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We are analyzing https://link.springer.com/article/10.1186/1477-5956-12-5.

Title:
Plasma protein profiling of Mild Cognitive Impairment and Alzheimer’s disease using iTRAQ quantitative proteomics | Proteome Science
Description:
Background With the promise of disease modifying treatments, there is a need for more specific diagnosis and prognosis of Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Plasma biomarkers are likely to be utilised to increase diagnostic accuracy and specificity of AD and cognitive decline. Methods Isobaric tags (iTRAQ) and proteomic methods were used to identify potential plasma biomarkers of MCI and AD. Relative protein expression level changes were quantified in plasma of 411 cognitively normal subjects, 19 AD patients and 261 MCI patients. Plasma was pooled into 4 groups including normal control, AD, amnestic single and multiple domain MCI (aMCI), and nonamnestic single and multiple domain MCI (nMCI). Western-blotting was used to validate iTRAQ data. Integrated function and protein interactions were explored using WEB based bioinformatics tools (DAVID v6.7 and STRING v9.0). Results In at least two iTRAQ replicate experiments, 30 proteins were significantly dysregulated in MCI and AD plasma, relative to controls. These proteins included ApoA1, ApoB100, complement C3, C4b-binding protein, afamin, vitamin D-binding protein precursor, isoform 1 of Gelsolin actin regulator, Ig mμ chain C region (IGHM), histidine-rich glycoprotein and fibrinogen β and γ chains. Western-blotting confirmed that afamin was decreased and IGHM was increased in MCI and AD groups. Bioinformatics results indicated that these dysregulated proteins represented a diversity of biological processes, including acute inflammatory response, cholesterol transport and blood coagulation. Conclusion These findings demonstrate that expression level changes in multiple proteins are observed in MCI and AD plasma. Some of these, such as afamin and IGHM, may be candidate biomarkers for AD and the predementia condition of MCI.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Science
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Content Management System {šŸ“}

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Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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How Does Link.springer.com Make Money? {šŸ’ø}

We're unsure how the site profits.

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Keywords {šŸ”}

pubmed, article, google, scholar, plasma, proteins, disease, cas, mci, itraq, protein, alzheimers, analysis, cognitive, results, afamin, study, table, apolipoprotein, dysregulated, impairment, biomarkers, central, samples, mild, vitamin, group, chain, ighm, fibrinogen, expression, biological, data, normal, subjects, domain, complement, patients, human, proteomics, full, brain, identified, multiple, western, blot, levels, published, diagnosis, bioinformatics,

Topics {āœ’ļø}

open access article article download pdf variable post-translational modifications hupo-psi modification nomenclature cyclooxygenase-2-positive macrophages infiltrate histidine-rich glycoprotein polymorphism vitamin d-binding protein automatic literature-mining searches mediates alpha-tocopherol transport pigment epithelium-derived factor large gene/protein lists vitamin e-binding properties includes histidine-rich glycoprotein complex multifactorial conditions/diseases n-terminal variable region neuronal growth-promoting factors applied biosystems/mds sciex diffuse amyloid-beta plaques web-based bioinformatics tools leaky blood–brain barrier important fat-soluble antioxidant enzyme inhibitor activity large population-based studies c18 pre-column cartridge plasma protein profiling genome-wide association discovery-based proteomics method c4b-binding protein proteome-based plasma biomarkers mu heavy chain full homosapiens genome tandem mass spectrometry cognitive impairment profiles nincds-adrda work group ig heavy chain protein-protein associations article song itraq replicate experiments privacy choices/manage cookies voegele af histidine-rich glycoprotein 10Ā mm tris/hcl phĀ 7 western blot analysis hp1090 hplc system tandem mass spectra american psychiatric association authors’ original file natural human antibodies ms/ms analysis identical heavy chains

Questions {ā“}

  • Li X, Buxbaum JN: Transthyretin and the brain re-visited: is neuronal synthesis of transthyretin protective in Alzheimer’s disease?
  • Pogge E: Vitamin D and Alzheimer’s disease: is there a link?

Schema {šŸ—ŗļø}

WebPage:
      mainEntity:
         headline:Plasma protein profiling of Mild Cognitive Impairment and Alzheimer’s disease using iTRAQ quantitative proteomics
         description:With the promise of disease modifying treatments, there is a need for more specific diagnosis and prognosis of Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Plasma biomarkers are likely to be utilised to increase diagnostic accuracy and specificity of AD and cognitive decline. Isobaric tags (iTRAQ) and proteomic methods were used to identify potential plasma biomarkers of MCI and AD. Relative protein expression level changes were quantified in plasma of 411 cognitively normal subjects, 19Ā AD patients and 261 MCI patients. Plasma was pooled into 4 groups including normal control, AD, amnestic single and multiple domain MCI (aMCI), and nonamnestic single and multiple domain MCI (nMCI). Western-blotting was used to validate iTRAQ data. Integrated function and protein interactions were explored using WEB based bioinformatics tools (DAVID v6.7 and STRING v9.0). In at least two iTRAQ replicate experiments, 30 proteins were significantly dysregulated in MCI and AD plasma, relative to controls. These proteins included ApoA1, ApoB100, complement C3, C4b-binding protein, afamin, vitamin D-binding protein precursor, isoform 1 of Gelsolin actin regulator, Ig mμ chain C region (IGHM), histidine-rich glycoprotein and fibrinogen β and γ chains. Western-blotting confirmed that afamin was decreased and IGHM was increased in MCI and AD groups. Bioinformatics results indicated that these dysregulated proteins represented a diversity of biological processes, including acute inflammatory response, cholesterol transport and blood coagulation. These findings demonstrate that expression level changes in multiple proteins are observed in MCI and AD plasma. Some of these, such as afamin and IGHM, may be candidate biomarkers for AD and the predementia condition of MCI.
         datePublished:2014-01-17T00:00:00Z
         dateModified:2014-01-17T00:00:00Z
         pageStart:1
         pageEnd:13
         license:https://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1477-5956-12-5
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            Biomarkers
            Isobaric tags for relative and absolute quantitation (iTRAQ)
            Plasma
            Mild Cognitive Impairment
            Alzheimer’s disease
            Proteomics
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      headline:Plasma protein profiling of Mild Cognitive Impairment and Alzheimer’s disease using iTRAQ quantitative proteomics
      description:With the promise of disease modifying treatments, there is a need for more specific diagnosis and prognosis of Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Plasma biomarkers are likely to be utilised to increase diagnostic accuracy and specificity of AD and cognitive decline. Isobaric tags (iTRAQ) and proteomic methods were used to identify potential plasma biomarkers of MCI and AD. Relative protein expression level changes were quantified in plasma of 411 cognitively normal subjects, 19Ā AD patients and 261 MCI patients. Plasma was pooled into 4 groups including normal control, AD, amnestic single and multiple domain MCI (aMCI), and nonamnestic single and multiple domain MCI (nMCI). Western-blotting was used to validate iTRAQ data. Integrated function and protein interactions were explored using WEB based bioinformatics tools (DAVID v6.7 and STRING v9.0). In at least two iTRAQ replicate experiments, 30 proteins were significantly dysregulated in MCI and AD plasma, relative to controls. These proteins included ApoA1, ApoB100, complement C3, C4b-binding protein, afamin, vitamin D-binding protein precursor, isoform 1 of Gelsolin actin regulator, Ig mμ chain C region (IGHM), histidine-rich glycoprotein and fibrinogen β and γ chains. Western-blotting confirmed that afamin was decreased and IGHM was increased in MCI and AD groups. Bioinformatics results indicated that these dysregulated proteins represented a diversity of biological processes, including acute inflammatory response, cholesterol transport and blood coagulation. These findings demonstrate that expression level changes in multiple proteins are observed in MCI and AD plasma. Some of these, such as afamin and IGHM, may be candidate biomarkers for AD and the predementia condition of MCI.
      datePublished:2014-01-17T00:00:00Z
      dateModified:2014-01-17T00:00:00Z
      pageStart:1
      pageEnd:13
      license:https://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1477-5956-12-5
      keywords:
         Biomarkers
         Isobaric tags for relative and absolute quantitation (iTRAQ)
         Plasma
         Mild Cognitive Impairment
         Alzheimer’s disease
         Proteomics
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                  address:
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                     type:PostalAddress
                  type:Organization
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            name:Perminder S Sachdev
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                  name:University of New South Wales
                  address:
                     name:Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, Australia
                     type:PostalAddress
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                  name:University of New South Wales
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         name:Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, Australia
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         name:School of Psychiatry, University of New South Wales, Sydney, Australia
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      address:
         name:Bioanalytical Mass Spectrometry Facility, University of New South Wales, Sydney, Australia
         type:PostalAddress
      name:University of New South Wales
      address:
         name:School of Psychiatry, University of New South Wales, Sydney, Australia
         type:PostalAddress
      name:University of New South Wales
      address:
         name:School of Medical Sciences, University of New South Wales, Sydney, Australia
         type:PostalAddress
      name:University of New South Wales
      address:
         name:Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, Australia
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Person:
      name:Fei Song
      affiliation:
            name:University of New South Wales
            address:
               name:Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
      name:Anne Poljak
      affiliation:
            name:University of New South Wales
            address:
               name:Bioanalytical Mass Spectrometry Facility, University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
            name:University of New South Wales
            address:
               name:School of Medical Sciences, University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Nicole A Kochan
      affiliation:
            name:University of New South Wales
            address:
               name:Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
            name:University of New South Wales
            address:
               name:School of Psychiatry, University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
      name:Mark Raftery
      affiliation:
            name:University of New South Wales
            address:
               name:Bioanalytical Mass Spectrometry Facility, University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
      name:Henry Brodaty
      affiliation:
            name:University of New South Wales
            address:
               name:School of Psychiatry, University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
      name:George A Smythe
      affiliation:
            name:University of New South Wales
            address:
               name:School of Medical Sciences, University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
      name:Perminder S Sachdev
      affiliation:
            name:University of New South Wales
            address:
               name:Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
            name:University of New South Wales
            address:
               name:School of Psychiatry, University of New South Wales, Sydney, Australia
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, Australia
      name:Bioanalytical Mass Spectrometry Facility, University of New South Wales, Sydney, Australia
      name:School of Medical Sciences, University of New South Wales, Sydney, Australia
      name:Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, Australia
      name:School of Psychiatry, University of New South Wales, Sydney, Australia
      name:Bioanalytical Mass Spectrometry Facility, University of New South Wales, Sydney, Australia
      name:School of Psychiatry, University of New South Wales, Sydney, Australia
      name:School of Medical Sciences, University of New South Wales, Sydney, Australia
      name:Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, Sydney, Australia
      name:School of Psychiatry, University of New South Wales, Sydney, Australia

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