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FältnamnIndikatorerMetadata
00005788naa a2200841 4500
001oai:gup.ub.gu.se/230001
003SwePub
008240910s2015 | |||||||||||000 ||eng|
0247 a https://gup.ub.gu.se/publication/2300012 URI
0247 a https://doi.org/10.1186/s13024-015-0059-y2 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Heywood, W. E.4 aut
2451 0a Identification of novel CSF biomarkers for neurodegeneration and their validation by a high-throughput multiplexed targeted proteomic assay
264 c 2015-12-01
264 1b Springer Science and Business Media LLC,c 2015
520 a Background: Currently there are no effective treatments for many neurodegenerative diseases. Reliable biomarkers for identifying and stratifying these diseases will be important in the development of future novel therapies. Lewy Body Dementia (LBD) is considered an under diagnosed form of dementia for which markers are needed to discriminate LBD from other forms of dementia such as Alzheimer's Disease (AD). This work describes a Label-Free proteomic profiling analysis of cerebral spinal fluid (CSF) from non-neurodegenerative controls and patients with LBD. Using this technology we identified several potential novel markers for LBD. These were then combined with other biomarkers from previously published studies, to create a 10 min multiplexed targeted and translational MRM-LC-MS/MS assay. This test was used to validate our new assay in a larger cohort of samples including controls and the other neurodegenerative conditions of Alzheimer's and Parkinson's disease (PD). Results: Thirty eight proteins showed significantly (p < 0.05) altered expression in LBD CSF by proteomic profiling. The targeted MRM-LC-MS/MS assay revealed 4 proteins that were specific for the identification of AD from LBD: ectonucleotide pyrophosphatase/phosphodiesterase 2 (p < 0.0001), lysosome-associated membrane protein 1 (p < 0.0001), pro-orexin (p < 0.0017) and transthyretin (p < 0.0001). Nineteen proteins were elevated significantly in both AD and LBD versus the control group of which 4 proteins are novel (malate dehydrogenase 1, serum amyloid A4, GM2-activator protein, and prosaposin). Protein-DJ1 was only elevated significantly in the PD group and not in either LBD or AD samples. Correlations with Alzheimer-associated amyloid beta-42 levels, determined by ELISA, were observed for transthyretin, GM2 activator protein and IGF2 in the AD disease group (r(2) >= 0.39, p <= 0.012). Cystatin C, ubiquitin and osteopontin showed a strong significant linear relationship (r(2) >= 0.4, p <= 0.03) with phosphorylated-tau levels in all groups, whilst malate dehydrogenase and apolipoprotein E demonstrated a linear relationship with phosphorylated-tau and total-tau levels in only AD and LBD disease groups. Conclusions: Using proteomics we have identified several potential and novel markers of neurodegeneration and subsequently validated them using a rapid, multiplexed mass spectral test. This targeted proteomic platform can measure common markers of neurodegeneration that correlate with existing diagnostic makers as well as some that have potential to show changes between AD from LBD.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Neurologi0 (SwePub)302072 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Neurology0 (SwePub)302072 hsv//eng
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
653 a Lewy body dementia
653 a Alzheimer's disease
653 a Targeted proteomics
653 a CSF biomarker
653 a ONSET ALZHEIMERS-DISEASE
653 a CEREBROSPINAL-FLUID
653 a MASS-SPECTROMETRY
653 a PARKINSONS-DISEASE
653 a CLINICAL-DIAGNOSIS
653 a PLASMA BIOMARKERS
653 a COGNITIVE
653 a DECLINE
653 a ALPHA-SYNUCLEIN
653 a TAU-PROTEIN
653 a DEMENTIA
653 a Neurosciences
653 a KHANN G
653 a 1984
653 a NEUROLOGY
653 a V34
653 a P939
653 a KEITH IG
653 a 1994
653 a NEUROLOGY
653 a V44
653 a P872
7001 a Galimberti, D.4 aut
7001 a Bliss, E.4 aut
7001 a Sirka, E.4 aut
7001 a Paterson, R. W.4 aut
7001 a Magdalinou, N. K.4 aut
7001 a Carecchio, M.4 aut
7001 a Reid, E.4 aut
7001 a Heslegrave, A.4 aut
7001 a Fenoglio, C.4 aut
7001 a Scarpini, E.4 aut
7001 a Schott, J. M.4 aut
7001 a Fox, N. C.4 aut
7001 a Hardy, J.4 aut
7001 a Bahtia, K.4 aut
7001 a Heales, S.4 aut
7001 a Sebire, N. J.4 aut
7001 a Zetterberg, Henrik,d 1973u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xzethe
7001 a Mills, K.4 aut
7102 a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi4 org
7730 t Molecular Neurodegenerationd : Springer Science and Business Media LLCg 10q 10x 1750-1326
8564 u https://molecularneurodegeneration.biomedcentral.com/track/pdf/10.1186/s13024-015-0059-y
8564 8u https://gup.ub.gu.se/publication/230001
8564 8u https://doi.org/10.1186/s13024-015-0059-y

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