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1. Cerebrospinal fluid proteomic profiling of individuals with mild cognitive impairment and suspected non‐Alzheimer's disease pathophysiology

Author

Aurore Delvenne, Johan Gobom, Betty Tijms, Isabelle Bos, Lianne M. Reus, Valerija Dobricic, Mara ten Kate, Frans Verhey, Inez Ramakers, Philip Scheltens, Charlotte E. Teunissen, Rik Vandenberghe, Jolien Schaeverbeke, Silvy Gabel, Julius Popp, Gwendoline Peyratout, Pablo Martinez‐Lage, Mikel Tainta, Magda Tsolaki, Yvonne Freund‐Levi, Simon Lovestone, Johannes Streffer, Frederik Barkhof, Lars Bertram, Kaj Blennow, Henrik Zetterberg, Pieter Jelle Visser, Stephanie J. B. Vos, Neurology, Amsterdam Neuroscience - Brain Imaging, Amsterdam Neuroscience - Neurodegeneration, Radiology and nuclear medicine, Clinical chemistry, Amsterdam Neuroscience - Neuroinfection & -inflammation, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, Psychology 6, Psychiatrie & Neuropsychologie, MUMC+: MA Med Staf Spec Psychiatrie (9), and Psychology 2

Subjects
Epidemiology, Clinical Neurology, PROTEIN, behavioral disciplines and activities, cerebrospinal fluid, Cellular and Molecular Neuroscience, mild cognitive impairment, proteomics, ADULT, Developmental Neuroscience, mental disorders, tau, pathophysiology, Science & Technology, suspected non-Alzheimer's disease pathophysiology, Health Policy, biomarkers, Alzheimer's disease, nervous system diseases, Psychiatry and Mental health, Neurosciences & Neurology, Human medicine, Neurology (clinical), Geriatrics and Gerontology, Life Sciences & Biomedicine, human activities
Abstract

BACKGROUND: Suspected non-Alzheimer's disease pathophysiology (SNAP) is a biomarker concept that encompasses individuals with neuronal injury but without amyloidosis. We aim to investigate the pathophysiology of SNAP, defined as abnormal tau without amyloidosis, in individuals with mild cognitive impairment (MCI) by cerebrospinal fluid (CSF) proteomics. METHODS: Individuals were classified based on CSF amyloid beta (Aβ)1-42 (A) and phosphorylated tau (T), as cognitively normal A-T- (CN), MCI A-T+ (MCI-SNAP), and MCI A+T+ (MCI-AD). Proteomics analyses, Gene Ontology (GO), brain cell expression, and gene expression analyses in brain regions of interest were performed. RESULTS: A total of 96 proteins were decreased in MCI-SNAP compared to CN and MCI-AD. These proteins were enriched for extracellular matrix (ECM), hemostasis, immune system, protein processing/degradation, lipids, and synapse. Fifty-one percent were enriched for expression in the choroid plexus. CONCLUSION: The pathophysiology of MCI-SNAP (A-T+) is distinct from that of MCI-AD. Our findings highlight the need for a different treatment in MCI-SNAP compared to MCI-AD. ispartof: ALZHEIMERS & DEMENTIA vol:19 issue:3 pages:807-820 ispartof: location:United States status: published

Published
2022
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2. Longitudinal changes in the brain language system as amyloid accumulates

Author

Mariska Reinartz, Silvy Gabel, Jolien Schaeverbeke, Emma Susanne Luckett, Koen Van Laere, Stefan Sunaert, Patrick Dupont, and Rik Vandenberghe

Subjects
Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Epidemiology, Health Policy, Neurology (clinical), Geriatrics and Gerontology
Published
2021
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3. Discovery and validation of plasma proteomic biomarkers relating to brain amyloid burden by SOMAscan assay

Author

Isabelle Bos, Henrik Zetterberg, Daniel Alcolea, Gwendoline Peyratout, B. Paul Morgan, Susan Baker, Simon Lovestone, Liu Shi, Fabian Kilpert, Lars Bertram, Shengjun Hong, Ellen Elisa De Roeck, Alberto Lleó, Mikel Tainta, Pablo Martinez-Lage, Kaj Blennow, Alison L. Baird, Olivier Blin, Lorena Rami, José Luis Molinuevo, Kristel Sleegers, Yvonne Freund-Levi, Lutz Frölich, Angharad R. Morgan, Pieter Jelle Visser, Rik Vandenberghe, Philip Scheltens, Silvy Gabel, Charlotte E. Teunissen, Petronella Kettunen, Julius Popp, Jill C. Richardson, Noel J. Buckley, Stephanie J. B. Vos, Abdul Hye, Johannes Streffer, Sarah Westwood, Nicholas J. Ashton, Valerija Dobricic, Alejo J. Nevado-Holgado, Magda Tsolaki, Giovanni B. Frisoni, Andre Franke, Frans R.J. Verhey, Sebastiaan Engelborghs, Mara ten Kate, Régis Bordet, Cristina Legido-Quigley, Laura Winchester, Anders Wallin, Karen Meersmans, Frederik Barkhof, Peter Johannsen, University of Oxford, Universität zu Lübeck = University of Lübeck [Lübeck], Christian-Albrechts University of Kiel, King‘s College London, University of Gothenburg (GU), Cardiff University, Maastricht University [Maastricht], VU University Medical Center [Amsterdam], University Hospitals Leuven [Leuven], Catholic University of Leuven - Katholieke Universiteit Leuven (KU Leuven), Vrije Universiteit Brussel (VUB), University of Antwerp (UA), Université de Genève = University of Geneva (UNIGE), Istituto Centro San Giovanni di Dio Fatebenefratelli, Partenaires INRAE, Institut de Neurosciences des Systèmes (INS), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance Publique - Hôpitaux de Marseille (APHM), GlaxoSmithKline [Stevenage, UK] (GSK), GlaxoSmithKline [Headquarters, London, UK] (GSK), CHU Lille, Université de Lille, Hospital Clinic (IDIBAPS), Universitat Pompeu Fabra [Barcelona] (UPF), Sahlgrenska Academy at University of Gothenburg [Göteborg], AHEPA University General Hospital [Thessaloniki], Hospital de la Santa Creu i Sant Pau, Lausanne University Hospital, Geneva University Hospital (HUG), Center for Research and Advanced Therapies CITA-Alzheimer Foundation [San Sebastián], Copenhagen University Hospital, Amsterdam UMC - Amsterdam University Medical Center, Vrije Universiteit Amsterdam [Amsterdam] (VU), Karolinska Institutet [Stockholm], Örebro University, Universität Heidelberg [Heidelberg] = Heidelberg University, Institutes of Neurology and Healthcare Engineering, UCL, London, Sahlgrenska University Hospital [Gothenburg], UCL, Institute of Neurology [London], Janssen Research & Development, University of Oslo (UiO), Neurology, Radiology and nuclear medicine, Amsterdam Neuroscience - Neurodegeneration, Clinical chemistry, Faculty of Arts and Philosophy, Clinical sciences, Educational Science, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, Psychiatrie & Neuropsychologie, Promovendi MHN, and MUMC+: MA Med Staf Spec Psychiatrie (9)

Subjects
0301 basic medicine, Apolipoprotein E, Male, Proteomics, Neurology, Epidemiology, Apolipoprotein E4, Disease, SOMAscan assay, ddc:616.89, BLOOD-BASED BIOMARKERS, 0302 clinical medicine, CASCADE HYPOTHESIS, MARKERS, Tau, Medicine, Biomarker discovery, DRUG, Medicine(all), Health Policy, Age Factors, Brain, Middle Aged, Blood proteins, 3. Good health, Europe, ALZHEIMERS-DISEASE, Psychiatry and Mental health, MENDELIAN RANDOMIZATION, Biomarker (medicine), Female, Life Sciences & Biomedicine, medicine.medical_specialty, Amyloid, MODELS, Clinical Neurology, Replication, Plasma proteomics, Computational biology, Article, SIGNALING PATHWAYS, 03 medical and health sciences, Cellular and Molecular Neuroscience, AGE, Developmental Neuroscience, Alzheimer Disease, Amyloid β, Causal relationship, Mendelian randomization, Humans, Biology, Aged, Science & Technology, business.industry, [SCCO.NEUR]Cognitive science/Neuroscience, Amyloid beta, 030104 developmental biology, Neurology (clinical), Human medicine, Neurosciences & Neurology, Geriatrics and Gerontology, TAU, business, 030217 neurology & neurosurgery, Biomarkers
Abstract

Plasma proteins have been widely studied as candidate biomarkers to predict brain amyloid deposition to increase recruitment efficiency in secondary prevention clinical trials for Alzheimer's disease. Most such biomarker studies are targeted to specific proteins or are biased toward high abundant proteins. 4001 plasma proteins were measured in two groups of participants (discovery group = 516, replication group = 365) selected from the European Medical Information Framework for Alzheimer's disease Multimodal Biomarker Discovery study, all of whom had measures of amyloid. A panel of proteins (n = 44), along with age and apolipoprotein E (APOE) ε4, predicted brain amyloid deposition with good performance in both the discovery group (area under the curve = 0.78) and the replication group (area under the curve = 0.68). Furthermore, a causal relationship between amyloid and tau was confirmed by Mendelian randomization. The results suggest that high-dimensional plasma protein testing could be a useful and reproducible approach for measuring brain amyloid deposition. This research was conducted as part of the EMIF-AD project, which has received support from the Innovative Medicines Initiative Joint Undertaking under EMIF grant agreement no. 115372, resources of which are composed of financial contribution from the European Union’s Seventh Framework Program (FP7/2007-2013), and EFPIA companies’ in-kind contribution. The DESCRIPA study was funded by the European Commission within the 5th framework program (QLRT-2001-2455). The EDAR study was funded by the European Commission within the 5th framework program (contract # 37670). The Leuven cohort was funded by the Stichting voor Alzheimer Onderzoek (grant numbers #11020, #13007, and #15005). R.V. is a senior clinical investigator of the Flemish Research Foundation (FWO). J.S. is currently an employee of UCB, Braine-l’Alleud, Belgium. The San Sebastian GAP study is partially funded by the Department of Health of the Basque Government (allocation 17.0.1.08.12.0000.2.454.01.41142.001.H). The authors acknowledge the contribution of the personnel of the Genomic Service Facility at the VIB-U Antwerp Center for Molecular Neurology. The research at VIBCMN is funded in part by the University of Antwerp Research Fund. F.B. is supported by the NIHR biomedical research centre at UCLH. L.S. is funded by DPUK through MRC (grant no. MR/L023784/2) and the UK Medical Research Council Award to the University of Oxford (grant no. MC_PC_17215).

Published
2019
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4. Genome-wide association study of Alzheimer's disease CSF biomarkers in the EMIF-AD Multimodal Biomarker Discovery dataset

Author

Pablo Martinez-Lage, Ulf Andreasson, Richard Dobson, Ellis Niemantsverdriet, Fabian Kilpert, Mikel Tainta, Michael Wittig, Mara ten Kate, Simon Lovestone, Lars Bertram, Henrik Zetterberg, Stephanie J.B. Vos, Dmitry Prokopenko, Frederik Barkhof, Jolien Schaeverbeke, Philip Scheltens, Shengjun Hong, Jill C. Richardson, Olivier Blin, Valerija Dobricic, Pieter Jelle Visser, Silvy Gabel, Cristina Legido-Quigley, Giovanni B. Frisoni, Johannes Streffer, Isabel Sala, Sebastiaan Engelborghs, José Luis Molinuevo, Andre Franke, Alberto Lleó, Isabelle Bos, Rudolph E. Tanzi, Lorena Rami, Kristel Sleegers, Betty M. Tijms, Régis Bordet, Charlotte E. Teunissen, Petronella Kettunen, Rik Vandenberghe, Julius Popp, Isabelle Cleynen, Gwendoline Peyratout, Kaj Blennow, Anders Wallin, Christine Van Broeckhoven, Psychiatrie & Neuropsychologie, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, Alzheimers Dis Neuroimaging Initia, Universität zu Lübeck = University of Lübeck [Lübeck], Massachusetts General Hospital [Boston], Maastricht University [Maastricht], Vrije Universiteit Amsterdam [Amsterdam] (VU), University of Gothenburg (GU), Sahlgrenska University Hospital [Gothenburg], Catholic University of Leuven - Katholieke Universiteit Leuven (KU Leuven), University Hospitals Leuven [Leuven], University of Antwerp (UA), Vrije Universiteit Brussel (VUB), Université de Genève = University of Geneva (UNIGE), Istituto Centro San Giovanni di Dio Fatebenefratelli, Partenaires INRAE, Institut de Neurosciences des Systèmes (INS), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), GlaxoSmithKline [Stevenage, UK] (GSK), GlaxoSmithKline [Headquarters, London, UK] (GSK), CHU Lille, Université de Lille, Clinic Barcelona Hospital Universitari, University of Oxford, Centro de Investigacion Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III [Madrid] (ISC), Geneva University Hospital (HUG), Lausanne University Hospital, Center for Research and Advanced Therapies CITA-Alzheimer Foundation [San Sebastián], King‘s College London, University College of London [London] (UCL), Steno Diabetes Center, VIB [Belgium], Amsterdam UMC - Amsterdam University Medical Center, UCL Institute of Neurology, Queen Square [London], UK Dementia Research Institute (UK DRI), UCB BioPharma [Braine l’Alleud, Belgium], Christian-Albrechts University of Kiel, University of Oslo (UiO), Alzheimer's Disease Neuroimaging Initiative (ADNI), Amsterdam Neuroscience - Neurodegeneration, Neurology, Laboratory Medicine, Radiology and nuclear medicine, Clinical sciences, Neuroprotection & Neuromodulation, and Pathologic Biochemistry and Physiology

Subjects
0301 basic medicine, Male, Genome-wide association study, 0302 clinical medicine, RISK VARIANTS, Biomarker discovery, MIF-AD Multimodal Biomarker Discovery dataset, Psychiatry, Alzheimer's disease, Psychiatry and Mental health, Female, Life Sciences & Biomedicine, SUSCEPTIBILITY LOCI, Neuroscience(all), Single-nucleotide polymorphism, Genomics, tau Proteins, Computational biology, Biology, Molecular neuroscience, elderly, Article, lcsh:RC321-571, 03 medical and health sciences, Cellular and Molecular Neuroscience, Alzheimer Disease, medicine, Dementia, SNP, Humans, CSF biomarkers, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Biological Psychiatry, Aged, Amyloid beta-Peptides, Science & Technology, business.industry, [SCCO.NEUR]Cognitive science/Neuroscience, Neurodegenerative disorder, medicine.disease, Personalized medicine, Genetic architecture, Peptide Fragments, 030104 developmental biology, Human medicine, TAU, business, 030217 neurology & neurosurgery, Biomarkers, dementia, Genome-Wide Association Study
Abstract

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder and the most common form of dementia in the elderly. Susceptibility to AD is considerably determined by genetic factors which hitherto were primarily identified using case–control designs. Elucidating the genetic architecture of additional AD-related phenotypic traits, ideally those linked to the underlying disease process, holds great promise in gaining deeper insights into the genetic basis of AD and in developing better clinical prediction models. To this end, we generated genome-wide single-nucleotide polymorphism (SNP) genotyping data in 931 participants of the European Medical Information Framework Alzheimer’s Disease Multimodal Biomarker Discovery (EMIF-AD MBD) sample to search for novel genetic determinants of AD biomarker variability. Specifically, we performed genome-wide association study (GWAS) analyses on 16 traits, including 14 measures derived from quantifications of five separate amyloid-beta (Aβ) and tau-protein species in the cerebrospinal fluid (CSF). In addition to confirming the well-established effects of apolipoprotein E (APOE) on diagnostic outcome and phenotypes related to Aβ42, we detected novel potential signals in the zinc finger homeobox 3 (ZFHX3) for CSF-Aβ38 and CSF-Aβ40 levels, and confirmed the previously described sex-specific association between SNPs in geminin coiled-coil domain containing (GMNC) and CSF-tau. Utilizing the results from independent case–control AD GWAS to construct polygenic risk scores (PRS) revealed that AD risk variants only explain a small fraction of CSF biomarker variability. In conclusion, our study represents a detailed first account of GWAS analyses on CSF-Aβ and -tau-related traits in the EMIF-AD MBD dataset. In subsequent work, we will utilize the genomics data generated here in GWAS of other AD-relevant clinical outcomes ascertained in this unique dataset.

Published
2020
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5. CSF proteomic profiling of mild cognitive impairment individuals with suspected non‐Alzheimer’s disease pathophysiology

Author

Julius Popp, Aurore Delvenne, Charlotte E. Teunissen, Gwendoline Peyratout, Magda Tsolaki, Mikel Tainta, Frans R.J. Verhey, Pieter Jelle Visser, Stephanie J.B. Vos, Betty M. Tijms, Pablo Martinez-Lage, Isabelle Bos, Silvy Gabel, Inez H.G.B. Ramakers, Rik Vandenberghe, Kaj Blennow, Henrik Zetterberg, Johan Gobom, Simon Lovestone, Johannes Streffer, Philip Scheltens, and Yvonne Freund-Levi

Subjects
Epidemiology, business.industry, Proteomic Profiling, Health Policy, Disease, Bioinformatics, Pathophysiology, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Medicine, Neurology (clinical), Geriatrics and Gerontology, Cognitive impairment, business
Published
2020
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6. Comparison of two analytical platforms for blood‐based surrogate biomarkers of amyloid pathology

Author

Charlotte E. Teunissen, Emma Susanne Luckett, Erik Stoops, Elisabeth H. Thijssen, Benjamin Gille, Hugo Vanderstichele, Koen Poesen, Inge M.W. Verberk, Rik Vandenberghe, Steffi De Meyer, Jolien Schaeverbeke, Rose Bruffaerts, Kimberley Mauroo, and Silvy Gabel

Subjects
Psychiatry and Mental health, Cellular and Molecular Neuroscience, Amyloid pathology, Pathology, medicine.medical_specialty, Developmental Neuroscience, Epidemiology, business.industry, Health Policy, Medicine, Neurology (clinical), Geriatrics and Gerontology, business
Published
2020
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7. Identification of plasma proteome signatures associated with ATN framework using SOMAscan

Author

Isabelle Bos, Simon Lovestone, Mara ten Kate, Ellen De Roeck, Lars Bertram, Giovanni B. Frisoni, Daniel Alcolea, Nicholas J. Ashton, Frederik Barkhof, Gwendoline Peyratout, Frans R.J. Verhey, Yvonne Freund, Noel J. Buckley, Sebastiaan Engelborghs, Fabian Kilpert, Valerija Dobricic, Régis Bordet, Paul Morgan, Mikel Tainta, Johannes Streffer, José Luis Molinuevo, Silvy Gabel, Kaj Blennow, Rik Vandenberghe, Kristel Sleegers, Olivier Blin, Cristina Legido-Quigley, Alberto Lleó, Abdul Hye, Andreas G. Franke, Alejo J. Nevado-Holgado, Julius Popp, Lutz Frölich, Sarah Westwood, Magda Tsolaki, Karen Meersmans, Laura Winchester, Liu Shi, Anders Wallin, Lorena Rami, Jill C. Richardson, Henrik Zetterberg, Stephanie J.B. Vos, Philip Scheltens, Alison L. Baird, Pablo Martinez-Lage, Peter Johannsen, Angharad R. Morgan, Pieter Jelle Visser, Charlotte E. Teunissen, Petronella Kettunen, and Shengjun Hong

Subjects
Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Epidemiology, Health Policy, Proteome, Identification (biology), Neurology (clinical), Computational biology, Geriatrics and Gerontology, Biology
Published
2020
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8. O5‐07‐02: APOLIPOPROTEIN E AND BIN1 POLYMORPHISMS DIFFERENTIALLY AFFECT CORTICAL AMYLOID AND TAU LOAD IN HEALTHY OLDER ADULTS

Author

Patrick Dupont, Silvy Gabel, Koen Van Laere, Kim Serdons, Rik Vandenberghe, Kristel Sleegers, Guy Bormans, Christine Van Broeckhoven, and Jolien Schaeverbeke

Subjects
Apolipoprotein E, medicine.medical_specialty, Amyloid, Epidemiology, business.industry, Health Policy, Affect (psychology), Psychiatry and Mental health, Cellular and Molecular Neuroscience, Endocrinology, Developmental Neuroscience, Internal medicine, Medicine, Neurology (clinical), Geriatrics and Gerontology, business
Published
2019
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9. Primary fatty amides in plasma associated with brain amyloid burden, hippocampal volume, and memory in the European Medical Information Framework for Alzheimer's Disease biomarker discovery cohort

Author

Lutz Frölich, Kaj Blennow, Karen Meersmans, Kristel Sleegers, Cristina Legido-Quigley, Mara ten Kate, Tommi Suvitaival, Julius Popp, Frederik Barkhof, Sarah Westwood, Tahmina Ahmad, Petra Proitsi, Jill C. Richardson, Magda Tsolaki, José Luis Molinuevo, Mikel Tainta, Alison L. Baird, Pablo Martinez-Lage, Philip Scheltens, Abdul Hye, Yvonne Freund-Levi, Lorena Rami, Adnan Ali, Stephanie J.B. Vos, Frans R.J. Verhey, Stuart G. Snowden, Rik Vandenberghe, Valerija Dobricic, Charlotte E. Teunissen, Pieter Jelle Visser, Petronella Kettunen, Min Kim, Peter Johannsen, Régis Bordet, David J. Merkler, Nicholas J. Ashton, Alberto Lleó, Henrik Zetterberg, Gwendoline Peyratout, Alejo J. Nevado-Holgado, Anders Wallin, Sebastiaan Engelborghs, Olivier Blin, Johannes Streffer, Isabel Sala, Isabelle Bos, Simon Lovestone, Ellen De Roeck, Lars Bertram, Silvy Gabel, Giovanni B. Frisoni, King‘s College London, University of Cambridge [UK] (CAM), Steno Diabetes Center of Copenhagen [Gentofte, Denmark], University of South Florida [Tampa] (USF), University of Oxford, Maastricht University [Maastricht], University Hospitals Leuven [Leuven], Amsterdam UMC - Amsterdam University Medical Center, Catholic University of Leuven - Katholieke Universiteit Leuven (KU Leuven), Institut de Neurosciences des Systèmes (INS), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance Publique - Hôpitaux de Marseille (APHM), GlaxoSmithKline [Stevenage, UK] (GSK), GlaxoSmithKline [Headquarters, London, UK] (GSK), University of Antwerp (UA), Troubles cognitifs vasculaires et dégénératifs, Université de Lille, Sciences et Technologies, CHU Lille, Hospital Clinic (IDIBAPS), University of Gothenburg (GU), AHEPA University General Hospital [Thessaloniki], Hospital de la Santa Creu i Sant Pau, Lausanne University Hospital, Center for Research and Advanced Therapies CITA-Alzheimer Foundation [San Sebastián], Copenhagen University Hospital, Karolinska University Hospital [Stockholm], Universität Heidelberg [Heidelberg] = Heidelberg University, Universität zu Lübeck = University of Lübeck [Lübeck], Université de Genève = University of Geneva (UNIGE), Geneva University Hospital (HUG), Sahlgrenska University Hospital [Gothenburg], UCL, Institute of Neurology [London], Janssen Pharmaceutica [Beerse], Universität Heidelberg [Heidelberg], Otten, Lisa, Clinical sciences, Neurology, Amsterdam Neuroscience - Neurodegeneration, Laboratory Medicine, Radiology and nuclear medicine, Psychiatrie & Neuropsychologie, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, and MUMC+: MA Med Staf Spec Psychiatrie (9)

Subjects
0301 basic medicine, Oncology, Male, Neurology, Epidemiology, Neuropsychological Tests, Hippocampus, RECOMMENDATIONS, Cohort Studies, ddc:616.89, 0302 clinical medicine, Cerebrospinal fluid, MARKERS, Biomarker discovery, Brain volume measurements, Medicine(all), OLEAMIDE, biology, medicine.diagnostic_test, Health Policy, Brain, INDUCED LIPOKINE, EMIF-AD, Amyloidosis, Middle Aged, Alzheimer's disease, Magnetic Resonance Imaging, PERTURBATIONS, 3. Good health, Psychiatry and Mental health, ACID, Female, Alzheimer’s disease, Life Sciences & Biomedicine, medicine.medical_specialty, Amyloid, Tau protein, Clinical Neurology, tau Proteins, CSF, METABOLISM, Article, Aged, Amyloid beta-Peptides/blood, Amyloid beta-Peptides/cerebrospinal fluid, Amyloidosis/blood, Amyloidosis/cerebrospinal fluid, Amyloidosis/metabolism, Biomarkers/blood, Biomarkers/cerebrospinal fluid, Brain/pathology, Cognitive Dysfunction/diagnosis, Hippocampus/metabolism, Humans, Memory/physiology, Metabolomics, tau Proteins/blood, tau Proteins/cerebrospinal fluid, Biomarkers, Cognitive function measurements, Dementia, Tau, 03 medical and health sciences, Cellular and Molecular Neuroscience, Developmental Neuroscience, Memory, Internal medicine, 12,13-DIHOME, medicine, 13-DIHOME, Cognitive Dysfunction, BIOSYNTHESIS, Biology, Mini–Mental State Examination, Amyloid beta-Peptides, Science & Technology, business.industry, [SCCO.NEUR]Cognitive science/Neuroscience, [SCCO.NEUR] Cognitive science/Neuroscience, medicine.disease, 030104 developmental biology, ddc:618.97, biology.protein, Human medicine, Neurology (clinical), Neurosciences & Neurology, Geriatrics and Gerontology, business, 030217 neurology & neurosurgery
Abstract

Introduction: A critical and as-yet unmet need in Alzheimer's disease (AD) is the discovery of peripheral small molecule biomarkers. Given that brain pathology precedes clinical symptom onset, we set out to test whether metabolites in blood associated with pathology as indexed by cerebrospinal fluid (CSF) AD biomarkers.Methods: This study analyzed 593 plasma samples selected from the European Medical Information Framework for Alzheimer's Disease Multimodal Biomarker Discovery study, of individuals who were cognitively healthy (n = 242), had mild cognitive impairment (n = 236), or had AD-type dementia (n = 115). Logistic regressions were carried out between plasma metabolites (n = 883) and CSF markers, magnetic resonance imaging, cognition, and clinical diagnosis.Results: Eight metabolites were associated with amyloid b and one with t-tau in CSF, these were primary fatty acid amides (PFAMs), lipokines, and amino acids. From these, PFAMs, glutamate, and aspartate also associated with hippocampal volume and memory.Discussion: PFAMs have been found increased and associated with amyloid b burden in CSF and clinical measures. Crown Copyright (C) 2019 Published by Elsevier Inc. on behalf of the Alzheimer's Association. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-ncnd/4.0/).

Published
2019
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10. IC‐P‐068: A POLYGENIC AD RISK SCORE PREDICTS AMYLOID ACCUMULATION OVER A 6‐YEAR INTERVAL IN COGNITIVELY INTACT OLDER ADULTS

Author

Patrick Dupont, Christine Van Broeckhoven, Koen Van Laere, Kristel Sleegers, Silvy Gabel, Katarzyna Adamczuk, Jolien Schaeverbeke, and Rik Vandenberghe

Subjects
medicine.medical_specialty, Framingham Risk Score, Amyloid, Epidemiology, business.industry, Health Policy, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Internal medicine, Cardiology, medicine, Interval (graph theory), Neurology (clinical), Geriatrics and Gerontology, business
Published
2018
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11. [P4–493]: IN VIVO VISUALIZATION OF [ 18 ]F‐THK5351 BINDING IN PRIMARY PROGRESSIVE APHASIA

Author

Rose Bruffaerts, Silvy Gabel, Karen Meersmans, Jolien Schaeverbeke, Charlotte Evenepoel, Karen Van Bouwel, Koen Van Laere, Ronald Peeters, Eva Dries, and Rik Vandenberghe

Subjects
Epidemiology, business.industry, Health Policy, medicine.disease, Visualization, Primary progressive aphasia, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, In vivo, medicine, Neurology (clinical), Geriatrics and Gerontology, business, Neuroscience
Published
2017
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12. [IC‐P‐191]: IN VIVO MAPPING OF TAU DEPOSITION, PERFUSION, AND CORTICAL THINNING IN MILD COGNITIVE IMPAIRMENT AND ALZHEIMER'S DISEASE

Author

Elijah Mak, Silvy Gabel, Simon Cervenka, Li Su, Ajenthan Surendranathan, William Richard Bevan‐Jones, Young T. Hong, Robert Arnold, Patricia Vazquez Rodriguez, Simon Jones, Guy B. Williams, Tim D. Fryer, Franklin I. Aigbirhio, James B. Rowe, and John T. O'Brien

Subjects
Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Epidemiology, Health Policy, Neurology (clinical), Geriatrics and Gerontology
Published
2017
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13. [P2–358]: IN VIVO MAPPING OF TAU DEPOSITION, PERFUSION, AND CORTICAL THINNING IN MILD COGNITIVE IMPAIRMENT AND ALZHEIMER'S DISEASE

Author

Simon Jones, Franklin I. Aigbirhio, John T. O'Brien, Li Su, Elijah Mak, Silvy Gabel, Ajenthan Surendranathan, Young T. Hong, Patricia Vázquez Rodríguez, James B. Rowe, William Richard Bevan-Jones, Luca Passamonti, Tim D. Fryer, Guy B. Williams, Simon Cervenka, and Robert M. Arnold

Subjects
Pathology, medicine.medical_specialty, Epidemiology, business.industry, Health Policy, Cortical thinning, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, In vivo, medicine, Neurology (clinical), Geriatrics and Gerontology, Cognitive impairment, business, Deposition (chemistry), Perfusion
Published
2017
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14. [O4–04–04]: [ 18 F]AV‐1451 PET IMAGING OF TAU PATHOLOGY PREDICTS WHITE MATTER HYPERINTENSITIES IN HEALTHY AGING, MILD COGNITIVE IMPAIRMENT AND ALZHEIMER'S DISEASE: THE NIMROD STUDY

Author

James B. Rowe, William Richard Bevan-Jones, John T. O'Brien, Guy B. Williams, Michael J. Firbank, Patricia Vázquez Rodríguez, Ajenthan Surendranathan, Elijah Mak, Luca Passamonti, Robert Arnold, Simon Cervenka, Silvy Gabel, P. Simon Jones, and Li Su

Subjects
Tau pathology, Epidemiology, Health Policy, Disease, Pet imaging, Hyperintensity, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Neurology (clinical), Geriatrics and Gerontology, Healthy aging, Cognitive impairment, Psychology, Neuroscience
Published
2017
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15. P2‐226: Hippocampal CA1 Involvement in Dementia with Lewy Bodies, Alzheimer's Disease and Mild Cognitive Impairment: The Nimrod Study

Author

Luca Passamonti, Patricia Rodríguezi, John T. O'Brien, Li Su, Guy B. Williams, Elijah Mak, Ajenthan Surendranathan, James B. Rowe, William Richard Bevan-Jones, Robert Arnold, and Silvy Gabel

Subjects
Epidemiology, Dementia with Lewy bodies, business.industry, Health Policy, Disease, Hippocampal formation, medicine.disease, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, medicine, Nimrod, Neurology (clinical), Geriatrics and Gerontology, Cognitive impairment, business, Neuroscience
Published
2016
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16. P3‐311: A Comparison of Neuropsychiatric Symptoms And Cognitive Profiles Between Dementia With Lewy Bodies And Progressive Supranuclear Palsy: The Nimrod Study

Author

Silvy Gabel, Luca Passamonti, Li Su, Robert Arnold, Elijah Mak, William Richard Bevan-Jones, Guy B. Williams, John T. O'Brien, James B. Rowe, Ajenthan Surendranathan, and Patricia Rodríguezi

Subjects
medicine.medical_specialty, Epidemiology, business.industry, Dementia with Lewy bodies, Health Policy, Cognition, medicine.disease, Progressive supranuclear palsy, Psychiatry and Mental health, Cellular and Molecular Neuroscience, Developmental Neuroscience, Medicine, Nimrod, Neurology (clinical), Geriatrics and Gerontology, business, Psychiatry
Published
2016
Full Text
View/download PDF

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