroblasts | keratinocytes

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Section: Methodsmentioning

confidence: 99%

Endogenous N -acyl taurines regulate skin wound healing

Sasso

Pontis

Armirotti

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Recently, another study showed nine potential biomarkers phan remained decreased in AD upon further testing [41] .…”

Section: Lipidomics In Ad Using Uplc-ms/multi-dimensional Mass Spectrmentioning

confidence: 99%

“…Decreased NAA, glutamate, glutamine, taurine, γ-amino butyric acid, choline and phosphocholine, creatine, phosphocreatine and succinate; and increased lactate, aspartate, glycine and other amino-acids including alanine, leucine, iso-leucine, valine and watersoluble free fatty-acids (0.8-0.9 and 1.2-1.3 ppm) in six affected regions [35] Alterations in tyrosine, tryptophan, purine, and tocopherol pathways; reductions in norepinephrine and its metabolites [38] Nine potential diagnostic biomarkers (LPCs, trypto phan, dihydrosphingosine, phytosphingosine and hexadecasphinganine) identified for AD [41] Eight sphingomyelin species significantly lower in AD; two ceramide species (N16:0 and N21:0) increased in AD; ratios of ceramide to sphingomyelin species differed significantly between groups; both N20:2 SM and OH-N25:0 ceramides were correlated with MMSE in AD [43] Omega-3 fatty acids indicative of MCI; elevated glyco proteins may be a risk for AD [46] CSF, cerebrospinal fluid; LC-ECA, liquid chromatography-electrochemical array; LPC, lysophosphatidyl choline; MDMS-SL, multi-dimensional mass spectrometry-based shotgun lipidomics; MMSE, mini-mental state examination; MS, mass spectrometry; NAA, N-acetyl-L-aspartate; NMR, nuclear magnetic resonance spectroscopy; SM, sphingomyelin; UPLC, ultra-performance liquid chromatography.…”

Section: H-nmrmentioning

confidence: 99%

Metabolomics: a novel approach to identify potential diagnostic biomarkers and pathogenesis in Alzheimer’s disease

Huang

Wang

et al. 2012

Neurosci. Bull.

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Although the pathogenesis of Alzheimer's disease (AD) is still not fully understood, it is acknowledged that intervention should be made at the early stage. Therefore, identifying biomarkers for the clinical diagnosis is critical.Metabolomics, a novel "omics", uses methods based on low-molecular-weight molecules, with high-throughput evaluation of a large number of metabolites that may lead to the identification of new disease-specific biomarkers and the elucidation of pathophysiological mechanisms. This review discusses metabolomics investigations of AD and potential future developments in this field.

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“…The broad information obtained by metabolic fingerprinting approach make it the most attractive and suitable strategy for biomarker discovery [85], while at the same time, represents the most challenging and time-consuming approach in Metabolomics. In AD research, the obtaining of metabolic fingerprints is a recent practice by using both NMR [87][88][89] and MS-based [90][91][92][93][94] techniques.…”

Section: Metabolomics In Admentioning

confidence: 99%

“…With the aim to detect potential metabolite biomarkers of AD in plasma, Li et al lysophosphatidylcholines and sphingosines were highlighted as the metabolites that most differentiated AD from control groups of plasma samples [91]. In a different work, in order to monitor the progression markers to AD, plasma samples from control, MCI without progression to AD (in a 1-4-year follow-up), MCI who progressed to AD (in that follow-up period) and AD diagnosed subjects was carried out [124].…”

Section: Metabolomics and Ad In Plasma And Serummentioning

confidence: 99%

Metabolomics in the Study of Alzheimer's Disease

Ibáñez

Valdés

García‐Cañas

et al. 2014

Comprehensive Analytical Chemistry

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With an increasing aging population, Alzheimer's disease (AD) has become a social and economic problem to societies worldwide, affecting millions of people. However, pathophysiological events associated with AD are not well elucidated yet and current definitive diagnosis is only obtained after death through examination of brain tissue. In the last years, Metabolomics has been demonstrated to provide deep insights into the full complexity of the disease phenotype and has been established as a promising approach to provide disease-specific metabolite signatures. The incipient application of Metabolomics may potentially contribute in the elucidation of AD physiopathological processes and ideally may offer therapeutic/preventing mechanisms to slow or reverse AD progress. In this chapter non-targeted metabolomics approaches applied to AD investigation are described.

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Plasma metabolic profiling of Alzheimer's disease by liquid chromatography/mass spectrometry

Cited by 116 publications

References 27 publications

Endogenous N -acyl taurines regulate skin wound healing

Endogenous N -acyl taurines regulate skin wound healing

Metabolomics: a novel approach to identify potential diagnostic biomarkers and pathogenesis in Alzheimer’s disease

Metabolomics in the Study of Alzheimer's Disease

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