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491 results on '"Johannsen, Peter"'

1. Fermionic Quantum Simulation on Andreev Bound State Superlattices

Author

Johannsen, Peter D. and Schrade, Constantin

Subjects
Condensed Matter - Mesoscale and Nanoscale Physics
Abstract

Arrays of superconducting qubits and cavities offer a promising route for realizing highly controllable artificial materials. However, many analog simulations of superconducting circuit hardware have focused on bosonic systems. Fermionic simulations, on the other hand, have largely relied on digital approaches that require non-local qubit couplings, which could limit their scalability. Here, we propose and study an alternative approach for analog fermionic quantum simulation based on arrays of coherently coupled mesoscopic Josephson junctions. These Josephson junction arrays implement an effective superlattice of Andreev bound state "atoms" that can trap individual fermionic quasiparticles and, due to their wavefunction overlap, mediate quasiparticle hoppings. By developing a Wannier function approach, we show that these Andreev bound state arrays form an all-superconducting and circuit QED-compatible platform for emulating lattice models of fermionic quasiparticles that are phase- and gate-programmable. Interestingly, we also find that the junction lattices can undergo a topological transition and host fermionic boundary modes that can be probed by conductance measurements. We hope our results will inspire the realization of artificial and possibly topological materials on Andreev bound state quantum simulators.

Published
2024

2. Rare variants in IFFO1, DTNB, NLRC3 and SLC22A10 associate with Alzheimer’s disease CSF profile of neuronal injury and inflammation

Author

Neumann, Alexander, Küçükali, Fahri, Bos, Isabelle, Vos, Stephanie J. B., Engelborghs, Sebastiaan, De Pooter, Tim, Joris, Geert, De Rijk, Peter, De Roeck, Ellen, Tsolaki, Magda, Verhey, Frans, Martinez-Lage, Pablo, Tainta, Mikel, Frisoni, Giovanni, Blin, Oliver, Richardson, Jill, Bordet, Régis, Scheltens, Philip, Popp, Julius, Peyratout, Gwendoline, Johannsen, Peter, Frölich, Lutz, Vandenberghe, Rik, Freund-Levi, Yvonne, Streffer, Johannes, Lovestone, Simon, Legido-Quigley, Cristina, ten Kate, Mara, Barkhof, Frederik, Strazisar, Mojca, Zetterberg, Henrik, Bertram, Lars, Visser, Pieter Jelle, van Broeckhoven, Christine, and Sleegers, Kristel

Published
2022
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3. Blood DNA methylomic signatures associated with CSF biomarkers of Alzheimer's disease in the EMIF‐AD study.

Author

Smith, Rebecca G., Pishva, Ehsan, Kouhsar, Morteza, Imm, Jennifer, Dobricic, Valerija, Johannsen, Peter, Wittig, Michael, Franke, Andre, Vandenberghe, Rik, Schaeverbeke, Jolien, Freund‐Levi, Yvonne, Frölich, Lutz, Scheltens, Philip, Teunissen, Charlotte E., Frisoni, Giovanni, Blin, Olivier, Richardson, Jill C., Bordet, Régis, Engelborghs, Sebastiaan, and de Roeck, Ellen

Abstract

INTRODUCTION: We investigated blood DNA methylation patterns associated with 15 well‐established cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD) pathophysiology, neuroinflammation, and neurodegeneration. METHODS: We assessed DNA methylation in 885 blood samples from the European Medical Information Framework for Alzheimer's Disease (EMIF‐AD) study using the EPIC array. RESULTS: We identified Bonferroni‐significant differential methylation associated with CSF YKL‐40 (five loci) and neurofilament light chain (NfL; seven loci) levels, with two of the loci associated with CSF YKL‐40 levels correlating with plasma YKL‐40 levels. A co‐localization analysis showed shared genetic variants underlying YKL‐40 DNA methylation and CSF protein levels, with evidence that DNA methylation mediates the association between genotype and protein levels. Weighted gene correlation network analysis identified two modules of co‐methylated loci correlated with several amyloid measures and enriched in pathways associated with lipoproteins and development. DISCUSSION: We conducted the most comprehensive epigenome‐wide association study (EWAS) of AD‐relevant CSF biomarkers to date. Future work should explore the relationship between YKL‐40 genotype, DNA methylation, and protein levels in the brain. Highlights: Blood DNA methylation was assessed in the EMIF‐AD MBD study.Epigenome‐wide association studies (EWASs) were performed for 15 Alzheimer's disease (AD)–relevant cerebrospinal fluid (CSF) biomarker measures.Five Bonferroni‐significant loci were associated with YKL‐40 levels and seven with neurofilament light chain (NfL).DNA methylation in YKL‐40 co‐localized with previously reported genetic variation.DNA methylation potentially mediates the effect of single‐nucleotide polymorphisms (SNPs) in YKL‐40 on CSF protein levels. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Potential genetic modifiers of disease risk and age at onset in patients with frontotemporal lobar degeneration and GRN mutations: a genome-wide association study

Author

Pottier, Cyril, Zhou, Xiaolai, Perkerson, Ralph B, Baker, Matt, Jenkins, Gregory D, Serie, Daniel J, Ghidoni, Roberta, Benussi, Luisa, Binetti, Giuliano, de Munain, Adolfo López, Zulaica, Miren, Moreno, Fermin, Le Ber, Isabelle, Pasquier, Florence, Hannequin, Didier, Sánchez-Valle, Raquel, Antonell, Anna, Lladó, Albert, Parsons, Tammee M, Finch, NiCole A, Finger, Elizabeth C, Lippa, Carol F, Huey, Edward D, Neumann, Manuela, Heutink, Peter, Synofzik, Matthis, Wilke, Carlo, Rissman, Robert A, Slawek, Jaroslaw, Sitek, Emilia, Johannsen, Peter, Nielsen, Jørgen E, Ren, Yingxue, van Blitterswijk, Marka, DeJesus-Hernandez, Mariely, Christopher, Elizabeth, Murray, Melissa E, Bieniek, Kevin F, Evers, Bret M, Ferrari, Camilla, Rollinson, Sara, Richardson, Anna, Scarpini, Elio, Fumagalli, Giorgio G, Padovani, Alessandro, Hardy, John, Momeni, Parastoo, Ferrari, Raffaele, Frangipane, Francesca, Maletta, Raffaele, Anfossi, Maria, Gallo, Maura, Petrucelli, Leonard, Suh, EunRan, Lopez, Oscar L, Wong, Tsz H, van Rooij, Jeroen GJ, Seelaar, Harro, Mead, Simon, Caselli, Richard J, Reiman, Eric M, Sabbagh, Marwan Noel, Kjolby, Mads, Nykjaer, Anders, Karydas, Anna M, Boxer, Adam L, Grinberg, Lea T, Grafman, Jordan, Spina, Salvatore, Oblak, Adrian, Mesulam, M-Marsel, Weintraub, Sandra, Geula, Changiz, Hodges, John R, Piguet, Olivier, Brooks, William S, Irwin, David J, Trojanowski, John Q, Lee, Edward B, Josephs, Keith A, Parisi, Joseph E, Ertekin-Taner, Nilüfer, Knopman, David S, Nacmias, Benedetta, Piaceri, Irene, Bagnoli, Silvia, Sorbi, Sandro, Gearing, Marla, Glass, Jonathan, Beach, Thomas G, Black, Sandra E, Masellis, Mario, Rogaeva, Ekaterina, Vonsattel, Jean-Paul, Honig, Lawrence S, Kofler, Julia, Bruni, Amalia C, Snowden, Julie, Mann, David, and Pickering-Brown, Stuart

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Frontotemporal Dementia (FTD), Neurodegenerative, Dementia, Genetics, Aging, Prevention, Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Human Genome, Alzheimer's Disease Related Dementias (ADRD), Acquired Cognitive Impairment, 2.1 Biological and endogenous factors, Aetiology, Neurological, Age of Onset, Aged, Case-Control Studies, Cerebellum, Female, Frontotemporal Lobar Degeneration, Genetic Predisposition to Disease, Genome-Wide Association Study, Glial Cell Line-Derived Neurotrophic Factor Receptors, Humans, Male, Middle Aged, Mutation, Progranulins, RNA, Messenger, Neurology & Neurosurgery, Clinical sciences
Abstract

BackgroundLoss-of-function mutations in GRN cause frontotemporal lobar degeneration (FTLD). Patients with GRN mutations present with a uniform subtype of TAR DNA-binding protein 43 (TDP-43) pathology at autopsy (FTLD-TDP type A); however, age at onset and clinical presentation are variable, even within families. We aimed to identify potential genetic modifiers of disease onset and disease risk in GRN mutation carriers.MethodsThe study was done in three stages: a discovery stage, a replication stage, and a meta-analysis of the discovery and replication data. In the discovery stage, genome-wide logistic and linear regression analyses were done to test the association of genetic variants with disease risk (case or control status) and age at onset in patients with a GRN mutation and controls free of neurodegenerative disorders. Suggestive loci (p

Published
2018

5. Association of Cerebral Amyloid-β Aggregation With Cognitive Functioning in Persons Without Dementia

Author

Jansen, Willemijn J, Ossenkoppele, Rik, Tijms, Betty M, Fagan, Anne M, Hansson, Oskar, Klunk, William E, van der Flier, Wiesje M, Villemagne, Victor L, Frisoni, Giovanni B, Fleisher, Adam S, Lleó, Alberto, Mintun, Mark A, Wallin, Anders, Engelborghs, Sebastiaan, Na, Duk L, Chételat, Gäel, Molinuevo, José Luis, Landau, Susan M, Mattsson, Niklas, Kornhuber, Johannes, Sabri, Osama, Rowe, Christopher C, Parnetti, Lucilla, Popp, Julius, Fladby, Tormod, Jagust, William J, Aalten, Pauline, Lee, Dong Young, Vandenberghe, Rik, de Oliveira, Catarina Resende, Kapaki, Elisabeth, Froelich, Lutz, Ivanoiu, Adrian, Gabryelewicz, Tomasz, Verbeek, Marcel M, Sanchez-Juan, Páscual, Hildebrandt, Helmut, Camus, Vincent, Zboch, Marzena, Brooks, David J, Drzezga, Alexander, Rinne, Juha O, Newberg, Andrew, de Mendonça, Alexandre, Sarazin, Marie, Rabinovici, Gil D, Madsen, Karine, Kramberger, Milica G, Nordberg, Agneta, Mok, Vincent, Mroczko, Barbara, Wolk, David A, Meyer, Philipp T, Tsolaki, Magda, Scheltens, Philip, Verhey, Frans RJ, Visser, Pieter Jelle, Aarsland, Dag, Alcolea, Daniel, Alexander, Myriam, Almdahl, Ina S, Arnold, Steven E, Baldeiras, Inês, Barthel, Henryk, van Berckel, Bart NM, Blennow, Kaj, van Buchem, Mark A, Cavedo, Enrica, Chen, Kewei, Chipi, Elena, Cohen, Ann D, Förster, Stefan, Fortea, Juan, Frederiksen, Kristian S, Freund-Levi, Yvonne, Gkatzima, Olymbia, Gordon, Mark Forrest, Grimmer, Timo, Hampel, Harald, Hausner, Lucrezia, Hellwig, Sabine, Herukka, Sanna-Kaisa, Johannsen, Peter, Klimkowicz-Mrowiec, Aleksandra, Köhler, Sebastian, Koglin, Norman, van Laere, Koen, de Leon, Mony, Lisetti, Viviana, Maier, Wolfgang, Marcusson, Jan, Meulenbroek, Olga, Møllergård, Hanne M, Morris, John C, Nordlund, Arto, Novak, Gerald P, Paraskevas, George P, Perera, Gayan, Peters, Oliver, and Ramakers, Inez HGB

Subjects
Health Services and Systems, Health Sciences, Acquired Cognitive Impairment, Alzheimer's Disease Related Dementias (ADRD), Neurosciences, Aging, Dementia, Brain Disorders, Behavioral and Social Science, Neurodegenerative, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Neurological, Mental health, Aged, Alzheimer Disease, Amyloid beta-Peptides, Brain, Cognition Disorders, Cognitive Dysfunction, Cross-Sectional Studies, Female, Humans, Male, Memory, Episodic, Mental Status and Dementia Tests, Middle Aged, Positron-Emission Tomography, Reference Values, Amyloid Biomarker Study Group, Other Medical and Health Sciences, Psychology, Cognitive Sciences, Clinical sciences, Clinical and health psychology
Abstract

ImportanceCerebral amyloid-β aggregation is an early event in Alzheimer disease (AD). Understanding the association between amyloid aggregation and cognitive manifestation in persons without dementia is important for a better understanding of the course of AD and for the design of prevention trials.ObjectiveTo investigate whether amyloid-β aggregation is associated with cognitive functioning in persons without dementia.Design, setting, and participantsThis cross-sectional study included 2908 participants with normal cognition and 4133 with mild cognitive impairment (MCI) from 53 studies in the multicenter Amyloid Biomarker Study. Normal cognition was defined as having no cognitive concerns for which medical help was sought and scores within the normal range on cognitive tests. Mild cognitive impairment was diagnosed according to published criteria. Study inclusion began in 2013 and is ongoing. Data analysis was performed in January 2017.Main outcomes and measuresGlobal cognitive performance as assessed by the Mini-Mental State Examination (MMSE) and episodic memory performance as assessed by a verbal word learning test. Amyloid aggregation was measured with positron emission tomography or cerebrospinal fluid biomarkers and dichotomized as negative (normal) or positive (abnormal) according to study-specific cutoffs. Generalized estimating equations were used to examine the association between amyloid aggregation and low cognitive scores (MMSE score ≤27 or memory z score≤-1.28) and to assess whether this association was moderated by age, sex, educational level, or apolipoprotein E genotype.ResultsAmong 2908 persons with normal cognition (mean [SD] age, 67.4 [12.8] years), amyloid positivity was associated with low memory scores after age 70 years (mean difference in amyloid positive vs negative, 4% [95% CI, 0%-7%] at 72 years and 21% [95% CI, 10%-33%] at 90 years) but was not associated with low MMSE scores (mean difference, 3% [95% CI, -1% to 6%], P = .16). Among 4133 patients with MCI (mean [SD] age, 70.2 [8.5] years), amyloid positivity was associated with low memory (mean difference, 16% [95% CI, 12%-20%], P

Published
2018

6. Baseline Characteristics from Evoke and Evoke+: Two Phase 3 Randomized Placebo-controlled Trials of Oral Semaglutide in Patients with Early Alzheimer’s Disease (P11-9.013)

Author

Scheltens, Philip, primary, Atri, Alireza, additional, Feldman, Howard, additional, Hansson, Oskar, additional, Knop, Filip, additional, Sano, Mary, additional, Dethlefsen, Claus, additional, Johannsen, Peter, additional, León, Teresa, additional, Hansen, Charlotte Thim, additional, and Cummings, Jeffrey, additional

Published
2024
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7. Prevalence of Cerebral Amyloid Pathology in Persons Without Dementia: A Meta-analysis

Author

Jansen, Willemijn J, Ossenkoppele, Rik, Knol, Dirk L, Tijms, Betty M, Scheltens, Philip, Verhey, Frans RJ, Visser, Pieter Jelle, Aalten, Pauline, Aarsland, Dag, Alcolea, Daniel, Alexander, Myriam, Almdahl, Ina S, Arnold, Steven E, Baldeiras, Inês, Barthel, Henryk, van Berckel, Bart NM, Bibeau, Kristen, Blennow, Kaj, Brooks, David J, van Buchem, Mark A, Camus, Vincent, Cavedo, Enrica, Chen, Kewei, Chetelat, Gael, Cohen, Ann D, Drzezga, Alexander, Engelborghs, Sebastiaan, Fagan, Anne M, Fladby, Tormod, Fleisher, Adam S, van der Flier, Wiesje M, Ford, Lisa, Förster, Stefan, Fortea, Juan, Foskett, Nadia, Frederiksen, Kristian S, Freund-Levi, Yvonne, Frisoni, Giovanni B, Froelich, Lutz, Gabryelewicz, Tomasz, Gill, Kiran Dip, Gkatzima, Olymbia, Gómez-Tortosa, Estrella, Gordon, Mark Forrest, Grimmer, Timo, Hampel, Harald, Hausner, Lucrezia, Hellwig, Sabine, Herukka, Sanna-Kaisa, Hildebrandt, Helmut, Ishihara, Lianna, Ivanoiu, Adrian, Jagust, William J, Johannsen, Peter, Kandimalla, Ramesh, Kapaki, Elisabeth, Klimkowicz-Mrowiec, Aleksandra, Klunk, William E, Köhler, Sebastian, Koglin, Norman, Kornhuber, Johannes, Kramberger, Milica G, Van Laere, Koen, Landau, Susan M, Lee, Dong Young, de Leon, Mony, Lisetti, Viviana, Lleó, Alberto, Madsen, Karine, Maier, Wolfgang, Marcusson, Jan, Mattsson, Niklas, de Mendonça, Alexandre, Meulenbroek, Olga, Meyer, Philipp T, Mintun, Mark A, Mok, Vincent, Molinuevo, José Luis, Møllergård, Hanne M, Morris, John C, Mroczko, Barbara, Van der Mussele, Stefan, Na, Duk L, Newberg, Andrew, Nordberg, Agneta, Nordlund, Arto, Novak, Gerald P, Paraskevas, George P, Parnetti, Lucilla, Perera, Gayan, Peters, Oliver, Popp, Julius, Prabhakar, Sudesh, Rabinovici, Gil D, Ramakers, Inez HGB, Rami, Lorena, de Oliveira, Catarina Resende, Rinne, Juha O, Rodrigue, Karen M, and Rodríguez-Rodríguez, Eloy

Subjects
Health Services and Systems, Health Sciences, Clinical Research, Alzheimer's Disease, Vascular Cognitive Impairment/Dementia, Acquired Cognitive Impairment, Neurosciences, Alzheimer's Disease Related Dementias (ADRD), Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Cerebrovascular, Neurodegenerative, Prevention, Dementia, Aging, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Aetiology, 2.1 Biological and endogenous factors, Neurological, Adult, Age Factors, Aged, Aged, 80 and over, Amyloid beta-Peptides, Apolipoprotein E4, Biomarkers, Brain, Cerebrospinal Fluid, Cognitive Dysfunction, Female, Genotype, Humans, Male, Middle Aged, Positron-Emission Tomography, Prevalence, Risk Factors, Amyloid Biomarker Study Group, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

ImportanceCerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies.ObjectiveTo use individual participant data meta-analysis to estimate the prevalence of amyloid pathology as measured with biomarkers in participants with normal cognition, subjective cognitive impairment (SCI), or mild cognitive impairment (MCI).Data sourcesRelevant biomarker studies identified by searching studies published before April 2015 using the MEDLINE and Web of Science databases and through personal communication with investigators.Study selectionStudies were included if they provided individual participant data for participants without dementia and used an a priori defined cutoff for amyloid positivity.Data extraction and synthesisIndividual records were provided for 2914 participants with normal cognition, 697 with SCI, and 3972 with MCI aged 18 to 100 years from 55 studies.Main outcomes and measuresPrevalence of amyloid pathology on positron emission tomography or in cerebrospinal fluid according to AD risk factors (age, apolipoprotein E [APOE] genotype, sex, and education) estimated by generalized estimating equations.ResultsThe prevalence of amyloid pathology increased from age 50 to 90 years from 10% (95% CI, 8%-13%) to 44% (95% CI, 37%-51%) among participants with normal cognition; from 12% (95% CI, 8%-18%) to 43% (95% CI, 32%-55%) among patients with SCI; and from 27% (95% CI, 23%-32%) to 71% (95% CI, 66%-76%) among patients with MCI. APOE-ε4 carriers had 2 to 3 times higher prevalence estimates than noncarriers. The age at which 15% of the participants with normal cognition were amyloid positive was approximately 40 years for APOE ε4ε4 carriers, 50 years for ε2ε4 carriers, 55 years for ε3ε4 carriers, 65 years for ε3ε3 carriers, and 95 years for ε2ε3 carriers. Amyloid positivity was more common in highly educated participants but not associated with sex or biomarker modality.Conclusions and relevanceAmong persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. These findings suggest a 20- to 30-year interval between first development of amyloid positivity and onset of dementia.

Published
2015

8. Discovery and validation of plasma proteomic biomarkers relating to brain amyloid burden by SOMAscan assay

Author

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

Published
2019
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10. Inflammatory biomarkers in Alzheimer's disease plasma

Author

Bullmore, Edward T., Bhatti, Junaid, Chamberlain, Samuel J., Correia, Marta M., Crofts, Anna L., Dickinson, Amber, Foster, Andrew C., Kitzbichler, Manfred G., Knight, Clare, Lynall, Mary-Ellen, Maurice, Christina, O'Donnell, Ciara, Pointon, Linda J., St George Hyslop, Peter, Turner, Lorinda, Vertes, Petra, Widmer, Barry, Williams, Guy B., Morgan, B. Paul, Leckey, Claire A., Morgan, Angharad R., O'Hagan, Caroline, Touchard, Samuel, Cavanagh, Jonathan, Deith, Catherine, Farmer, Scott, McClean, John, McColl, Alison, McPherson, Andrew, Scouller, Paul, Sutherland, Murray, Boddeke, H.W.G.M., Richardson, Jill C., Khan, Shahid, Murphy, Phil, Parker, Christine A., Patel, Jai, Jones, Declan, de Boer, Peter, Kemp, John, Drevets, Wayne C., Nye, Jeffrey S., Wittenberg, Gayle, Isaac, John, Bhattacharya, Anindya, Carruthers, Nick, Kolb, Hartmuth, Pariante, Carmine M., Turkheimer, Federico, Barker, Gareth J., Byrom, Heidi, Cash, Diana, Cattaneo, Annamaria, Gee, Antony, Hastings, Caitlin, Mariani, Nicole, McLaughlin, Anna, Mondelli, Valeria, Nettis, Maria, Nikkheslat, Naghmeh, Randall, Karen, Sheridan, Hannah, Simmons, Camilla, Singh, Nisha, Van Loo, Victoria, Vicente-Rodriguez, Marta, Wood, Tobias C., Worrell, Courtney, Zajkowska, Zuzanna, Plath, Niels, Egebjerg, Jan, Eriksson, Hans, Gastambide, Francois, Adams, Karen Husted, Jeggo, Ross, Thomsen, Christian, Pederson, Jan Torleif, Campbell, Brian, Möller, Thomas, Nelson, Bob, Zorn, Stevin, O'Connor, Jason, Attenburrow, Mary Jane, Baird, Alison, Benjamin, Jithen, Clare, Stuart, Cowen, Philip, Huang, I-Shu (Dante), Hurley, Samuel, Jones, Helen, Lovestone, Simon, Mada, Francisca, Nevado-Holgado, Alejo, Oladejo, Akintayo, Ribe, Elena, Smith, Katy, Vyas, Anviti, Hughes, Zoe, Balice-Gordon, Rita, Duerr, James, Piro, Justin R., Sporn, Jonathan, Perry, V. Hugh, Cleal, Madeleine, Fryatt, Gemma, Gomez-Nicola, Diego, Mancuso, Renzo, Reynolds, Richard, Harrison, Neil A., Cercignani, Mara, Clarke, Charlotte L., Hoskins, Elizabeth, Kohn, Charmaine, Murray, Rosemary, Wilcock, Lauren, Wlazly, Dominika, Mount, Howard, Leckey, Claire, Nevado-Holgado, Alejo J., Barkhof, Frederik, Bertram, Lars, Blin, Olivier, Bos, Isabelle, Dobricic, Valerija, Engelborghs, Sebastiaan, Frisoni, Giovanni, Frölich, Lutz, Gabel, Silvey, Johannsen, Peter, Kettunen, Petronella, Kłoszewska, Iwona, Legido-Quigley, Cristina, Lleó, Alberto, Martinez-Lage, Pablo, Mecocci, Patrizia, Meersmans, Karen, Molinuevo, José Luis, Peyratout, Gwendoline, Popp, Julius, Richardson, Jill, Sala, Isabel, Scheltens, Philip, Streffer, Johannes, Soininen, Hikka, Tainta-Cuezva, Mikel, Teunissen, Charlotte, Tsolaki, Magda, Vandenberghe, Rik, Visser, Pieter Jelle, Vos, Stephanie, Wahlund, Lars-Olof, Wallin, Anders, Westwood, Sarah, and Zetterberg, Henrik

Published
2019
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11. 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

Kim, Min, Snowden, Stuart, Suvitaival, Tommi, Ali, Ashfaq, Merkler, David J., Ahmad, Tahmina, Westwood, Sarah, Baird, Alison, Proitsi, Petroula, Nevado-Holgado, Alejo, Hye, Abdul, Bos, Isabelle, Vos, Stephanie, Vandenberghe, Rik, Teunissen, Charlotte, ten Kate, Mara, Scheltens, Philip, Gabel, Silvy, Meersmans, Karen, Blin, Olivier, Richardson, Jill, De Roeck, Ellen, Sleegers, Kristel, Bordet, Régis, Rami, Lorena, Kettunen, Petronella, Tsolaki, Magda, Verhey, Frans, Sala, Isabel, Lléo, Alberto, Peyratout, Gwendoline, Tainta, Mikel, Johannsen, Peter, Freund-Levi, Yvonne, Frölich, Lutz, Dobricic, Valerija, Engelborghs, Sebastiaan, Frisoni, Giovanni B., Molinuevo, José L., Wallin, Anders, Popp, Julius, Martinez-Lage, Pablo, Bertram, Lars, Barkhof, Frederik, Ashton, Nicholas, Blennow, Kaj, Zetterberg, Henrik, Streffer, Johannes, Visser, Pieter J., Lovestone, Simon, and Legido-Quigley, Cristina

Published
2019
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12. Cerebrospinal fluid biomarkers of neurodegeneration, synaptic integrity, and astroglial activation across the clinical Alzheimer's disease spectrum

Author

Bos, Isabelle, Vos, Stephanie, Verhey, Frans, Scheltens, Philip, Teunissen, Charlotte, Engelborghs, Sebastiaan, Sleegers, Kristel, Frisoni, Giovanni, Blin, Olivier, Richardson, Jill C., Bordet, Régis, Tsolaki, Magda, Popp, Julius, Peyratout, Gwendoline, Martinez-Lage, Pablo, Tainta, Mikel, Lleó, Alberto, Johannsen, Peter, Freund-Levi, Yvonne, Frölich, Lutz, Vandenberghe, Rik, Westwood, Sarah, Dobricic, Valerija, Barkhof, Frederik, Legido-Quigley, Cristina, Bertram, Lars, Lovestone, Simon, Streffer, Johannes, Andreasson, Ulf, Blennow, Kaj, Zetterberg, Henrik, and Visser, Pieter Jelle

Published
2019
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13. Therapeutic drug monitoring for dose optimization in Alzheimer's disease and in dementia with Lewy bodies: A randomized single-blinded clinical trial

Author

Fischer, Michael Hén Forbord, Zibrandtsen, Ivan Chrilles, Johannsen, Peter, Siersma, Volkert, Rasmussen, Jan Borg, Larsen, Jens Borggaard, and Høgh, Peter

Abstract

Background Previous evidence suggests serum concentrations of donepezil varies in clinical populations and that a dose higher than standard may have additional positive effect on cognition. Therapeutic drug monitoring (TDM) is a tool for dose optimization (DO) whereby treatment is adjusted based on previous quantification of the prescribed drug.Objective Investigate whether TDM-based DO of donepezil or memantine improves clinical outcomes and/or reduce the frequency of adverse reactions (ARs) in neurodegenerative conditions commonly treated with these two study drugs.Methods Single-blinded 1:1 randomized controlled study in an outpatient memory clinic. Eligible participants either newly diagnosed with Alzheimer's disease dementia (AD), dementia with Lewy bodies (DLB), or Parkinson's disease dementia (PDD) scheduled for treatment with donepezil or memantine. The intervention group received TDM based DO. The control group received DO solely based on clinical assessment. Clinical outcomes were change in Mini-Mental State Examination, Addenbrooke's Cognitive Examination, Neuropsychiatric Inventory, and Disability Assessment in Dementia from baseline to 12 months. Additionally, data on incidence and severity of ARs and proportion of participants with a serum concentration within the therapeutic reference range were collected.Results 132 participants recruited (125 AD, 7 DLB, none with PDD) of whom 107 completed the study (101 AD and 6 DLB), fewer in the control group than planned. Statistical analysis did not reveal significant differences between groups neither for clinical outcomes nor for frequency of ARs.Conclusions TDM based DO did not significantly improve clinical outcomes nor reduce the frequency of ARs albeit important caveats to the results apply.ClincialTrials.gov identifier NCT04117178 (first posted October 7, 2019).

Published
2024
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14. Blood DNA methylomic signatures associated with CSF biomarkers of Alzheimer’s disease in the EMIF‐AD Multimodal Biomarker Discovery study

Author

Smith, Rebecca G., primary, Imm, Jennifer L, additional, Dobricic, Valerija, additional, Sommerer, Yasmine, additional, Bos, Isabelle, additional, Vos, Stephanie J. B., additional, Verhey, Frans R.J., additional, Scheltens, Philip, additional, Engelborgs, Sebastiaan, additional, Frisoni, Giovanni B, additional, Blin, Olivier, additional, Richardson, Jill C, additional, Bordet, Régis, additional, Tsolaki, Magda, additional, Popp, Julius, additional, Martinez‐Lage, Pablo, additional, Lleo, Alberto, additional, Johannsen, Peter, additional, Freund‐Levi, Yvonne, additional, Lutz, Frölich, additional, Vandenberghe, Rik, additional, Wittig, Michael, additional, Frank, Andre, additional, Lovestone, Simon, additional, Streffer, Johannes, additional, Andreasson, Ulf, additional, Blennow, Kaj, additional, Visser, Pieter Jelle, additional, Zetterberg, Henrik, additional, Bertram, Lars, additional, and Lunnon, Katie, additional

Published
2023
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16. Prevalence of the apolipoprotein E ε4 allele in amyloid β positive subjects across the spectrum of Alzheimer's disease

Author

Mattsson, Niklas, Groot, Colin, Jansen, Willemijn J., Landau, Susan M., Villemagne, Victor L., Engelborghs, Sebastiaan, Mintun, Mark M., Lleo, Alberto, Molinuevo, José Luis, Jagust, William J., Frisoni, Giovanni B., Ivanoiu, Adrian, Chételat, Gaël, Resende de Oliveira, Catarina, Rodrigue, Karen M., Kornhuber, Johannes, Wallin, Anders, Klimkowicz-Mrowiec, Aleksandra, Kandimalla, Ramesh, Popp, Julius, Aalten, Pauline P., Aarsland, Dag, Alcolea, Daniel, Almdahl, Ina S., Baldeiras, Inês, van Buchem, Mark A., Cavedo, Enrica, Chen, Kewei, Cohen, Ann D., Förster, Stefan, Fortea, Juan, Frederiksen, Kristian S., Freund-Levi, Yvonne, Gill, Kiran Dip, Gkatzima, Olymbia, Grimmer, Timo, Hampel, Harald, Herukka, Sanna-Kaisa, Johannsen, Peter, van Laere, Koen, de Leon, Mony J., Maier, Wolfgang, Marcusson, Jan, Meulenbroek, Olga, Møllergård, Hanne M., Morris, John C., Mroczko, Barbara, Nordlund, Arto, Prabhakar, Sudesh, Peters, Oliver, Rami, Lorena, Rodríguez-Rodríguez, Eloy, Roe, Catherine M., Rüther, Eckart, Santana, Isabel, Schröder, Johannes, Seo, Sang W., Soininen, Hilkka, Spiru, Luiza, Stomrud, Erik, Struyfs, Hanne, Teunissen, Charlotte E., Verhey, Frans R.J., Vos, Stephanie J.B., van Waalwijk van Doorn, Linda J.C., Waldemar, Gunhild, Wallin, Åsa K., Wiltfang, Jens, Vandenberghe, Rik, Brooks, David J., Fladby, Tormod, Rowe, Christopher C., Drzezga, Alexander, Verbeek, Marcel M., Sarazin, Marie, Wolk, David A., Fleisher, Adam S., Klunk, William E., Na, Duk L., Sánchez-Juan, Pascual, Lee, Dong Young, Nordberg, Agneta, Tsolaki, Magda, Camus, Vincent, Rinne, Juha O., Fagan, Anne M., Zetterberg, Henrik, Blennow, Kaj, Rabinovici, Gil D., Hansson, Oskar, van Berckel, Bart N.M., van der Flier, Wiesje M., Scheltens, Philip, Visser, Pieter Jelle, and Ossenkoppele, Rik

Published
2018
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17. FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration.

Author

Urwin, Hazel, Josephs, Keith A, Rohrer, Jonathan D, Mackenzie, Ian R, Neumann, Manuela, Authier, Astrid, Seelaar, Harro, Van Swieten, John C, Brown, Jeremy M, Johannsen, Peter, Nielsen, Jorgen E, Holm, Ida E, FReJA Consortium, Dickson, Dennis W, Rademakers, Rosa, Graff-Radford, Neill R, Parisi, Joseph E, Petersen, Ronald C, Hatanpaa, Kimmo J, White, Charles L, Weiner, Myron F, Geser, Felix, Van Deerlin, Vivianna M, Trojanowski, John Q, Miller, Bruce L, Seeley, William W, van der Zee, Julie, Kumar-Singh, Samir, Engelborghs, Sebastiaan, De Deyn, Peter P, Van Broeckhoven, Christine, Bigio, Eileen H, Deng, Han-Xiang, Halliday, Glenda M, Kril, Jillian J, Munoz, David G, Mann, David M, Pickering-Brown, Stuart M, Doodeman, Valerie, Adamson, Gary, Ghazi-Noori, Shabnam, Fisher, Elizabeth MC, Holton, Janice L, Revesz, Tamas, Rossor, Martin N, Collinge, John, Mead, Simon, and Isaacs, Adrian M

Subjects
FReJA Consortium, Hippocampus, Frontal Lobe, Humans, Dyskinesias, RNA-Binding Protein FUS, tau Proteins, DNA-Binding Proteins, Prevalence, Sequence Analysis, DNA, Mental Disorders, Age of Onset, Mutation, Adult, Middle Aged, Female, Male, Frontotemporal Lobar Degeneration, Sequence Analysis, DNA, Clinical Sciences, Neurosciences, Neurology & Neurosurgery
Abstract

Through an international consortium, we have collected 37 tau- and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, and present here the first comprehensive analysis of these cases in terms of neuropathology, genetics, demographics and clinical data. 92% (34/37) had fused in sarcoma (FUS) protein pathology, indicating that FTLD-FUS is an important FTLD subtype. This FTLD-FUS collection specifically focussed on aFTLD-U cases, one of three recently defined subtypes of FTLD-FUS. The aFTLD-U subtype of FTLD-FUS is characterised clinically by behavioural variant frontotemporal dementia (bvFTD) and has a particularly young age of onset with a mean of 41 years. Further, this subtype had a high prevalence of psychotic symptoms (36% of cases) and low prevalence of motor symptoms (3% of cases). We did not find FUS mutations in any aFTLD-U case. To date, the only subtype of cases reported to have ubiquitin-positive but tau-, TDP-43- and FUS-negative pathology, termed FTLD-UPS, is the result of charged multivesicular body protein 2B gene (CHMP2B) mutation. We identified three FTLD-UPS cases, which are negative for CHMP2B mutation, suggesting that the full complement of FTLD pathologies is yet to be elucidated.

Published
2010

18. Blood-based multivariate methylation risk score for cognitive impairment and dementia

Author

Koetsier, Jarno, primary, Cavill, Rachel, additional, Reijnders, Rick A, additional, Harvey, Joshua, additional, Deckers, Kay, additional, Köhler, Sebastian, additional, Eijssen, Lars, additional, Smith, Rebecca G, additional, Smith, Adam R, additional, Burrage, Joe, additional, Walker, Emma M, additional, Shireby, Gemma, additional, Hannon, Eilis, additional, Dempster, Emma, additional, Frayling, Timothy, additional, Mill, Jonathan, additional, Dobricic, Valerija, additional, Sommerer, Yasmine, additional, Johannsen, Peter, additional, Wittig, Michael, additional, Franke, Andre, additional, Vandenberghe, Rick, additional, Schaeverbeke, Jolien, additional, Freund-Levi, Yvonne, additional, Frölich, Lutz, additional, Scheltens, Philip, additional, Teunissen, Charlotte, additional, Frisoni, Giovanni, additional, Blin, Olivier, additional, Richardson, Jill, additional, Bordet, Régis, additional, Engelborghs, Sebastiaan, additional, de Roeck, Ellen, additional, Martinez-Lage, Pablo, additional, Tainta, Mikel, additional, Lleó, Alberto, additional, Sala, Isabel, additional, Popp, Julius, additional, Peyratout, Gwedoline, additional, Verhey, Frans, additional, Tsolaki, Magda, additional, Andreasson, Ulf, additional, Blennow, Kaj, additional, Zetterberg, Henrik, additional, Streffer, Johannes, additional, Vos, Stephanie JB, additional, Lovestone, Simon, additional, Visser, Pieter-Jelle, additional, Bertram, Lars, additional, Lunnon, Katie, additional, and Pishva, Ehsan, additional

Published
2023
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19. The frequency and influence of dementia risk factors in prodromal Alzheimer's disease

Author

Bos, Isabelle, Vos, Stephanie J., Frölich, Lutz, Kornhuber, Johannes, Wiltfang, Jens, Maier, Wolfgang, Peters, Oliver, Rüther, Eckhart, Engelborghs, Sebastiaan, Niemantsverdriet, Ellis, De Roeck, Ellen Elisa, Tsolaki, Magda, Freund-Levi, Yvonne, Johannsen, Peter, Vandenberghe, Rik, Lleó, Alberto, Alcolea, Daniel, Frisoni, Giovanni B., Galluzzi, Samantha, Nobili, Flavio, Morbelli, Silvia, Drzezga, Alexander, Didic, Mira, van Berckel, Bart N., Salmon, Eric, Bastin, Christine, Dauby, Solene, Santana, Isabel, Baldeiras, Inês, de Mendonça, Alexandre, Silva, Dina, Wallin, Anders, Nordlund, Arto, Coloma, Preciosa M., Wientzek, Angelika, Alexander, Myriam, Novak, Gerald P., Gordon, Mark Forrest, Wallin, Åsa K., Hampel, Harald, Soininen, Hilkka, Herukka, Sanna-Kaisa, Scheltens, Philip, Verhey, Frans R., and Visser, Pieter Jelle

Published
2017
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20. Whole-exome rare-variant analysis of Alzheimer's disease and related biomarker traits

Author

Küçükali, Fahri, Neumann, Alexander, Van Dongen, Jasper, De Pooter, Tim, Joris, Geert, De Rijk, Peter, Ohlei, Olena, Dobricic, Valerija, Bos, Isabelle, Vos, Stephanie J.B., Engelborghs, Sebastiaan, De Roeck, Ellen, Vandenberghe, Rik, Gabel, Silvy, Meersmans, Karen, Tsolaki, Magda, Verhey, Frans, Martinez-Lage, Pablo, Tainta, Mikel, Frisoni, Giovanni, Blin, Oliver, Richardson, Jill C., Bordet, Régis, Scheltens, Philip, Popp, Julius, Peyratout, Gwendoline, Johannsen, Peter, Frölich, Lutz, Freund-Levi, Yvonne, Streffer, Johannes, Lovestone, Simon, Legido-Quigley, Cristina, Kate, Mara ten, Barkhof, Frederik, Zetterberg, Henrik, Bertram, Lars, Strazisar, Mojca, Visser, Pieter Jelle, Van Broeckhoven, Christine, Sleegers, Kristel, Küçükali, Fahri, Neumann, Alexander, Van Dongen, Jasper, De Pooter, Tim, Joris, Geert, De Rijk, Peter, Ohlei, Olena, Dobricic, Valerija, Bos, Isabelle, Vos, Stephanie J.B., Engelborghs, Sebastiaan, De Roeck, Ellen, Vandenberghe, Rik, Gabel, Silvy, Meersmans, Karen, Tsolaki, Magda, Verhey, Frans, Martinez-Lage, Pablo, Tainta, Mikel, Frisoni, Giovanni, Blin, Oliver, Richardson, Jill C., Bordet, Régis, Scheltens, Philip, Popp, Julius, Peyratout, Gwendoline, Johannsen, Peter, Frölich, Lutz, Freund-Levi, Yvonne, Streffer, Johannes, Lovestone, Simon, Legido-Quigley, Cristina, Kate, Mara ten, Barkhof, Frederik, Zetterberg, Henrik, Bertram, Lars, Strazisar, Mojca, Visser, Pieter Jelle, Van Broeckhoven, Christine, and Sleegers, Kristel

Abstract

Introduction: Despite increasing evidence of a role of rare genetic variation in the risk of Alzheimer's disease (AD), limited attention has been paid to its contribution to AD-related biomarker traits indicative of AD-relevant pathophysiological processes. Methods: We performed whole-exome gene-based rare-variant association studies (RVASs) of 17 AD-related traits on whole-exome sequencing (WES) data generated in the European Medical Information Framework for Alzheimer's Disease Multimodal Biomarker Discovery (EMIF-AD MBD) study (n = 450) and whole-genome sequencing (WGS) data from ADNI (n = 808). Results: Mutation screening revealed a novel probably pathogenic mutation (PSEN1 p.Leu232Phe). Gene-based RVAS revealed the exome-wide significant contribution of rare coding variation in RBKS and OR7A10 to cognitive performance and protection against left hippocampal atrophy, respectively. Discussion: The identification of these novel gene–trait associations offers new perspectives into the role of rare coding variation in the distinct pathophysiological processes culminating in AD, which may lead to identification of novel therapeutic and diagnostic targets.

Published
2023

21. Effect of aerobic exercise on physical performance in patients with Alzheimer's disease

Author

Sobol, Nanna Aue, Hoffmann, Kristine, Frederiksen, Kristian Steen, Vogel, Asmus, Vestergaard, Karsten, Brændgaard, Hans, Gottrup, Hanne, Lolk, Annette, Wermuth, Lene, Jakobsen, Søren, Laugesen, Lars, Gergelyffy, Robert, Høgh, Peter, Bjerregaard, Eva, Siersma, Volkert, Andersen, Birgitte Bo, Johannsen, Peter, Waldemar, Gunhild, Hasselbalch, Steen Gregers, and Beyer, Nina

Published
2016
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22. Whole‐exome rare‐variant analysis of Alzheimer's disease and related biomarker traits

Author

Alzheimer's Disease Neuroimaging Initiative (ADNI), Küçükali, Fahri, Neumann, Alexander, Van Dongen, Jasper, De Pooter, Tim, Joris, Geert, De Rijk, Peter, Ohlei, Olena, Dobricic, Valerija, Bos, Isabelle, Vos, Stephanie J B, Engelborghs, Sebastiaan, De Roeck, Ellen, Vandenberghe, Rik, Gabel, Silvy, Meersmans, Karen, Tsolaki, Magda, Verhey, Frans, Martinez-Lage, Pablo, Tainta, Mikel, Frisoni, Giovanni, Blin, Oliver, Richardson, Jill C, Bordet, Régis, Scheltens, Philip, Popp, Julius, Peyratout, Gwendoline, Johannsen, Peter, Frölich, Lutz, Freund-Levi, Yvonne, Streffer, Johannes, Lovestone, Simon, Legido-Quigley, Cristina, Kate, Mara Ten, Barkhof, Frederik, Zetterberg, Henrik, Bertram, Lars, Strazisar, Mojca, Visser, Pieter Jelle, Van Broeckhoven, Christine, Sleegers, Kristel, Alzheimer’s Disease Neuroimaging Initiative (ADNI), EMIF-ADStudyGroup, Epidemiology, Psychiatrie & Neuropsychologie, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, Clinical sciences, Neuroprotection & Neuromodulation, Neurology, Amsterdam Neuroscience - Neurodegeneration, Radiology and nuclear medicine, Amsterdam Neuroscience - Brain Imaging, and Amsterdam Neuroscience - Neuroinfection & -inflammation

Subjects
D-RIBOSE, Epidemiology, Endophenotypes, Neuroscience(all), Clinical Neurology, ABCA7, Cellular and Molecular Neuroscience, Developmental Neuroscience, SDG 3 - Good Health and Well-being, GWAS, whole-exome sequencing, GENOME-WIDE ASSOCIATION, METAANALYSIS, Science & Technology, ENDOPHENOTYPES, MUTATIONS, Health Policy, neurology, biomarkers, rare coding variants, Alzheimer's disease, FRAMEWORK, Psychiatry and Mental health, Whole-exome sequencing, COGNITIVE DECLINE, Neurology (clinical), Neurosciences & Neurology, Human medicine, Geriatrics and Gerontology, Life Sciences & Biomedicine
Abstract

INTRODUCTION: Despite increasing evidence of a role of rare genetic variation in the risk of Alzheimer's disease (AD), limited attention has been paid to its contribution to AD-related biomarker traits indicative of AD-relevant pathophysiological processes. METHODS: We performed whole-exome gene-based rare-variant association studies (RVASs) of 17 AD-related traits on whole-exome sequencing (WES) data generated in the European Medical Information Framework for Alzheimer's Disease Multimodal Biomarker Discovery (EMIF-AD MBD) study (n = 450) and whole-genome sequencing (WGS) data from ADNI (n = 808). RESULTS: Mutation screening revealed a novel probably pathogenic mutation (PSEN1 p.Leu232Phe). Gene-based RVAS revealed the exome-wide significant contribution of rare coding variation in RBKS and OR7A10 to cognitive performance and protection against left hippocampal atrophy, respectively. DISCUSSION: The identification of these novel gene-trait associations offers new perspectives into the role of rare coding variation in the distinct pathophysiological processes culminating in AD, which may lead to identification of novel therapeutic and diagnostic targets. ispartof: ALZHEIMERS & DEMENTIA vol:19 issue:6 ispartof: location:United States status: Published online

Published
2023
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23. evoke and evoke+: design of two large‐scale, double‐blind, placebo‐controlled, phase 3 studies evaluating the neuroprotective effects of semaglutide in early Alzheimer’s disease

Author

Atri, Alireza, primary, Feldman, Howard H., additional, Hansen, Charlotte Thim, additional, Honore, Julie Broe, additional, Johannsen, Peter, additional, Knop, Filip Krag, additional, Poulsen, Pernille, additional, Raket, Lars Lau, additional, Sano, Mary, additional, Soininen, Hilkka, additional, and Cummings, Jeffrey, additional

Published
2022
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24. Investigating changes in fluid biomarkers in early Alzheimer’s disease: design of plasma biomarker analyses and a cerebrospinal fluid sub‐study in the evoke and evoke+ trials of semaglutide versus placebo

Author

Cummings, Jeffrey, primary, Zetterberg, Henrik, additional, Atri, Alireza, additional, Hansen, Charlotte Thim, additional, Honore, Julie Broe, additional, Johannsen, Peter, additional, Knop, Filip Krag, additional, Raket, Lars Lau, additional, Sano, Mary, additional, Soininen, Hilkka, additional, and Feldman, Howard H., additional

Published
2022
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25. Prevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum

Author

Jansen, Willemijn J., Janssen, Olin, Tijms, Betty M., Vos, Stephanie J.B., Ossenkoppele, Rik, Visser, Pieter Jelle, Aarsland, Dag, Alcolea, Daniel, Altomare, Daniele, Von Arnim, Christine, Baiardi, Simone, Baldeiras, Ines, Barthel, Henryk, Bateman, Randall J., Van Berckel, Bart, Binette, Alexa Pichet, Blennow, Kaj, Boada, Merce, Boecker, Henning, Bottlaender, Michel, Den Braber, Anouk, Brooks, David J., Van Buchem, Mark A., Camus, Vincent, Carill, Jose Manuel, Cerman, Jiri, Chen, Kewei, Chételat, Gaël, Chipi, Elena, Cohen, Ann D., Daniels, Alisha, Delarue, Marion, Didic, Mira, Drzezga, Alexander, Dubois, Bruno, Eckerström, Marie, Ekblad, Laura L., Engelborghs, Sebastiaan, Epelbaum, Stéphane, Fagan, Anne M., Fan, Yong, Fladby, Tormod, Fleisher, Adam S., Van Der Flier, Wiesje M., Förster, Stefan, Fortea, Juan, Frederiksen, Kristian Steen, Freund-Levi, Yvonne, Frings, Lars, Frisoni, Giovanni B., Fröhlich, Lutz, Gabryelewicz, Tomasz, Gertz, Hermann Josef, Gill, Kiran Dip, Gkatzima, Olymbia, Gómez-Tortosa, Estrella, Grimmer, Timo, Guedj, Eric, Habeck, Christian G., Hampel, Harald, Handels, Ron, Hansson, Oskar, Hausner, Lucrezia, Hellwig, Sabine, Heneka, Michael T., Herukka, Sanna Kaisa, Hildebrandt, Helmut, Hodges, John, Hort, Jakub, Huang, Chin Chang, Iriondo, Ane Juaristi, Itoh, Yoshiaki, Ivanoiu, Adrian, Jagust, William J., Jessen, Frank, Johannsen, Peter, Johnson, Keith A., Kandimalla, Ramesh, Kapaki, Elisabeth N., Kern, Silke, Kilander, Lena, Klimkowicz-Mrowiec, Aleksandra, Klunk, William E., Koglin, Norman, Kornhuber, Johannes, Kramberger, Milica G., Kuo, Hung Chou, Van Laere, Koen, Landau, Susan M., Landeau, Brigitte, Lee, Dong Young, De Leon, Mony, Leyton, Cristian E., Lin, Kun Ju, Lleó, Alberto, Löwenmark, Malin, Madsen, Karine, Maier, Wolfgang, Marcusson, Jan, Marquié, Marta, Martinez-Lage, Pablo, Maserejian, Nancy, Mattsson, Niklas, De Mendonça, Alexandre, Meyer, Philipp T., Miller, Bruce L., Minatani, Shinobu, Mintun, Mark A., Mok, Vincent C.T., Molinuevo, Jose Luis, Morbelli, Silvia Daniela, Morris, John C., Mroczko, Barbara, Na, Duk L., Newberg, Andrew, Nobili, Flavio, Nordberg, Agneta, Olde Rikkert, Marcel G.M., De Oliveira, Catarina Resende, Olivieri, Pauline, Orellana, Adela, Paraskevas, George, Parchi, Piero, Pardini, Matteo, Parnetti, Lucilla, Peters, Oliver, Poirier, Judes, Popp, Julius, Prabhakar, Sudesh, Rabinovici, Gil D., Ramakers, Inez H., Rami, Lorena, Reiman, Eric M., Rinne, Juha O., Rodrigue, Karen M., Rodríguez-Rodriguez, Eloy, Roe, Catherine M., Rosa-Neto, Pedro, Rosen, Howard J., Rot, Uros, Rowe, Christopher C., Rüther, Eckart, Ruiz, Agustín, Sabri, Osama, Sakhardande, Jayant, Sánchez-Juan, Pascual, Sando, Sigrid Botne, Santana, Isabel, Sarazin, Marie, Scheltens, Philip, Schröder, Johannes, Selnes, Per, Seo, Sang Won, Silva, Dina, Skoog, Ingmar, Snyder, Peter J., Soininen, Hilkka, Sollberger, Marc, Sperling, Reisa A., Spiru, Luisa, Stern, Yaakov, Stomrud, Erik, Takeda, Akitoshi, Teichmann, Marc, Teunissen, Charlotte E., Thompson, Louisa I., Tomassen, Jori, Tsolaki, Magda, Vandenberghe, Rik, Verbeek, Marcel M., Verhey, Frans R.J., Villemagne, Victor, Villeneuve, Sylvia, Vogelgsang, Jonathan, Waldemar, Gunhild, Wallin, Anders, Wallin, Åsa K., Wiltfang, Jens, Wolk, David A., Yen, Tzu Chen, Zboch, Marzena, Zetterberg, Henrik, Jansen, Willemijn J., Janssen, Olin, Tijms, Betty M., Vos, Stephanie J.B., Ossenkoppele, Rik, Visser, Pieter Jelle, Aarsland, Dag, Alcolea, Daniel, Altomare, Daniele, Von Arnim, Christine, Baiardi, Simone, Baldeiras, Ines, Barthel, Henryk, Bateman, Randall J., Van Berckel, Bart, Binette, Alexa Pichet, Blennow, Kaj, Boada, Merce, Boecker, Henning, Bottlaender, Michel, Den Braber, Anouk, Brooks, David J., Van Buchem, Mark A., Camus, Vincent, Carill, Jose Manuel, Cerman, Jiri, Chen, Kewei, Chételat, Gaël, Chipi, Elena, Cohen, Ann D., Daniels, Alisha, Delarue, Marion, Didic, Mira, Drzezga, Alexander, Dubois, Bruno, Eckerström, Marie, Ekblad, Laura L., Engelborghs, Sebastiaan, Epelbaum, Stéphane, Fagan, Anne M., Fan, Yong, Fladby, Tormod, Fleisher, Adam S., Van Der Flier, Wiesje M., Förster, Stefan, Fortea, Juan, Frederiksen, Kristian Steen, Freund-Levi, Yvonne, Frings, Lars, Frisoni, Giovanni B., Fröhlich, Lutz, Gabryelewicz, Tomasz, Gertz, Hermann Josef, Gill, Kiran Dip, Gkatzima, Olymbia, Gómez-Tortosa, Estrella, Grimmer, Timo, Guedj, Eric, Habeck, Christian G., Hampel, Harald, Handels, Ron, Hansson, Oskar, Hausner, Lucrezia, Hellwig, Sabine, Heneka, Michael T., Herukka, Sanna Kaisa, Hildebrandt, Helmut, Hodges, John, Hort, Jakub, Huang, Chin Chang, Iriondo, Ane Juaristi, Itoh, Yoshiaki, Ivanoiu, Adrian, Jagust, William J., Jessen, Frank, Johannsen, Peter, Johnson, Keith A., Kandimalla, Ramesh, Kapaki, Elisabeth N., Kern, Silke, Kilander, Lena, Klimkowicz-Mrowiec, Aleksandra, Klunk, William E., Koglin, Norman, Kornhuber, Johannes, Kramberger, Milica G., Kuo, Hung Chou, Van Laere, Koen, Landau, Susan M., Landeau, Brigitte, Lee, Dong Young, De Leon, Mony, Leyton, Cristian E., Lin, Kun Ju, Lleó, Alberto, Löwenmark, Malin, Madsen, Karine, Maier, Wolfgang, Marcusson, Jan, Marquié, Marta, Martinez-Lage, Pablo, Maserejian, Nancy, Mattsson, Niklas, De Mendonça, Alexandre, Meyer, Philipp T., Miller, Bruce L., Minatani, Shinobu, Mintun, Mark A., Mok, Vincent C.T., Molinuevo, Jose Luis, Morbelli, Silvia Daniela, Morris, John C., Mroczko, Barbara, Na, Duk L., Newberg, Andrew, Nobili, Flavio, Nordberg, Agneta, Olde Rikkert, Marcel G.M., De Oliveira, Catarina Resende, Olivieri, Pauline, Orellana, Adela, Paraskevas, George, Parchi, Piero, Pardini, Matteo, Parnetti, Lucilla, Peters, Oliver, Poirier, Judes, Popp, Julius, Prabhakar, Sudesh, Rabinovici, Gil D., Ramakers, Inez H., Rami, Lorena, Reiman, Eric M., Rinne, Juha O., Rodrigue, Karen M., Rodríguez-Rodriguez, Eloy, Roe, Catherine M., Rosa-Neto, Pedro, Rosen, Howard J., Rot, Uros, Rowe, Christopher C., Rüther, Eckart, Ruiz, Agustín, Sabri, Osama, Sakhardande, Jayant, Sánchez-Juan, Pascual, Sando, Sigrid Botne, Santana, Isabel, Sarazin, Marie, Scheltens, Philip, Schröder, Johannes, Selnes, Per, Seo, Sang Won, Silva, Dina, Skoog, Ingmar, Snyder, Peter J., Soininen, Hilkka, Sollberger, Marc, Sperling, Reisa A., Spiru, Luisa, Stern, Yaakov, Stomrud, Erik, Takeda, Akitoshi, Teichmann, Marc, Teunissen, Charlotte E., Thompson, Louisa I., Tomassen, Jori, Tsolaki, Magda, Vandenberghe, Rik, Verbeek, Marcel M., Verhey, Frans R.J., Villemagne, Victor, Villeneuve, Sylvia, Vogelgsang, Jonathan, Waldemar, Gunhild, Wallin, Anders, Wallin, Åsa K., Wiltfang, Jens, Wolk, David A., Yen, Tzu Chen, Zboch, Marzena, and Zetterberg, Henrik

Abstract

Importance: One characteristic histopathological event in Alzheimer disease (AD) is cerebral amyloid aggregation, which can be detected by biomarkers in cerebrospinal fluid (CSF) and on positron emission tomography (PET) scans. Prevalence estimates of amyloid pathology are important for health care planning and clinical trial design. Objective: To estimate the prevalence of amyloid abnormality in persons with normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia and to examine the potential implications of cutoff methods, biomarker modality (CSF or PET), age, sex, APOE genotype, educational level, geographical region, and dementia severity for these estimates. Design, Setting, and Participants: This cross-sectional, individual-participant pooled study included participants from 85 Amyloid Biomarker Study cohorts. Data collection was performed from January 1, 2013, to December 31, 2020. Participants had normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia. Normal cognition and subjective cognitive decline were defined by normal scores on cognitive tests, with the presence of cognitive complaints defining subjective cognitive decline. Mild cognitive impairment and clinical AD dementia were diagnosed according to published criteria. Exposures: Alzheimer disease biomarkers detected on PET or in CSF. Main Outcomes and Measures: Amyloid measurements were dichotomized as normal or abnormal using cohort-provided cutoffs for CSF or PET or by visual reading for PET. Adjusted data-driven cutoffs for abnormal amyloid were calculated using gaussian mixture modeling. Prevalence of amyloid abnormality was estimated according to age, sex, cognitive status, biomarker modality, APOE carrier status, educational level, geographical location, and dementia severity using generalized estimating equations. Results: Among the 19097 participants (mean [SD] age, 69.1 [9.8] years; 10148 women [53.1%])

Published
2022

26. Frequency of missed or delayed diagnosis in dementia is associated with neighborhood socioeconomic status

Author

Holm, Ellen, Jacobsen, Katja Kemp, de Lony, Thea Bang, Lembeck, Maurice, Pedersen, Hanne, Andersson, Charlotte, Johannsen, Peter, Jørgensen, Terese Sara Høj, Torp-Pedersen, Christian, Holm, Ellen, Jacobsen, Katja Kemp, de Lony, Thea Bang, Lembeck, Maurice, Pedersen, Hanne, Andersson, Charlotte, Johannsen, Peter, Jørgensen, Terese Sara Høj, and Torp-Pedersen, Christian

Abstract

Introduction Underdetection of dementia in areas with low socioeconomic status (SES) may interfere with findings concerning associations between SES and dementia. Methods Using administrative registers we assessed the associations between age- and sex-adjusted dementia incidence and neighborhood socioeconomic status (nSES) in 94 Danish municipalities. Wealth was divided into income quartiles and other nSES variables were dichotomized into high versus low according to the median. Results High population density (odds ratio [OR] 1.21, 95% confidence interval [CI] 1.18?1.24), higher proportion of inhabitants in higher income quartiles (P for trend

Published
2022

27. Six generations of CHMP2B-mediated Frontotemporal Dementia:Clinical features, predictive testing, progression, and survival

Author

Roos, Peter, Johannsen, Peter, Lindquist, Suzanne G., Brown, Jeremy M., Waldemar, Gunhild, Duno, Morten, Nielsen, Troels T., Budtz-Jorgensen, Esben, Gydesen, Susanne, Holm, Ida E., Collinge, John, Isaacs, Adrian M., Nielsen, Jørgen E., Roos, Peter, Johannsen, Peter, Lindquist, Suzanne G., Brown, Jeremy M., Waldemar, Gunhild, Duno, Morten, Nielsen, Troels T., Budtz-Jorgensen, Esben, Gydesen, Susanne, Holm, Ida E., Collinge, John, Isaacs, Adrian M., and Nielsen, Jørgen E.

Abstract

Objectives Chromosome 3-linked frontotemporal dementia (FTD-3) is caused by a c.532-1G > C mutation in the CHMP2B gene. It is extensively studied in a Danish family comprising one of the largest families with an autosomal dominantly inherited frontotemporal dementia (FTD). This retrospective cohort study utilizes demographics to identify risk factors for onset, progression, life expectancy, and death in CHMP2B-mediated FTD. The pedigree of 528 individuals in six generations is provided, and clinical descriptions are presented. Choices of genetic testing are evaluated. Materials and Methods Demographic and lifestyle factors were assessed in survival analysis in all identified CHMP2B mutation carriers (44 clinically affected FTD-3 patients and 16 presymptomatic CHMP2B mutation carriers). Predictors of onset and progression included sex, parental disease course, education, and vascular risk factors. Life expectancy was established by matching CHMP2B mutation carriers with average life expectancies in Denmark. Results Disease course was not correlated to parental disease course and seemed unmodified by lifestyle factors. Diagnosis was recognized at an earlier age in members with higher levels of education, probably reflecting an early dysexecutive syndrome, unmasked earlier in people with higher work-related requirements. Carriers of the CHMP2B mutation had a significant reduction in life expectancy of 13 years. Predictive genetic testing was chosen by 20% of at-risk family members. Conclusions CHMP2B-mediated FTD is substantiated as an autosomal dominantly inherited disease of complete penetrance. The clinical phenotype is a behavioral variant FTD. The disease course is unpredictable, and life expectancy is reduced. The findings may be applicable to other genetic FTD subtypes.

Published
2022

28. Early microgliosis precedes neuronal loss and behavioural impairment in mice with a frontotemporal dementia-causing CHMP2B mutation

Author

Clayton, Emma L., Mancuso, Renzo, Nielsen, Troels Tolstrup, Mizielinska, Sarah, Holmes, Holly, Powell, Nicholas, Norona, Frances, Larsen, Jytte Overgaard, Milioto, Carmelo, Wilson, Katherine M., Lythgoe, Mark F., Ourselin, Sebastian, Nielsen, Jörgen E., Johannsen, Peter, Holm, Ida, Collinge, John, Oliver, Peter L., Gomez-Nicola, Diego, and Isaacs, Adrian M.

Published
2017
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30. Prevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum

Author

Jansen, Willemijn J, Janssen, Olin, von Arnim, Christine, Marquié, Marta, Martinez-Lage, Pablo, Maserejian, Nancy, Mattsson, Niklas, de Mendonça, Alexandre, Meyer, Philipp T, Miller, Bruce L, Minatani, Shinobu, Mintun, Mark A, Mok, Vincent C T, Baiardi, Simone, Molinuevo, Jose Luis, Morbelli, Silvia Daniela, Morris, John C, Mroczko, Barbara, Na, Duk L, Newberg, Andrew, Nobili, Flavio, Nordberg, Agneta, Olde Rikkert, Marcel G M, de Oliveira, Catarina Resende, Baldeiras, Ines, Olivieri, Pauline, Orellana, Adela, Paraskevas, George, Parchi, Piero, Pardini, Matteo, Parnetti, Lucilla, Peters, Oliver, Poirier, Judes, Popp, Julius, Prabhakar, Sudesh, Barthel, Henryk, Rabinovici, Gil D, Ramakers, Inez H, Rami, Lorena, Reiman, Eric M, Rinne, Juha O, Rodrigue, Karen M, Rodríguez-Rodriguez, Eloy, Roe, Catherine M, Rosa-Neto, Pedro, Rosen, Howard J, Bateman, Randall J, Rot, Uros, Rowe, Christopher C, Rüther, Eckart, Ruiz, Agustín, Sabri, Osama, Sakhardande, Jayant, Sánchez-Juan, Pascual, Sando, Sigrid Botne, Santana, Isabel, Sarazin, Marie, Van Berckel, Bart, Scheltens, Philip, Schröder, Johannes, Selnes, Per, Seo, Sang Won, Silva, Dina, Skoog, Ingmar, Snyder, Peter J, Soininen, Hilkka, Sollberger, Marc, Sperling, Reisa A, Binette, Alexa Pichet, Spiru, Luisa, Stern, Yaakov, Stomrud, Erik, Takeda, Akitoshi, Teichmann, Marc, Teunissen, Charlotte E, Thompson, Louisa I, Tomassen, Jori, Tsolaki, Magda, Vandenberghe, Rik, Blennow, Kaj, Verbeek, Marcel M, Verhey, Frans R J, Villemagne, Victor, Villeneuve, Sylvia, Vogelgsang, Jonathan, Waldemar, Gunhild, Wallin, Anders, Wallin, Åsa K, Wiltfang, Jens, Wolk, David A, Boada, Merce, Yen, Tzu-Chen, Zboch, Marzena, Zetterberg, Henrik, Boecker, Henning, Tijms, Betty M, Bottlaender, Michel, den Braber, Anouk, Brooks, David J, Van Buchem, Mark A, Camus, Vincent, Carill, Jose Manuel, Cerman, Jiri, Chen, Kewei, Chételat, Gaël, Chipi, Elena, Vos, Stephanie J B, Cohen, Ann D, Daniels, Alisha, Delarue, Marion, Didic, Mira, Drzezga, Alexander, Dubois, Bruno, Eckerström, Marie, Ekblad, Laura L, Engelborghs, Sebastiaan, Epelbaum, Stéphane, Ossenkoppele, Rik, Fagan, Anne M, Fan, Yong, Fladby, Tormod, Fleisher, Adam S, Van der Flier, Wiesje M, Förster, Stefan, Fortea, Juan, Frederiksen, Kristian Steen, Freund-Levi, Yvonne, Frings, Lars, Visser, Pieter Jelle, Frisoni, Giovanni B, Fröhlich, Lutz, Gabryelewicz, Tomasz, Gertz, Hermann-Josef, Gill, Kiran Dip, Gkatzima, Olymbia, Gómez-Tortosa, Estrella, Grimmer, Timo, Guedj, Eric, Habeck, Christian G, Group, Amyloid Biomarker Study, Hampel, Harald, Handels, Ron, Hansson, Oskar, Hausner, Lucrezia, Hellwig, Sabine, Heneka, Michael, Herukka, Sanna-Kaisa, Hildebrandt, Helmut, Hodges, John, Hort, Jakub, Aarsland, Dag, Huang, Chin-Chang, Iriondo, Ane Juaristi, Itoh, Yoshiaki, Ivanoiu, Adrian, Jagust, William J, Jessen, Frank, Johannsen, Peter, Johnson, Keith A, Kandimalla, Ramesh, Kapaki, Elisabeth N, Alcolea, Daniel, Kern, Silke, Kilander, Lena, Klimkowicz-Mrowiec, Aleksandra, Klunk, William E, Koglin, Norman, Kornhuber, Johannes, Kramberger, Milica G, Kuo, Hung-Chou, Van Laere, Koen, Landau, Susan M, Altomare, Daniele, Landeau, Brigitte, Lee, Dong Young, de Leon, Mony, Leyton, Cristian E, Lin, Kun-Ju, Lleó, Alberto, Löwenmark, Malin, Madsen, Karine, Maier, Wolfgang, Marcusson, Jan, Clinical sciences, Neuroprotection & Neuromodulation, Neurology, Amsterdam Neuroscience - Brain Imaging, Amsterdam Neuroscience - Neurodegeneration, Radiology and nuclear medicine, Laboratory Medicine, Amsterdam Neuroscience - Neuroinfection & -inflammation, APH - Personalized Medicine, APH - Methodology, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, and Psychiatrie & Neuropsychologie

Subjects
Male, MILD COGNITIVE IMPAIRMENT, epidemiology [Cognitive Dysfunction], positron emission tomography, Alzheimer`s disease Donders Center for Medical Neuroscience [Radboudumc 1], epidemiology [Alzheimer Disease], Neuroscience(all), diagnostic imaging [Cognitive Dysfunction], Amyloidogenic Proteins, tau Proteins, cerebrospinal fluid [Amyloid beta-Peptides], DIAGNOSIS, cerebrospinal fluid, Apolipoproteins E, Alzheimer Disease, Prevalence, Humans, Amyloid, Alzheimer, PET, Cognitive Dysfunction, ddc:610, cerebrospinal fluid [Peptide Fragments], Aged, Amyloid beta-Peptides, neurology, DEMENTIA, Correction, ASSOCIATION, Amyloidosis, Middle Aged, Disorders of movement Donders Center for Medical Neuroscience [Radboudumc 3], health care planning, clinical trial design, Peptide Fragments, cerebrospinal fluid [Alzheimer Disease], PET, DRIFT, Cross-Sectional Studies, cerebrospinal fluid [Biomarkers], cerebrospinal fluid [tau Proteins], Radiology Nuclear Medicine and imaging, Positron-Emission Tomography, genetics [Apolipoproteins E], Female, Neurology (clinical), diagnostic imaging [Alzheimer Disease], cerebral amyloid aggregation, Biomarkers
Abstract

Importance: One characteristic histopathological event in Alzheimer disease (AD) is cerebral amyloid aggregation, which can be detected by biomarkers in cerebrospinal fluid (CSF) and on positron emission tomography (PET) scans. Prevalence estimates of amyloid pathology are important for health care planning and clinical trial design.Objective: To estimate the prevalence of amyloid abnormality in persons with normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia and to examine the potential implications of cutoff methods, biomarker modality (CSF or PET), age, sex, APOE genotype, educational level, geographical region, and dementia severity for these estimates.Design, Setting, and Participants: This cross-sectional, individual-participant pooled study included participants from 85 Amyloid Biomarker Study cohorts. Data collection was performed from January 1, 2013, to December 31, 2020. Participants had normal cognition, subjective cognitive decline, mild cognitive impairment, or clinical AD dementia. Normal cognition and subjective cognitive decline were defined by normal scores on cognitive tests, with the presence of cognitive complaints defining subjective cognitive decline. Mild cognitive impairment and clinical AD dementia were diagnosed according to published criteria.Exposures: Alzheimer disease biomarkers detected on PET or in CSF.Main Outcomes and Measures: Amyloid measurements were dichotomized as normal or abnormal using cohort-provided cutoffs for CSF or PET or by visual reading for PET. Adjusted data-driven cutoffs for abnormal amyloid were calculated using gaussian mixture modeling. Prevalence of amyloid abnormality was estimated according to age, sex, cognitive status, biomarker modality, APOE carrier status, educational level, geographical location, and dementia severity using generalized estimating equations.Results: Among the 19 097 participants (mean [SD] age, 69.1 [9.8] years; 10 148 women [53.1%]) included, 10 139 (53.1%) underwent an amyloid PET scan and 8958 (46.9%) had an amyloid CSF measurement. Using cohort-provided cutoffs, amyloid abnormality prevalences were similar to 2015 estimates for individuals without dementia and were similar across PET- and CSF-based estimates (24%; 95% CI, 21%-28%) in participants with normal cognition, 27% (95% CI, 21%-33%) in participants with subjective cognitive decline, and 51% (95% CI, 46%-56%) in participants with mild cognitive impairment, whereas for clinical AD dementia the estimates were higher for PET than CSF (87% vs 79%; mean difference, 8%; 95% CI, 0%-16%; P = .04). Gaussian mixture modeling-based cutoffs for amyloid measures on PET scans were similar to cohort-provided cutoffs and were not adjusted. Adjusted CSF cutoffs resulted in a 10% higher amyloid abnormality prevalence than PET-based estimates in persons with normal cognition (mean difference, 9%; 95% CI, 3%-15%; P = .004), subjective cognitive decline (9%; 95% CI, 3%-15%; P = .005), and mild cognitive impairment (10%; 95% CI, 3%-17%; P = .004), whereas the estimates were comparable in persons with clinical AD dementia (mean difference, 4%; 95% CI, -2% to 9%; P = .18).Conclusions and Relevance: This study found that CSF-based estimates using adjusted data-driven cutoffs were up to 10% higher than PET-based estimates in people without dementia, whereas the results were similar among people with dementia. This finding suggests that preclinical and prodromal AD may be more prevalent than previously estimated, which has important implications for clinical trial recruitment strategies and health care planning policies.

Published
2022
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35. Cortical Frontoparietal Network Dysfunction in CHMP2B-Frontotemporal Dementia

Author

Musaeus, Christian Sandøe, Pedersen, Jette Stokholm, Kjær, Troels Wesenberg, Johannsen, Peter, Waldemar, Gunhild, Haverberg, Maria Joy Normann, Bacher, Theis, Nielsen, Jørgen Erik, and Roos, Peter

Subjects
microstates analysis, mental disorders, CHMP2B, FTD, microstates, spectral power, EEG, Frontotemporal dementia
Abstract

A rare cause of inherited frontotemporal dementia (FTD) is a mutation in the CHMP2B gene on chromosome 3 leading to the autosomal dominantly inherited FTD (CHMP2B-FTD). Since CHMP2B-FTD is clinically well-characterized, and patients show a distinct pattern of executive dysfunction, the condition offers possible insight in the early electroencephalographic (EEG) changes in the cortical networks. Specifically, EEG microstate analysis parses the EEG signals into topographies believed to represent discrete network activations. We investigated the EEG dynamics in patients with symptomatic CHMP2B-FTD (n = 5) as well as pre-symptomatic mutation carriers (n = 5) compared to non-carrier family members (n = 6). The data was parsed into four archetypal microstates and global power was calculated. A trend was found for lower occurrence in microstate D in CHMP2B-FTD (p-value = 0.177, F-value = 2.036). Patients with recent symptom onset (2 years) showed decreased duration. Patients with CHMP2B-FTD present with executive dysfunction, and microstate D has previously been shown to be associated with the fronto-parietal network. The biphasic pattern may represent the pathophysiological changes in brain dynamics during neurodegeneration, which may apply to other neurodegenerative diseases.

Published
2021
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37. Sex-specific metabolic pathways associate with Alzheimer’s Disease (AD) endophenotypes in the European Medical Information Framework for AD Multimodal Biomarker Discovery cohort

Author

Xu, Jin, primary, Green, Rebecca, additional, Kim, Min, additional, Lord, Jodie, additional, Ebshiana, Amera, additional, Westwood, Sarah, additional, Baird, Alison L, additional, Nevado-Holgado, Alejo J, additional, Shi, Liu, additional, Hye, Abdul, additional, Snowden, Stuart G., additional, Bos, Isabelle, additional, Vos, Stephanie J. B., additional, Vandenberghe, Rik, additional, Teunissen, Charlotte E., additional, Kate, Mara Ten, additional, Scheltens, Philip, additional, Gabel, Silvy, additional, Meersmans, Karen, additional, Blin, Olivier, additional, Richardson, Jill, additional, De Roeck, Ellen Elisa, additional, Engelborghs, Sebastiaan, additional, Sleegers, Kristel, additional, Bordet, Régis, additional, Rami, Lorena, additional, Kettunen, Petronella, additional, Tsolaki, Magda, additional, Verhey, Frans R.J., additional, Alcolea, Daniel, additional, Lleó, Alberto, additional, Peyratout, Gwendoline, additional, Tainta, Mikel, additional, Johannsen, Peter, additional, Freund-Levi, Yvonne, additional, Frölich, Lutz, additional, Dobricic, Valerija, additional, Frisoni, Giovanni B., additional, Molinuevo, José Luis, additional, Wallin, Anders, additional, Popp, Julius, additional, Martinez-Lage, Pablo, additional, Bertram, Lars, additional, Blennow, Kaj, additional, Zetterberg, Henrik, additional, Streffer, Johannes, additional, Visser, Pieter Jelle, additional, Lovestone, Simon, additional, Proitsi, Petroula, additional, and Legido-Quigley, Cristina, additional

Published
2021
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39. Dickkopf-1 Overexpression in vitro Nominates Candidate Blood Biomarkers Relating to Alzheimer's Disease Pathology

Author

Shi, Liu, Winchester, Laura M., Liu, Benjamine Y., Killick, Richard, Ribe, Elena M., Westwood, Sarah, Baird, Alison L., Buckley, Noel J., Hong, Shengjun, Dobricic, Valerija, Kilpert, Fabian, Franke, Andre, Kiddle, Steven, Sattlecker, Martina, Dobson, Richard, Cuadrado, Antonio, Hye, Abdul, Ashton, Nicholas J., Morgan, Angharad R., Bos, Isabelle, Vos, Stephanie J.B., Ten Kate, Mara, Scheltens, Philip, Vandenberghe, Rik, Gabel, Silvy, Meersmans, Karen, Engelborghs, Sebastiaan, De Roeck, Ellen E., Sleegers, Kristel, Frisoni, Giovanni B., Blin, Olivier, Richardson, Jill C., Bordet, Régis, Molinuevo, José L., Rami, Lorena, Wallin, Anders, Kettunen, Petronella, Tsolaki, Magda, Verhey, Frans, Lleó, Alberto, Alcolea, Daniel, Popp, Julius, Peyratout, Gwendoline, Martinez-Lage, Pablo, Tainta, Mikel, Johannsen, Peter, Teunissen, Charlotte E., Freund-Levi, Yvonne, Frölich, Lutz, Legido-Quigley, Cristina, Barkhof, Frederik, Blennow, Kaj, Rasmussen, Katrine Laura, Nordestgaard, Børge Grønne, Frikke-Schmidt, Ruth, Nielsen, Sune Fallgaard, Soininen, Hilkka, Vellas, Bruno, Kloszewska, Iwona, Mecocci, Patrizia, Zetterberg, Henrik, Morgan, B. Paul, Streffer, Johannes, Visser, Pieter Jelle, Bertram, Lars, Nevado-Holgado, Alejo J., Lovestone, Simon, Shi, Liu, Winchester, Laura M., Liu, Benjamine Y., Killick, Richard, Ribe, Elena M., Westwood, Sarah, Baird, Alison L., Buckley, Noel J., Hong, Shengjun, Dobricic, Valerija, Kilpert, Fabian, Franke, Andre, Kiddle, Steven, Sattlecker, Martina, Dobson, Richard, Cuadrado, Antonio, Hye, Abdul, Ashton, Nicholas J., Morgan, Angharad R., Bos, Isabelle, Vos, Stephanie J.B., Ten Kate, Mara, Scheltens, Philip, Vandenberghe, Rik, Gabel, Silvy, Meersmans, Karen, Engelborghs, Sebastiaan, De Roeck, Ellen E., Sleegers, Kristel, Frisoni, Giovanni B., Blin, Olivier, Richardson, Jill C., Bordet, Régis, Molinuevo, José L., Rami, Lorena, Wallin, Anders, Kettunen, Petronella, Tsolaki, Magda, Verhey, Frans, Lleó, Alberto, Alcolea, Daniel, Popp, Julius, Peyratout, Gwendoline, Martinez-Lage, Pablo, Tainta, Mikel, Johannsen, Peter, Teunissen, Charlotte E., Freund-Levi, Yvonne, Frölich, Lutz, Legido-Quigley, Cristina, Barkhof, Frederik, Blennow, Kaj, Rasmussen, Katrine Laura, Nordestgaard, Børge Grønne, Frikke-Schmidt, Ruth, Nielsen, Sune Fallgaard, Soininen, Hilkka, Vellas, Bruno, Kloszewska, Iwona, Mecocci, Patrizia, Zetterberg, Henrik, Morgan, B. Paul, Streffer, Johannes, Visser, Pieter Jelle, Bertram, Lars, Nevado-Holgado, Alejo J., and Lovestone, Simon

Abstract

Background: Previous studies suggest that Dickkopf-1 (DKK1), an inhibitor of Wnt signaling, plays a role in amyloid-induced toxicity and hence Alzheimer's disease (AD). However, the effect of DKK1 expression on protein expression, and whether such proteins are altered in disease, is unknown. Objective: We aim to test whether DKK1 induced protein signature obtained in vitro were associated with markers of AD pathology as used in the amyloid/tau/neurodegeneration (ATN) framework as well as with clinical outcomes. Methods: We first overexpressed DKK1 in HEK293A cells and quantified 1,128 proteins in cell lysates using aptamer capture arrays (SomaScan) to obtain a protein signature induced by DKK1. We then used the same assay to measure the DKK1-signature proteins in human plasma in two large cohorts, EMIF (n = 785) and ANM (n = 677). Results: We identified a 100-protein signature induced by DKK1 in vitro. Subsets of proteins, along with age and apolipoprotein E ϵ4 genotype distinguished amyloid pathology (A + T-N-, A+T+N-, A+T-N+, and A+T+N+) from no AD pathology (A-T-N-) with an area under the curve of 0.72, 0.81, 0.88, and 0.85, respectively. Furthermore, we found that some signature proteins (e.g., Complement C3 and albumin) were associated with cognitive score and AD diagnosis in both cohorts. Conclusions: Our results add further evidence for a role of DKK regulation of Wnt signaling in AD and suggest that DKK1 induced signature proteins obtained in vitro could reflect theATNframework as well as predict disease severity and progression in vivo.

Published
2020

40. Validation of Plasma Proteomic Biomarkers Relating to Brain Amyloid Burden in the EMIF-Alzheimer's Disease Multimodal Biomarker Discovery Cohort

Author

Westwood, Sarah, Baird, Alison L., Anand, Sneha N., Nevado-Holgado, Alejo J., Kormilitzin, Andrey, Shi, Liu, Hye, Abdul, Ashton, Nicholas J., Morgan, Angharad R., Bos, Isabelle, Vos, Stephanie J. B., Baker, Susan, Buckley, Noel J., Ten Kate, Mara, Scheltens, Philip, Teunissen, Charlotte E., Vandenberghe, Rik, Gabel, Silvy, Meersmans, Karen, Engelborghs, Sebastiaan, De Roeck, Ellen E., Sleegers, Kristel, Frisoni, Giovanni B., Blin, Olivier, Richardson, Jill C., Bordet, Régis, Molinuevo, José L., Rami, Lorena, Wallin, Anders, Kettunen, Petronella, Tsolaki, Magda, Verhey, Frans, Lléo, Alberto, Sala, Isabel, Popp, Julius, Peyratout, Gwendoline, Martinez-Lage, Pablo, Tainta, Mikel, Johannsen, Peter, Freund-Levi, Yvonne, Frölich, Lutz, Dobricic, Valerija, Legido-Quigley, Cristina, Bertram, Lars, Barkhof, Frederik, Zetterberg, Henrik, Morgan, B. Paul, Streffer, Johannes, Visser, Pieter Jelle, Lovestone, Simon, Westwood, Sarah, Baird, Alison L., Anand, Sneha N., Nevado-Holgado, Alejo J., Kormilitzin, Andrey, Shi, Liu, Hye, Abdul, Ashton, Nicholas J., Morgan, Angharad R., Bos, Isabelle, Vos, Stephanie J. B., Baker, Susan, Buckley, Noel J., Ten Kate, Mara, Scheltens, Philip, Teunissen, Charlotte E., Vandenberghe, Rik, Gabel, Silvy, Meersmans, Karen, Engelborghs, Sebastiaan, De Roeck, Ellen E., Sleegers, Kristel, Frisoni, Giovanni B., Blin, Olivier, Richardson, Jill C., Bordet, Régis, Molinuevo, José L., Rami, Lorena, Wallin, Anders, Kettunen, Petronella, Tsolaki, Magda, Verhey, Frans, Lléo, Alberto, Sala, Isabel, Popp, Julius, Peyratout, Gwendoline, Martinez-Lage, Pablo, Tainta, Mikel, Johannsen, Peter, Freund-Levi, Yvonne, Frölich, Lutz, Dobricic, Valerija, Legido-Quigley, Cristina, Bertram, Lars, Barkhof, Frederik, Zetterberg, Henrik, Morgan, B. Paul, Streffer, Johannes, Visser, Pieter Jelle, and Lovestone, Simon

Abstract

We have previously investigated, discovered, and replicated plasma protein biomarkers for use to triage potential trials participants for PET or cerebrospinal fluid measures of Alzheimer's disease (AD) pathology. This study sought to undertake validation of these candidate plasma biomarkers in a large, multi-center sample collection. Targeted plasma analyses of 34 proteins with prior evidence for prediction of in vivo pathology were conducted in up to 1,000 samples from cognitively healthy elderly individuals, people with mild cognitive impairment, and in patients with AD-type dementia, selected from the EMIF-AD catalogue. Proteins were measured using Luminex xMAP, ELISA, and Meso Scale Discovery assays. Seven proteins replicated in their ability to predict in vivo amyloid pathology. These proteins form a biomarker panel that, along with age, could significantly discriminate between individuals with high and low amyloid pathology with an area under the curve of 0.74. The performance of this biomarker panel remained consistent when tested in apolipoprotein E ɛ4 non-carrier individuals only. This blood-based panel is biologically relevant, measurable using practical immunocapture arrays, and could significantly reduce the cost incurred to clinical trials through screen failure.

Published
2020
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41. Dickkopf-1 Overexpression in vitro Nominates Candidate Blood Biomarkers Relating to Alzheimer's Disease Pathology

Author

European Commission, Research Foundation - Flanders, Eusko Jaurlaritza, University of Antwerp, National Institute for Health Research (UK), NHS Foundation Trust, NIHR Biomedical Research Centre (UK), Medical Research Council (UK), University of Oxford, Shi, Liu, Winchester, Laura M., Liu, Benjamine Y., Killik, Richard, Ribe, Elena, Westwood, Sarah, Baird, Alison L., Buckley, Noel J., Hong, Shengjun, Dobricic, Valerija, Kilpert, Fabian, Franke, Andre, Kiddle, Steven, Sattlecker, Martina, Dobson, Richard, Cuadrado, Antonio, Hye, Abdul, Ashton, Nicholas J., Morgan, Angharad R., Bos, Isabelle, Vos, Stephanie J. B., Kate, Mara ten, Scheltens, Philip, Vandenberghe, Rik, Gabel, Silvy, Meersmans, Karen, Engelborghs, Sebastiaan, Roeck, Ellen E. De, Sleegersr, Kristel, Frisoni, Giovanni B., Blin, Olivier, Richardson, Jill C., Bordet, Regis, Molinuevo, José Luis, Rami, Lorena, Wallin, Anders, Kettunen, Petronella, Tsolaki, Magda, Verhey, Frans, Lleó, Alberto, Alcolea, Daniel, Popp, Julius, Peyratout, Gwendoline, Martinez-Lage, Pablo, Tainta, Mikel, Johannsen, Peter, Teunissen, Charlotte E., Freund-Levi, Yvonne, Frolich, Lutz, Legido-Quigley, Cristina, Barkhof, Frederik, Blennow, Kaj, Rasmussen, Katrine Laura, Nordestgaardv, Børge Grønne, Frikke-Schmidtu, Ruth, Fallgaard Nielsen, Sune, Soininen, Hilkka, Vellas, Bruno, Kloszewska, Iwona, Mecocci, Patrizia, Zetterberg, Henrik, Morgan, B. Paul, Strefferq, Johannes, Jelle Visser, Pieter, Bertramc, Lars, Nevado-Holgado, Alejo J., Lovestone, Simon, European Commission, Research Foundation - Flanders, Eusko Jaurlaritza, University of Antwerp, National Institute for Health Research (UK), NHS Foundation Trust, NIHR Biomedical Research Centre (UK), Medical Research Council (UK), University of Oxford, Shi, Liu, Winchester, Laura M., Liu, Benjamine Y., Killik, Richard, Ribe, Elena, Westwood, Sarah, Baird, Alison L., Buckley, Noel J., Hong, Shengjun, Dobricic, Valerija, Kilpert, Fabian, Franke, Andre, Kiddle, Steven, Sattlecker, Martina, Dobson, Richard, Cuadrado, Antonio, Hye, Abdul, Ashton, Nicholas J., Morgan, Angharad R., Bos, Isabelle, Vos, Stephanie J. B., Kate, Mara ten, Scheltens, Philip, Vandenberghe, Rik, Gabel, Silvy, Meersmans, Karen, Engelborghs, Sebastiaan, Roeck, Ellen E. De, Sleegersr, Kristel, Frisoni, Giovanni B., Blin, Olivier, Richardson, Jill C., Bordet, Regis, Molinuevo, José Luis, Rami, Lorena, Wallin, Anders, Kettunen, Petronella, Tsolaki, Magda, Verhey, Frans, Lleó, Alberto, Alcolea, Daniel, Popp, Julius, Peyratout, Gwendoline, Martinez-Lage, Pablo, Tainta, Mikel, Johannsen, Peter, Teunissen, Charlotte E., Freund-Levi, Yvonne, Frolich, Lutz, Legido-Quigley, Cristina, Barkhof, Frederik, Blennow, Kaj, Rasmussen, Katrine Laura, Nordestgaardv, Børge Grønne, Frikke-Schmidtu, Ruth, Fallgaard Nielsen, Sune, Soininen, Hilkka, Vellas, Bruno, Kloszewska, Iwona, Mecocci, Patrizia, Zetterberg, Henrik, Morgan, B. Paul, Strefferq, Johannes, Jelle Visser, Pieter, Bertramc, Lars, Nevado-Holgado, Alejo J., and Lovestone, Simon

Abstract

[Background]: Previous studies suggest that Dickkopf-1 (DKK1), an inhibitor of Wnt signaling, plays a role in amyloid-induced toxicity and hence Alzheimer’s disease (AD). However, the effect of DKK1 expression on protein expression, and whether such proteins are altered in disease, is unknown. [Objective]: We aim to test whether DKK1 induced protein signature obtained in vitro were associated with markers of AD pathology as used in the amyloid/tau/neurodegeneration (ATN) framework as well as with clinical outcomes. [Methods]: We first overexpressed DKK1 in HEK293A cells and quantified 1,128 proteins in cell lysates using aptamer capture arrays (SomaScan) to obtain a protein signature induced by DKK1. We then used the same assay to measure the DKK1-signature proteins in human plasma in two large cohorts, EMIF (n = 785) and ANM (n = 677). [Results]: We identified a 100-protein signature induced by DKK1 in vitro. Subsets of proteins, along with age and apolipoprotein E ɛ4 genotype distinguished amyloid pathology (A + T–N–, A+T+N–, A+T–N+, and A+T+N+) from no AD pathology (A–T–N–) with an area under the curve of 0.72, 0.81, 0.88, and 0.85, respectively. Furthermore, we found that some signature proteins (e.g., Complement C3 and albumin) were associated with cognitive score and AD diagnosis in both cohorts. [Conclusions]: Our results add further evidence for a role of DKK regulation of Wnt signaling in AD and suggest that DKK1 induced signature proteins obtained in vitro could reflect theATNframework as well as predict disease severity and progression in vivo.

Published
2020

42. Replication study of plasma proteins relating to Alzheimer's pathology

Author

Shi, Liu, primary, Winchester, Laura M., additional, Westwood, Sarah, additional, Baird, Alison L., additional, Anand, Sneha N., additional, Buckley, Noel J, additional, Hye, Abdul, additional, Ashton, Nicholas J., additional, Bos, Isabelle, additional, Vos, Stephanie J. B., additional, Kate, Mara ten, additional, Scheltens, Philip, additional, Teunissen, Charlotte E., additional, Vandenberghe, Rik, additional, Gabel, Silvy, additional, Meersmans, Karen, additional, Engelborghs, Sebastiaan, additional, De Roeck, Ellen E., additional, Sleegers, Kristel, additional, Frisoni, Giovanni B., additional, Blin, Olivier, additional, Richardson, Jill C., additional, Bordet, Régis, additional, Molinuevo, José L., additional, Rami, Lorena, additional, Wallin, Anders, additional, Kettunen, Petronella, additional, Tsolaki, Magda, additional, Verhey, Frans, additional, Lléo, Alberto, additional, Sala, Isabel, additional, Popp, Julius, additional, Peyratout, Gwendoline, additional, Martinez‐Lage, Pablo, additional, Tainta, Mikel, additional, Johannsen, Peter, additional, Freund‐Levi, Yvonne, additional, Frölich, Lutz, additional, Dobricic, Valerija, additional, Legido‐Quigley, Cristina, additional, Barkhof, Frederik, additional, Andreasson, Ulf, additional, Blennow, Kaj, additional, Zetterberg, Henrik, additional, Streffer, Johannes, additional, Lill, Christina M., additional, Bertram, Lars, additional, Visser, Pieter Jelle, additional, Kolb, Hartmuth C., additional, Narayan, Vaibhav A., additional, Lovestone, Simon, additional, and Nevado‐Holgado, Alejo J., additional

Published
2021
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45. Six generations of CHMP2B‐mediated Frontotemporal Dementia: Clinical features, predictive testing, progression, and survival.

Author

Roos, Peter, Johannsen, Peter, Lindquist, Suzanne G., Brown, Jeremy M., Waldemar, Gunhild, Duno, Morten, Nielsen, Troels T., Budtz‐Jørgensen, Esben, Gydesen, Susanne, Holm, Ida E., Collinge, John, Isaacs, Adrian M., Nielsen, Jørgen E., Gade, Anders, Stokholm, Jette, Thusgaard, Tove, Fisher, Elizabeth M.C., and Englund, Elisabet

Subjects
*FRONTOTEMPORAL dementia, *PREDICTIVE tests, *LIFE expectancy, *GENETIC testing, *DISEASE progression
Abstract

Objectives: Chromosome 3‐linked frontotemporal dementia (FTD‐3) is caused by a c.532‐1G > C mutation in the CHMP2B gene. It is extensively studied in a Danish family comprising one of the largest families with an autosomal dominantly inherited frontotemporal dementia (FTD). This retrospective cohort study utilizes demographics to identify risk factors for onset, progression, life expectancy, and death in CHMP2B‐mediated FTD. The pedigree of 528 individuals in six generations is provided, and clinical descriptions are presented. Choices of genetic testing are evaluated. Materials and Methods: Demographic and lifestyle factors were assessed in survival analysis in all identified CHMP2B mutation carriers (44 clinically affected FTD‐3 patients and 16 presymptomatic CHMP2B mutation carriers). Predictors of onset and progression included sex, parental disease course, education, and vascular risk factors. Life expectancy was established by matching CHMP2B mutation carriers with average life expectancies in Denmark. Results: Disease course was not correlated to parental disease course and seemed unmodified by lifestyle factors. Diagnosis was recognized at an earlier age in members with higher levels of education, probably reflecting an early dysexecutive syndrome, unmasked earlier in people with higher work‐related requirements. Carriers of the CHMP2B mutation had a significant reduction in life expectancy of 13 years. Predictive genetic testing was chosen by 20% of at‐risk family members. Conclusions: CHMP2B‐mediated FTD is substantiated as an autosomal dominantly inherited disease of complete penetrance. The clinical phenotype is a behavioral variant FTD. The disease course is unpredictable, and life expectancy is reduced. The findings may be applicable to other genetic FTD subtypes. [ABSTRACT FROM AUTHOR]

Published
2022
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47. A metabolite-based machine learning approach to diagnose Alzheimer-type dementia in blood: Results from the European Medical Information Framework for Alzheimer disease biomarker discovery cohort

Author

Stamate, Daniel, Kim, Min, Proitsi, Petroula, Westwood, Sarah, Baird, Alison, Nevado-Holgado, Alejo, Hye, Abdul, Bos, Isabelle, Vos, Stephanie J.B., Vandenberghe, Rik, Teunissen, Charlotte E., Kate, Mara Ten, Scheltens, Philip, Gabel, Silvy, Meersmans, Karen, Blin, Olivier, Richardson, Jill, De Roeck, Ellen, Engelborghs, Sebastiaan, Sleegers, Kristel, Bordet, Régis, Ramit, Lorena, Kettunen, Petronella, Tsolaki, Magda, Verhey, Frans, Alcolea, Daniel, Lléo, Alberto, Peyratout, Gwendoline, Tainta, Mikel, Johannsen, Peter, Freund-Levi, Yvonne, Frölich, Lutz, Dobricic, Valerija, Frisoni, Giovanni B., Molinuevo, José L., Wallin, Anders, Popp, Julius, Martinez-Lage, Pablo, Bertram, Lars, Blennow, Kaj, Zetterberg, Henrik, Streffer, Johannes, Visser, Pieter J., Lovestone, Simon, and Legido-Quigley, Cristina

Published
2019
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48. DNA methylation differences associated with peripheral biomarkers in the EMIF‐AD cohort

Author

Smith, Rebecca G., primary, Bos, Isabelle, additional, Vos, Stephanie J.B., additional, Verhey, Frans R.J., additional, Scheltens, Philip, additional, Engelborghs, Sebastiaan, additional, Frisoni, Giovanni B., additional, Blin, Olivier, additional, Richardson, Jill, additional, Bordet, Régis, additional, Tsolaki, Magda, additional, Popp, Julius, additional, Martinez‐Lage, Pablo, additional, Lleó, Alberto, additional, Johannsen, Peter, additional, Freund, Yvonne, additional, Frölich, Lutz, additional, Vandenberghe, Rik, additional, Lovestone, Simon, additional, Streffer, Johannes, additional, Andreasson, Ulf, additional, Blennow, Kaj, additional, Visser, Pieter Jelle, additional, Zetterberg, Henrik, additional, Bertram, Lars, additional, and Lunnon, Katie, additional

Published
2020
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49. Identification of plasma proteome signatures associated with ATN framework using SOMAscan

Author

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

Published
2020
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50. Dickkopf-1 Overexpression in vitro Nominates Candidate Blood Biomarkers Relating to Alzheimer’s Disease Pathology

Author

Shi, Liu, primary, Winchester, Laura M., additional, Liu, Benjamine Y., additional, Killick, Richard, additional, Ribe, Elena M., additional, Westwood, Sarah, additional, Baird, Alison L., additional, Buckley, Noel J., additional, Hong, Shengjun, additional, Dobricic, Valerija, additional, Kilpert, Fabian, additional, Franke, Andre, additional, Kiddle, Steven, additional, Sattlecker, Martina, additional, Dobson, Richard, additional, Cuadrado, Antonio, additional, Hye, Abdul, additional, Ashton, Nicholas J., additional, Morgan, Angharad R., additional, Bos, Isabelle, additional, Vos, Stephanie J.B., additional, ten Kate, Mara, additional, Scheltens, Philip, additional, Vandenberghe, Rik, additional, Gabel, Silvy, additional, Meersmans, Karen, additional, Engelborghs, Sebastiaan, additional, De Roeck, Ellen E., additional, Sleegers, Kristel, additional, Frisoni, Giovanni B., additional, Blin, Olivier, additional, Richardson, Jill C., additional, Bordet, Régis, additional, Molinuevo, José L., additional, Rami, Lorena, additional, Wallin, Anders, additional, Kettunen, Petronella, additional, Tsolaki, Magda, additional, Verhey, Frans, additional, Lleó, Alberto, additional, Alcolea, Daniel, additional, Popp, Julius, additional, Peyratout, Gwendoline, additional, Martinez-Lage, Pablo, additional, Tainta, Mikel, additional, Johannsen, Peter, additional, Teunissen, Charlotte E., additional, Freund-Levi, Yvonne, additional, Frölich, Lutz, additional, Legido-Quigley, Cristina, additional, Barkhof, Frederik, additional, Blennow, Kaj, additional, Rasmussen, Katrine Laura, additional, Nordestgaard, Børge Grønne, additional, Frikke-Schmidt, Ruth, additional, Nielsen, Sune Fallgaard, additional, Soininen, Hilkka, additional, Vellas, Bruno, additional, Kloszewska, Iwona, additional, Mecocci, Patrizia, additional, Zetterberg, Henrik, additional, Morgan, B. Paul, additional, Streffer, Johannes, additional, Visser, Pieter Jelle, additional, Bertram, Lars, additional, Nevado-Holgado, Alejo J., additional, and Lovestone, Simon, additional

Published
2020
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