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LIBRIS Formathandbok  (Information om MARC21)
00006171naa a22006493a 4500
008080901s2016 xx |||| s |0|| 0|eng d
024a 278457822 pmid
024a 849968372992 scopus
024a 850335614562 scopus
024a 278457822 pmid
024a 10.1038/tp.2016.1942 doi
040 a (SwePub)lud (SwePub)gu
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Paterson, R. W.,u University College London4 aut0 (SwePub:)
2451 0a A targeted proteomic multiplex CSF assay identifies increased malate dehydrogenase and other neurodegenerative biomarkers in individuals with Alzheimer's disease pathology.
500 a Published
500 a 15
500 a not verified at registration
5208 enga Alzheimer's disease (AD) is the most common cause of dementia. Biomarkers are required to identify individuals in the preclinical phase, explain phenotypic diversity, measure progression and estimate prognosis. The development of assays to validate candidate biomarkers is costly and time-consuming. Targeted proteomics is an attractive means of quantifying novel proteins in cerebrospinal and other fluids, and has potential to help overcome this bottleneck in biomarker development. We used a previously validated multiplexed 10-min, targeted proteomic assay to assess 54 candidate cerebrospinal fluid (CSF) biomarkers in two independent cohorts comprising individuals with neurodegenerative dementias and healthy controls. Individuals were classified as 'AD' or 'non-AD' on the basis of their CSF T-tau and amyloid Aβ1-42 profile measured using enzyme-linked immunosorbent assay; biomarkers of interest were compared using univariate and multivariate analyses. In all, 35/31 individuals in Cohort 1 and 46/36 in Cohort 2 fulfilled criteria for AD/non-AD profile CSF, respectively. After adjustment for multiple comparisons, five proteins were elevated significantly in AD CSF compared with non-AD CSF in both cohorts: malate dehydrogenase; total APOE; chitinase-3-like protein 1 (YKL-40); osteopontin and cystatin C. In an independent multivariate orthogonal projection to latent structures discriminant analysis (OPLS-DA), these proteins were also identified as major contributors to the separation between AD and non-AD in both cohorts. Independent of CSF Aβ1-42 and tau, a combination of these biomarkers differentiated AD and non-AD with an area under curve (AUC)=0.88. This targeted proteomic multiple reaction monitoring (MRM)-based assay can simultaneously and rapidly measure multiple candidate CSF biomarkers. Applying this technique to AD we demonstrate differences in proteins involved in glucose metabolism and neuroinflammation that collectively have potential clinical diagnostic utility.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Neurologi2 hsv//swe0 (SwePub)30207
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Neurology2 hsv//eng0 (SwePub)30207
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes2 hsv//swe0 (SwePub)30205
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes2 hsv//eng0 (SwePub)30205
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Psykiatri2 hsv//swe0 (SwePub)30215
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Psychiatry2 hsv//eng0 (SwePub)30215
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Klinisk laboratoriemedicin2 hsv//swe0 (SwePub)30223
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Clinical Laboratory Medicine2 hsv//eng0 (SwePub)30223
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Annan klinisk medicin2 hsv//swe0 (SwePub)30299
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Other Clinical Medicine2 hsv//eng0 (SwePub)30299
700a Heywood, W. E.,u University College London4 aut0 (SwePub:)
700a Heslegrave, A. J.,u University College London4 aut0 (SwePub:)
700a Magdalinou, N. K.,u University College London4 aut0 (SwePub:)
700a Andreasson, U.,u Sahlgrenska University Hospital4 aut0 (SwePub:)
700a Sirka, E.,u University College London4 aut0 (SwePub:)
700a Bliss, E.,u University College London4 aut0 (SwePub:)
700a Slattery, C. F.,u University College London4 aut0 (SwePub:)
700a Toombs, J.,u University College London4 aut0 (SwePub:)
700a Svensson, J.,u Sahlgrenska Academy, Skaraborg Hospital4 aut0 (SwePub:)
700a Johansson, P.,u Skaraborg Hospital, Sahlgrenska Academy4 aut0 (SwePub:)
700a Fox, N. C.,u University College London4 aut0 (SwePub:)
700a Zetterberg, H.,u University College London, Sahlgrenska University Hospital4 aut0 (SwePub:)
700a Mills, K.,u University College London4 aut0 (SwePub:)
700a Schott, J. M.,u University College London4 aut0 (SwePub:)
7108 swea Göteborgs universitet.b Sahlgrenska akademin.b Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi.0 (SwePub:gu.se)1630
7108 enga Gothenburg University.b Sahlgrenska Academy.b Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry.0 (SwePub:gu.se)1630
7108 swea Göteborgs universitet.b Sahlgrenska akademin.b Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition.0 (SwePub:gu.se)1793
7108 enga Gothenburg University.b Sahlgrenska Academy.b Institute of Medicine, Department of Internal Medicine and Clinical Nutrition.0 (SwePub:gu.se)1793
773t Translational psychiatryx 2158-3188g 6:11q 6:11
8564 0u http://dx.doi.org/10.1038/tp.2016.194z fulltextx free
8564 8u https://lup.lub.lu.se/record/b88d23ef-e620-428e-ae1a-deea01282aa6y Till lärosätets (lu) databasx lärosäteslänk
8564 8u https://gup.ub.gu.se/publication/253388y Till lärosätets (gu) databasx lärosäteslänk

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