Sökning: WFRF:(Verberk Inge) > Combination of plas...
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000 | 05514naa a2200541 4500 | |
001 | oai:lup.lub.lu.se:3531247a-6ec9-4101-85d6-25d1f4a9cabe | |
003 | SwePub | |
008 | 201027s2020 | |||||||||||000 ||eng| | |
024 | 7 | a https://lup.lub.lu.se/record/3531247a-6ec9-4101-85d6-25d1f4a9cabe2 URI |
024 | 7 | a https://doi.org/10.1186/s13195-020-00682-72 DOI |
040 | a (SwePub)lu | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a art2 swepub-publicationtype |
072 | 7 | a ref2 swepub-contenttype |
100 | 1 | a Verberk, Inge M.W.u Vrije Universiteit Amsterdam4 aut |
245 | 1 0 | a Combination of plasma amyloid beta(1-42/1-40)and glial fibrillary acidic protein strongly associates with cerebral amyloid pathology |
264 | c 2020-09-28 | |
264 | 1 | b Springer Science and Business Media LLC,c 2020 |
520 | a Background: Blood-based biomarkers for Alzheimer's disease (AD) might facilitate identification of participants for clinical trials targeting amyloid beta (Abeta) accumulation, and aid in AD diagnostics. We examined the potential of plasma markers Abeta(1-42/1-40), glial fibrillary acidic protein (GFAP) and neurofilament light (NfL) to identify cerebral amyloidosis and/or disease severity. Methods: We included individuals with a positive (n = 176: 63 ± 7 years, 87 (49%) females) or negative (n = 76: 61 ± 9 years, 27 (36%) females) amyloid PET status, with syndrome diagnosis subjective cognitive decline (18 PET+, 25 PET-), mild cognitive impairment (26 PET+, 24 PET-), or AD-dementia (132 PET+). Plasma Abeta(1-42/1-40), GFAP, and NfL were measured by Simoa. We applied two-way ANOVA adjusted for age and sex to investigate the associations of the plasma markers with amyloid PET status and syndrome diagnosis; logistic regression analysis with Wald's backward selection to identify an optimal panel that identifies amyloid PET positivity; age, sex, and education-adjusted linear regression analysis to investigate associations between the plasma markers and neuropsychological test performance; and Spearman's correlation analysis to investigate associations between the plasma markers and medial temporal lobe atrophy (MTA). Results: Abeta(1-42/1-40) and GFAP independently associated with amyloid PET status (p = 0.009 and p < 0.001 respectively), and GFAP and NfL independently associated with syndrome diagnosis (p = 0.001 and p = 0.048 respectively). The optimal panel identifying a positive amyloid status included Abeta(1-42/1-40) and GFAP, alongside age and APOE (AUC = 88% (95% CI 83-93%), 82% sensitivity, 86% specificity), while excluding NfL and sex. GFAP and NfL robustly associated with cognitive performance on global cognition and all major cognitive domains (GFAP: range standardized β (sβ) = - 0.40 to - 0.26; NfL: range sβ = - 0.35 to - 0.18; all: p < 0.002), whereas Abeta(1-42/1-40) associated with global cognition, memory, attention, and executive functioning (range sβ = 0.22 - 0.11; all: p < 0.05) but not language. GFAP and NfL showed moderate positive correlations with MTA (both: Spearman's rho> 0.33, p < 0.001). Abeta(1-42/1-40) showed a moderate negative correlation with MTA (Spearman's rho = - 0.24, p = 0.001). Discussion and conclusions: Combination of plasma Abeta(1-42/1-40) and GFAP provides a valuable tool for the identification of amyloid PET status. Furthermore, plasma GFAP and NfL associate with various disease severity measures suggesting potential for disease monitoring. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Klinisk laboratoriemedicin0 (SwePub)302232 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Clinical Laboratory Medicine0 (SwePub)302232 hsv//eng |
653 | a Alzheimer's continuum | |
653 | a Amyloid pathology | |
653 | a Blood-based biomarkers | |
653 | a Plasma amyloid beta | |
653 | a Plasma GFAP | |
700 | 1 | a Thijssen, Elisabethu Vrije Universiteit Amsterdam4 aut |
700 | 1 | a Koelewijn, Jannetu Vrije Universiteit Amsterdam4 aut |
700 | 1 | a Mauroo, Kimberleyu ADx NeuroSciences4 aut |
700 | 1 | a Vanbrabant, Jeroenu ADx NeuroSciences4 aut |
700 | 1 | a De Wilde, Arnou Vrije Universiteit Amsterdam4 aut |
700 | 1 | a Zwan, Marissa D.u Vrije Universiteit Amsterdam4 aut |
700 | 1 | a Verfaillie, Sander C.J.u Vrije Universiteit Amsterdam4 aut |
700 | 1 | a Ossenkoppele, Riku Lund University,Lunds universitet,Klinisk minnesforskning,Forskargrupper vid Lunds universitet,Clinical Memory Research,Lund University Research Groups,Vrije Universiteit Amsterdam4 aut0 (Swepub:lu)ri1513os |
700 | 1 | a Barkhof, Frederiku University College London4 aut |
700 | 1 | a Van Berckel, Bart N.M.u Vrije Universiteit Amsterdam4 aut |
700 | 1 | a Scheltens, Philipu Vrije Universiteit Amsterdam4 aut |
700 | 1 | a Van Der Flier, Wiesje M.u Vrije Universiteit Amsterdam4 aut |
700 | 1 | a Stoops, Eriku ADx NeuroSciences4 aut |
700 | 1 | a Vanderstichele, Hugo M.u ADx NeuroSciences4 aut |
700 | 1 | a Teunissen, Charlotte E.u Vrije Universiteit Amsterdam4 aut |
710 | 2 | a Vrije Universiteit Amsterdamb ADx NeuroSciences4 org |
773 | 0 | t Alzheimer's Research and Therapyd : Springer Science and Business Media LLCg 12:1q 12:1x 1758-9193 |
856 | 4 | u http://dx.doi.org/10.1186/s13195-020-00682-7x freey FULLTEXT |
856 | 4 | u https://alzres.biomedcentral.com/track/pdf/10.1186/s13195-020-00682-7 |
856 | 4 8 | u https://lup.lub.lu.se/record/3531247a-6ec9-4101-85d6-25d1f4a9cabe |
856 | 4 8 | u https://doi.org/10.1186/s13195-020-00682-7 |
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