247 results on '"Verhey, Frans R. J."'
Search Results
2. Correction: Cerebrospinal fluid tau levels are associated with abnormal neuronal plasticity markers in Alzheimer’s disease
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Visser, Pieter Jelle, Reus, Lianne M., Gobom, Johan, Jansen, Iris, Dicks, Ellen, van der Lee, Sven J., Tsolaki, Magda, Verhey, Frans R. J., Popp, Julius, Martinez-Lage, Pablo, Vandenberghe, Rik, Lleó, Alberto, Molinuevo, José Luís, Engelborghs, Sebastiaan, Freund-Levi, Yvonne, Froelich, Lutz, Sleegers, Kristel, Dobricic, Valerija, Lovestone, Simon, Streffer, Johannes, Vos, Stephanie J. B., Bos, Isabelle, Smit, August B., Blennow, Kaj, Scheltens, Philip, Teunissen, Charlotte E., Bertram, Lars, Zetterberg, Henrik, and Tijms, Betty M.
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- 2022
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3. Cerebrospinal fluid tau levels are associated with abnormal neuronal plasticity markers in Alzheimer’s disease
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Visser, Pieter Jelle, Reus, Lianne M., Gobom, Johan, Jansen, Iris, Dicks, Ellen, van der Lee, Sven J., Tsolaki, Magda, Verhey, Frans R. J., Popp, Julius, Martinez-Lage, Pablo, Vandenberghe, Rik, Lleó, Alberto, Molinuevo, José Luís, Engelborghs, Sebastiaan, Freund-Levi, Yvonne, Froelich, Lutz, Sleegers, Kristel, Dobricic, Valerija, Lovestone, Simon, Streffer, Johannes, Vos, Stephanie J. B., Bos, Isabelle, Smit, August B., Blennow, Kaj, Scheltens, Philip, Teunissen, Charlotte E., Bertram, Lars, Zetterberg, Henrik, and Tijms, Betty M.
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- 2022
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4. Associations between plasma kynurenines and cognitive function in individuals with normal glucose metabolism, prediabetes and type 2 diabetes: the Maastricht Study
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Bakker, Lieke, Ramakers, Inez H. G. B., van Boxtel, Martin P. J., Schram, Miranda T., Stehouwer, Coen D. A., van der Kallen, Carla J. H., Dagnelie, Pieter C., van Greevenbroek, Marleen M. J., Wesselius, Anke, Midttun, Øivind, Ueland, Per M., Verhey, Frans R. J., Eussen, Simone J. P. M., and Köhler, Sebastian
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- 2021
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5. Imaging the role of blood–brain barrier disruption in normal cognitive ageing
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Verheggen, Inge C. M., de Jong, Joost J. A., van Boxtel, Martin P. J., Postma, Alida A., Jansen, Jacobus F. A., Verhey, Frans R. J., and Backes, Walter H.
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- 2020
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6. Association of tear fluid amyloid and tau levels with disease severity and neurodegeneration
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Gijs, Marlies, Ramakers, Inez H. G. B., Visser, Pieter Jelle, Verhey, Frans R. J., van de Waarenburg, Marjo P. H., Schalkwijk, Casper G., Nuijts, Rudy M. M. A., and Webers, Carroll A. B.
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- 2021
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7. Genome-wide association study of frontotemporal dementia identifies a C9ORF72 haplotype with a median of 12-G4C2 repeats that predisposes to pathological repeat expansions
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Reus, Lianne M., Jansen, Iris E., Mol, Merel O., van Ruissen, Fred, van Rooij, Jeroen, van Schoor, Natasja M., Tesi, Niccolò, Reinders, Marcel J. T., Huisman, Martijn A., Holstege, Henne, Visser, Pieter Jelle, de Boer, Sterre C. M., Hulsman, Marc, Ahmad, Shahzad, Amin, Najaf, Uitterlinden, Andre G., Ikram, Arfan, van Duijn, Cornelia M., Seelaar, Harro, Ramakers, Inez H. G. B., Verhey, Frans R. J., van der Lugt, Aad, Claassen, Jurgen A. H. R., Jan Biessels, Geert, De Deyn, Peter Paul, Scheltens, Philip, van der Flier, Wiesje M., van Swieten, John C., Pijnenburg, Yolande A. L., and van der Lee, Sven J.
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- 2021
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8. The association of hyperglycaemia and insulin resistance with incident depressive symptoms over 4 years of follow-up: The Maastricht Study
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Geraets, Anouk F. J., Köhler, Sebastian, Muzambi, Rutendo, Schalkwijk, Casper G., Oenema, Anke, Eussen, Simone J. P. M., Dagnelie, Pieter C., Stehouwer, Coen D. A., Schaper, Nicolaas C., Henry, Ronald M. A., van der Kallen, Carla J. H., Wesselius, Anke, Koster, Annemarie, Verhey, Frans R. J., and Schram, Miranda T.
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- 2020
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9. Increase in blood–brain barrier leakage in healthy, older adults
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Verheggen, Inge C. M., de Jong, Joost J. A., van Boxtel, Martin P. J., Gronenschild, Ed H. B. M., Palm, Walter M., Postma, Alida A., Jansen, Jacobus F. A., Verhey, Frans R. J., and Backes, Walter H.
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- 2020
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10. Permeability of the windows of the brain: feasibility of dynamic contrast-enhanced MRI of the circumventricular organs
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Verheggen, Inge C. M., de Jong, Joost J. A., van Boxtel, Martin P. J., Postma, Alida A., Verhey, Frans R. J., Jansen, Jacobus F. A., and Backes, Walter H.
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- 2020
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11. Smartphone-Based Experience Sampling in People With Mild Cognitive Impairment: Feasibility and Usability Study
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Bartels, Sara Laureen, van Knippenberg, Rosalia J M, Malinowsky, Camilla, Verhey, Frans R J, and de Vugt, Marjolein E
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Geriatrics ,RC952-954.6 - Abstract
BackgroundDaily functioning of people with cognitive disorders such as mild cognitive impairment (MCI) is usually depicted by retrospective questionnaires, which can be memory-biased and neglect fluctuations over time or contexts. ObjectiveThis study examines the feasibility and usability of applying the experience sampling method (ESM) in people with MCI to provide a detailed and dynamic picture of behavioral, emotional, and cognitive patterns in everyday life. MethodsFor 6 consecutive days, 21 people with MCI used an ESM app on their smartphones. At 8 semi-random timepoints per day, participants filled in momentary questionnaires on mood, activities, social context, and subjective cognitive complaints. Feasibility was determined through self-reports and observable human-technology interactions. Usability was demonstrated on an individual and group level. ResultsOf the 21 participants, 3 dropped out due to forgetting to carry their smartphones or forgetting the study instructions. In the remaining 18 individuals, the compliance rate was high, at 78.7%. Participants reported that momentary questions reflected their daily experiences well. Of the 18 participants, 13 (72%) experienced the increase in awareness of their own memory functions as pleasant or neutral. ConclusionsSupport was found for the general feasibility of smartphone-based experience sampling in people with MCI. However, many older adults with MCI are currently not in possession of smartphones, and study adherence seems challenging for a minority of individuals. Momentary data can increase the insights into daily patterns and may guide the person-tailored development of self-management strategies in clinical settings.
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- 2020
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12. Associations between pattern separation and hippocampal subfield structure and function vary along the lifespan: A 7 T imaging study
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Riphagen, Joost M., Schmiedek, Lisa, Gronenschild, Ed H. B. M., Yassa, Michael A., Priovoulos, Nikos, Sack, Alexander T., Verhey, Frans R. J., and Jacobs, Heidi I. L.
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- 2020
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13. Determinants of quality of life in family caregivers in MCI:a comparison with mild dementia
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Tan, Eva Y. L., Janssen, Niels, Handels, Ron, Ramakers, Inez H. G. B., Verhey, Frans R. J., van der Flier, Wiesje M., Melis, René J. F., Olde Rikkert, Marcel G. M., Schols, Jos M. G. A., and de Vugt, Marjolein E.
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Objectives: The aim of the current study was to investigate the health-related quality of life (HRQol) of the family caregiver in MCI, explore possible determinants and study possible differences with mild dementia. Methods: This secondary data analysis included 145 persons with MCI and 154 persons with dementia and their family caregivers from two Dutch cohort studies. HRQoL was measured with the VAS of the EuroQol-5D-3L version. Regressions analyses were conducted to examine potential demographic and clinical determinants of the caregiver’s HRQoL. Results: The mean EQ5D-VAS in family caregivers of persons with MCI was 81.1 (SD 15.7), and did not significantly differ from family caregivers in mild dementia (81.9 (SD 13.0)). In MCI, patient measurements were not significantly associated with caregiver mean EQ5D-VAS. Concerning caregiver characteristics, being a spouse and a lower educational level were associated with a lower mean EQ5D-VAS (in a multiple linear regression model: unstandardized B −8.075, p = 0.013 and unstandardized B −6.162, p = 0.037 resp.). In mild dementia, the NPI item irritability showed an association with caregiver EQ5D-VAS in bivariate linear regression analyses. Conclusion: Results indicate that especially family caregiver characteristics seem to influence family caregiver HRQoL in MCI. Future research should include other potential determinants such as burden, coping strategies and relationship quality.
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- 2023
14. MRI predictors of amyloid pathology: results from the EMIF-AD Multimodal Biomarker Discovery study
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ten Kate, Mara, Redolfi, Alberto, Peira, Enrico, Bos, Isabelle, Vos, Stephanie J., Vandenberghe, Rik, Gabel, Silvy, Schaeverbeke, Jolien, Scheltens, Philip, Blin, Olivier, Richardson, Jill C., Bordet, Regis, Wallin, Anders, Eckerstrom, Carl, Molinuevo, José Luis, Engelborghs, Sebastiaan, Van Broeckhoven, Christine, Martinez-Lage, Pablo, Popp, Julius, Tsolaki, Magdalini, Verhey, Frans R. J., Baird, Alison L., Legido-Quigley, Cristina, Bertram, Lars, Dobricic, Valerija, Zetterberg, Henrik, Lovestone, Simon, Streffer, Johannes, Bianchetti, Silvia, Novak, Gerald P., Revillard, Jerome, Gordon, Mark F., Xie, Zhiyong, Wottschel, Viktor, Frisoni, Giovanni, Visser, Pieter Jelle, and Barkhof, Frederik
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- 2018
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15. Can education improve clinical practice concerning delirium in older hospitalised patients? Results of a pre-test post-test study on an educational intervention for nursing staff
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van Velthuijsen, Eveline L., Zwakhalen, Sandra M. G., Warnier, Ron M. J., Ambergen, Ton, Mulder, Wubbo J., Verhey, Frans R. J., and Kempen, Gertrudis I. J. M.
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- 2018
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16. Worry Modifies the Relationship between Locus Coeruleus Activity and Emotional Mnemonic Discrimination
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Pagen, Linda H. G., primary, Poser, Benedikt A., additional, van Boxtel, Martin P. J., additional, Priovoulos, Nikos, additional, van Hooren, Roy W. E., additional, Verhey, Frans R. J., additional, and Jacobs, Heidi I. L., additional
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- 2022
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17. Prevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum
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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
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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.
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- 2022
18. Additional file 2 of Cerebrospinal fluid tau levels are associated with abnormal neuronal plasticity markers in Alzheimer’s disease
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Visser, Pieter Jelle, Reus, Lianne M., Gobom, Johan, Jansen, Iris, Dicks, Ellen, van der Lee, Sven J., Tsolaki, Magda, Verhey, Frans R. J., Popp, Julius, Martinez-Lage, Pablo, Vandenberghe, Rik, Lleó, Alberto, Molinuevo, José Luís, Engelborghs, Sebastiaan, Freund-Levi, Yvonne, Froelich, Lutz, Sleegers, Kristel, Dobricic, Valerija, Lovestone, Simon, Streffer, Johannes, Vos, Stephanie J. B., Bos, Isabelle, Smit, August B., Blennow, Kaj, Scheltens, Philip, Teunissen, Charlotte E., Bertram, Lars, Zetterberg, Henrik, and Tijms, Betty M.
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mental disorders ,sense organs - Abstract
Additional file 2: Figure S1. Longitudinal change in CSF total tau. Figure S2. Enrichment of synaptic processes in individuals with AD according to t-tau status. Figure S3. Enriched GO biological processes and SUZ12 and REST transcription factors associated with proteins that differed between AD individuals with increased t-tau and normal t-tau and proteins that changed with disease severity.
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- 2022
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19. Characteristics of subjective cognitive decline associated with amyloid positivity
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Janssen, Olin, Jansen, Willemijn J, Epelbaum, Stéphane, Lleó, Alberto, Engelborghs, Sebastiaan, van der Flier, Wiesje M, Landau, Susan, Popp, Julius, Wallin, Anders, Scheltens, Philip, Rikkert, Marcel Olde, Snyder, Peter J, Vos, Stephanie J B, Rowe, Chris, Chételat, Gaël, Ruíz, Agustin, Marquié, Marta, Chipi, Elena, Wolfsgruber, Steffen, Heneka, Michael, Boecker, Henning, Peters, Oliver, Jarholm, Jonas, Boada, Merce, Rami, Lorena, Tort-Merino, Adrià, Binette, Alexa Pichet, Poirier, Judes, Rosa-Neto, Pedro, Cerman, Jiri, Dubois, Bruno, Teichmann, Marc, Alcolea, Daniel, Fortea, Juan, Parnetti, Lucilla, Sánchez-Saudinós, M Belén, Ebenau, Jarith, Pocnet, Cornelia, Eckerström, Marie, Thompson, Louisa, Villemagne, Victor, Buckley, Rachel, Burnham, Samantha, Delarue, Marion, Freund-Levi, Yvonne, Gabryelewicz, Tomasz, Wallin, Åsa K, Ramakers, Inez, Tsolaki, Magda, Soininen, Hilkka, Hampel, Harald, Spiru, Luiza, Initiative, Alzheimer's Disease Neuroimaging, group, FACEHBI study, group, PREVENT-AD research, Tijms, Betty, Fladby, Tormod, Ossenkoppele, Rik, Verhey, Frans R J, Jessen, Frank, Visser, Pieter Jelle, Molinuevo, José Luis, Villeneuve, Sylvia, Hort, Jakub, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, Psychiatrie & Neuropsychologie, Neurology, Amsterdam Neuroscience - Neurodegeneration, Amsterdam Neuroscience - Brain Imaging, Alzheimers Dis Neuroimaging Initia, Facehbi Study Grp, PREVENT-AD Res Grp, Clinical sciences, and Neuroprotection & Neuromodulation
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PRECLINICAL ALZHEIMERS-DISEASE ,Amyloid ,SYMPTOMS ,positron emission tomography ,Epidemiology ,Neuroscience(all) ,Apolipoprotein E4 ,Amyloidogenic Proteins ,cerebrospinal fluid ,Cellular and Molecular Neuroscience ,Developmental Neuroscience ,mental disorders ,Humans ,Cognitive Dysfunction ,ddc:610 ,DEPOSITION ,OLDER-ADULTS ,genetics [Apolipoprotein E4] ,POPULATION ,RISK ,neurology ,Health Policy ,DEMENTIA ,genetics [Cognitive Dysfunction] ,Brain ,amyloid ,Amyloidosis ,Alzheimer's disease ,PREVALENCE ,COMMUNITY ,Psychiatry and Mental health ,metabolism [Brain] ,Positron-Emission Tomography ,Neurology (clinical) ,Human medicine ,psychology [Cognitive Dysfunction] ,Geriatrics and Gerontology ,subjective cognitive decline ,MEMORY COMPLAINTS ,Biomarkers - Abstract
Introduction The evidence for characteristics of persons with subjective cognitive decline (SCD) associated with amyloid positivity is limited. Methods In 1640 persons with SCD from 20 Amyloid Biomarker Study cohort, we investigated the associations of SCD-specific characteristics (informant confirmation, domain-specific complaints, concerns, feelings of worse performance) demographics, setting, apolipoprotein E gene (APOE) epsilon 4 carriership, and neuropsychiatric symptoms with amyloid positivity. Results Between cohorts, amyloid positivity in 70-year-olds varied from 10% to 76%. Only older age, clinical setting, and APOE epsilon 4 carriership showed univariate associations with increased amyloid positivity. After adjusting for these, lower education was also associated with increased amyloid positivity. Only within a research setting, informant-confirmed complaints, memory complaints, attention/concentration complaints, and no depressive symptoms were associated with increased amyloid positivity. Feelings of worse performance were associated with less amyloid positivity at younger ages and more at older ages. Discussion Next to age, setting, and APOE epsilon 4 carriership, SCD-specific characteristics may facilitate the identification of amyloid-positive individuals.
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- 2022
20. Effectiveness of dementia follow-up care by memory clinics or general practitioners: randomised controlled trial
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Meeuwsen, Els J, Melis, René J F, Van Der Aa, Geert C H M, Golüke-Willemse, Gertie A M, De Leest, Benoit J M, Van Raak, Frank H J M, Schölzel-Dorenbos, Carla J M, Verheijen, Desiree C M, Verhey, Frans R J, Visser, Marieke C, Wolfs, Claire A, Adang, Eddy M M, and Rikkert, Marcel G M Olde
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- 2012
21. Are physically frail older persons more at risk of adverse outcomes if they also suffer from cognitive, social, and psychological frailty?
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Ament, Bart H. L., de Vugt, Marjolein E., Verhey, Frans R. J., and Kempen, Gertrudis I. J. M.
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- 2014
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22. Anxiety and cognitive functioning in the Maastricht study: A cross-sectional population study
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Gulpers, Bernice J. A., Verhey, Frans R. J., Eussen, Simone J. P. M., Schram, M.T., Galan, B.E. de, Boxtel, Martin P. J. van, Stehouwer, Coen D. A., Kohler, S., RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, Psychiatrie & Neuropsychologie, RS: CAPHRI - R5 - Optimising Patient Care, Epidemiologie, MUMC+: HVC Pieken Maastricht Studie (9), RS: Carim - V01 Vascular complications of diabetes and metabolic syndrome, Interne Geneeskunde, Psychology 2, Section Neuropsychology, RS: FPN NPPP I, MUMC+: MA Interne Geneeskunde (3), and Psychology 5
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Psychiatry and Mental health ,Clinical Psychology ,All institutes and research themes of the Radboud University Medical Center ,Cross-Sectional Studies ,Cognition ,Diabetes Mellitus, Type 2 ,Humans ,Metabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6] ,Anxiety ,Anxiety Disorders ,Aged - Abstract
BACKGROUND: Higher anxiety levels in older adults are associated with worse executive functioning and an increased risk for dementia. In this study individual anxiety disorders and clinically relevant generalized anxiety symptoms are studied in relation to multiple cognitive domains.METHOD: This cross-sectional study includes 7344 community-dwelling participants of The Maastricht Study aged 40-75 years and oversampling of type 2 diabetes. Panic disorder with and without agoraphobia, agoraphobia and lifetime panic disorder were measured with the Mini International Neuropsychiatric Interview. Generalized anxiety symptoms were measured with the Generalized Anxiety Disorder 7-item scale (GAD-7). Multiple cognitive domains (executive functioning, memory and processing speed) and cognitive impairment were assessed. Multivariable linear and logistic regression analyses were used with adjustment for potential confounders. Interaction analyses were performed to test the moderation of age, sex and type 2 diabetes (due to oversampling).RESULTS: Agoraphobia was associated with worse scores on all cognitive domains (range B = -0.12 to -0.10; range 95%CI = -0.20 to -0.04) and with higher odds of cognitive impairment (OR = 1.51, 95%CI = 1.18-1.93). High scores on the GAD-7 were associated with worse scores on processing speed (B = -0.11, 95%CI = -0.20 to -0.03) and higher odds of cognitive impairment (OR = 1.42, 95%CI = 1.02-1.97). Panic disorder was significantly associated with worse scores on memory tasks (B = -0.25, 95%CI = -0.48 to -0.02). Associations were stronger in the younger participants and for agoraphobia and GAD-7 scores also in those with type 2 diabetes.CONCLUSION: Multiple anxiety disorders and generalized anxiety symptoms were associated with worse cognitive functioning on several cognitive domains.
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- 2021
23. Obtaining EQ-5D-5L utilities from the disease specific quality of life Alzheimer's disease scale: development and results from a mapping study
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Rombach, Ines, Iftikhar, Marvi, Jhuti, Gurleen S., Gustavsson, Anders, Lecomte, Pascal, Belger, Mark, Handels, Ron, Castro Sanchez, Amparo Y., Kors, Jan, Hopper, Louise, Olde Rikkert, Marcel, Selbæk, Geir, Stephan, Astrid, Sikkes, Sietske A. M., Woods, Bob, Gonçalves-Pereira, Manuel, Zanetti, Orazio, Ramakers, Inez H. G. B., Verhey, Frans R. J., Gallacher, John, Actifcare Consortium, LeARN Consortium, Landeiro, Filipa, Gray, Alastair M., Psychiatrie & Neuropsychologie, RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, MUMC+: MA Med Staf Spec Psychiatrie (9), Neurology, and Amsterdam Neuroscience - Neurodegeneration
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Male ,Alzheimer`s disease Donders Center for Medical Neuroscience [Radboudumc 1] ,Mean squared error ,Scale (ratio) ,Computer science ,Preference based measures ,PATIENT ,Article ,VALIDATION ,03 medical and health sciences ,0302 clinical medicine ,Quality of life ,Alzheimer Disease ,EQ-5D ,PEOPLE ,Surveys and Questionnaires ,Statistics ,medicine ,Humans ,Dementia ,Health related quality of life ,030212 general & internal medicine ,DEMQOL ,Mapping algorithm ,ADAPTATION ,VERSION ,PROXY ,Multinomial logistic regression ,Estimation ,030503 health policy & services ,DEMENTIA ,Public Health, Environmental and Occupational Health ,Statistical model ,OUTCOME MEASURES ,medicine.disease ,Cross-walking ,humanities ,Quality of Life ,Female ,0305 other medical science ,Algorithms - Abstract
Purpose The Quality of Life Alzheimer’s Disease Scale (QoL-AD) is commonly used to assess disease specific health-related quality of life (HRQoL) as rated by patients and their carers. For cost-effectiveness analyses, utilities based on the EQ-5D are often required. We report a new mapping algorithm to obtain EQ-5D indices when only QoL-AD data are available. Methods Different statistical models to estimate utility directly, or responses to individual EQ-5D questions (response mapping) from QoL-AD, were trialled for patient-rated and proxy-rated questionnaires. Model performance was assessed by root mean square error and mean absolute error. Results The response model using multinomial regression including age and sex, performed best in both the estimation dataset and an independent dataset. Conclusions The recommended mapping algorithm allows researchers for the first time to estimate EQ-5D values from QoL-AD data, enabling cost-utility analyses using datasets where the QoL-AD but no utility measures were collected.
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- 2021
24. The Effects of Technological Interventions on Social Participation of Community-Dwelling Older Adults with and Without Dementia: A Systematic Review
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Heins, Pascale, primary, Boots, Lizzy M. M., additional, Koh, Wei Qi, additional, Neven, An, additional, Verhey, Frans R. J., additional, and de Vugt, Marjolein E. de, additional
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- 2021
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25. The Course and Predictors of Quality of Life in Nursing Home Residents with Young-onset Dementia
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Pu, Lihui, Bakker, Christian, Appelhof, Britt, Van Duinen-van den Ijssel, Jeannette C. L., Zwijsen, Sandra A., Teerenstra, Steven, Smalbrugge, Martin, Verhey, Frans R. J., de Vugt, Marjolein E., Zuidema, Sytse U., Koopmans, Raymond T. C. M., and Life Course Epidemiology (LCE)
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- 2020
26. Fatigue and physical disability in patients with multiple sclerosis: a structural equation modeling approach
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Bol, Yvonne, Duits, Annelien A., Lousberg, Richel, Hupperts, Raymond M. M., Lacroix, Michelle H. P., Verhey, Frans R. J., and Vlaeyen, Johan W. S.
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- 2010
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27. Additional file 1 of Permeability of the windows of the brain: feasibility of dynamic contrast-enhanced MRI of the circumventricular organs
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Verheggen, Inge C. M., de Jong, Joost J. A., van Boxtel, Martin P. J., Postma, Alida A., Verhey, Frans R. J., Jansen, Jacobus F. A., and Backes, Walter H.
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Data_FILES - Abstract
Additional file 1. Participant characteristics.
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- 2020
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28. Additional file 4 of Permeability of the windows of the brain: feasibility of dynamic contrast-enhanced MRI of the circumventricular organs
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Verheggen, Inge C. M., de Jong, Joost J. A., van Boxtel, Martin P. J., Postma, Alida A., Verhey, Frans R. J., Jansen, Jacobus F. A., and Backes, Walter H.
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Additional file 4. Contrast enhancement in the CVOs and normal-appearing brain matter.
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- 2020
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29. Cognitive changes in prevalent and incident cardiovascular disease: a 12-year follow-up in the Maastricht Aging Study (MAAS).
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Schievink, Syenna H J, Boxtel, Martin P J van, Deckers, Kay, Oostenbrugge, Robert J van, Verhey, Frans R J, and Köhler, Sebastian
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CARDIOVASCULAR diseases ,COGNITION ,DEMENTIA ,NEUROPSYCHOLOGY ,DISEASE management - Abstract
Aims Cardiovascular disease (CVD) has been suggested to accelerate cognitive decline and to be a risk factor for dementia, but still little is known about the cognitive course after a first cardiovascular event. Therefore, the present study aims to investigate the cognitive trajectories in both prevalent and incident CVD over a 12-year time period in the general population. Methods and results Cognitively healthy participants (age 24–82 years, n = 1823) of a prospective cohort study were serially assessed at baseline, 6 and 12 years. Verbal memory, executive function, and information processing speed were analysed in adults with prevalent, incident, and no CVD. Random effects models were used to test the association between CVD and change in cognitive function over time. At baseline, participants with prevalent CVD showed more decline in memory and information processing speed than healthy controls. Participants with incident CVD also showed more decline in these cognitive domains, but this was only significant in the follow-up period from 6 to 12 years. Associations were more pronounced in participants aged younger than 65 years at baseline, and in sub-analyses with angina pectoris or myocardial infarction as the most prevalent CVD conditions. Conclusion Prevalent and incident CVD predict cognitive decline in middle-aged individuals. Findings for incident CVD suggest that the onset of decline is linked in time with the vascular event itself. Timely CVD management may delay the onset of decline. [ABSTRACT FROM AUTHOR]
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- 2022
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30. Integrated multidisciplinary approach for dementia care
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Verhey, Frans R. J., Wolfs, Claire A. G., Kessels, Alfons, Dirksen, Carmen D., and Severens, Johan L.
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- 2008
31. Integrated multidisciplinary diagnostic approach for dementia care: randomised controlled trial
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Wolfs, Claire A. G., Kessels, Alfons, Dirksen, Carmen D., Severens, Johan L., and Verhey, Frans R. J.
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- 2008
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32. Cognitive functioning in spousal caregivers of dementia patients: findings from the prospective MAASBED study
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de Vugt, Marjolein E., Jolles, Jelle, van Osch, Liesbeth, Stevens, Fred, Aalten, Pauline, Lousberg, Richel, and Verhey, Frans R. J.
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- 2006
33. Cross-national comparisons of the Cambridge Cognitive Examination - revised: the CAMCOG-R
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VERHEY, FRANS R. J., HUPPERT, FELICIA A., KORTEN, EDITH C. C. M., HOUX, PETER, DE VUGT, MARJOLEIN, VAN LANG, NATASJA, DEDEYN, PETER P., SAERENS, JOS, NERI, MIRCO, DE VREESE, LUC, PEÑA-CASANOVA, JORDI, BÖHM, PETER, STOPPE, GABRIELA, FLEISCHMANN, ULRICH, WALLIN, ANDERS, HELLSTRÖM, PER, MIDDELKOOP, HUUB, BOLLEN, WARD, KLINKENBERG, EDWIN L., DERIX, MAYKE M. A., and JOLLES, JELLEMER
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- 2003
34. Exploring perspectives of young onset dementia caregivers with high versus low unmet needs
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Millenaar, Joany K., Bakker, Christian, van Vliet, Deliane, Koopmans, Raymond T. C. M., Kurz, Alexander, Verhey, Frans R. J., de Vugt, Marjolein E., RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, Psychiatrie & Neuropsychologie, and MUMC+: MA Med Staf Spec Psychiatrie (9)
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young onset dementia ,caregivers ,care needs ,ADULT-CHILD ,PEOPLE ,EXPERIENCE ,service use - Abstract
BackgroundThis study is part of the Research to Assess Policies and Strategies for Dementia in the Young project. Information about specific needs in young onset dementia (YOD) will provide the basis for the development of an e-health intervention to assist caregivers in coping with YOD in several European countries. ObjectiveThe aim was to investigate the issues caregivers of people with YOD face. MethodsA qualitative content analysis method was used to analyse interviews with YOD caregivers. Quantitative data of the Needs in Young Onset Dementia study were used to select caregivers based on a ranking of unmet needs, to capture differences and similarities between caregivers that experienced high levels of unmet needs versus those with low levels of unmet needs. Needs were assessed with the Camberwell Assessment of Needs in the Elderly. ResultsFindings revealed the following themes: (i) acceptance; (ii) perception of the relationship; (iii) role adaptation; (iv) Availability of appropriate services; (v) social support; and (vi) awareness in the person with dementia and acceptance of help. Several factors seemed more apparent in the caregivers who experienced few unmet needs opposed to the caregivers who experienced more unmet needs. ConclusionThe current study provides an in-depth perspective on the caregiver's experiences and emphasizes specific themes that could be addressed in future interventions. This might contribute to a caring situation in which the caregiver experiences less unmet needs. Copyright (c) 2017 John Wiley & Sons, Ltd.
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- 2018
35. Lifestyle for Brain Health (LIBRA): a new model for dementia prevention
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Schiepers, Olga J. G., Kohler, Sebastian, Deckers, Kay, Irving, Kate, O'Donnell, Catherine A., van den Akker, Marjan, Verhey, Frans R. J., Vos, Stephanie J. B., de Vugt, Marjolein E., van Boxtel, Martin P. J., RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, Psychiatrie & Neuropsychologie, Family Medicine, RS: CAPHRI - R6 - Promoting Health & Personalised Care, MUMC+: MA Med Staf Spec Psychiatrie (9), Section Neuropsychology, and RS: FPN NPPP I
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lifestyle ,prevention ,ageing ,cognitive function ,dementia - Abstract
ObjectiveModifiable risk factors for dementia were recently identified and compiled in a systematic review. The Lifestyle for Brain Health' (LIBRA) score, reflecting someone's potential for dementia prevention, was studied in a large longitudinal population-based sample with respect to predicting cognitive change over an observation period of up to 16years. MethodsLifestyle for Brain Health was calculated at baseline for 949 participants aged 50-81years from the Maastricht Ageing Study. The predictive value of LIBRA for incident dementia and cognitive impairment was examined by using Cox proportional hazard models and by testing its relation with cognitive decline. ResultsLifestyle for Brain Health predicted future risk of dementia, as well as risk of cognitive impairment. A one-point increase in LIBRA score related to 19% higher risk for dementia and 9% higher risk for cognitive impairment. LIBRA predicted rate of decline in processing speed, but not memory or executive functioning. ConclusionsLifestyle for Brain Health (LIBRA) may help in identifying and monitoring risk status in dementia-prevention programmes, by targeting modifiable, lifestyle-related risk factors.
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- 2018
36. APOEε-4 allele for the diagnosis of Alzheimer's and other dementia disorders in people with mild cognitive impairment in a primary care setting
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Elias-Sonnenschein, Lyzel S., Viechtbauer, Wolfgang, Ramakers, Inez, Ukoumunne, Obioha, Verhey, Frans R. J., Visser, Pieter Jelle, Neurology, NCA - neurodegeneration, and Amsterdam Neuroscience - Neurodegeneration
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Medicine General & Introductory Medical Sciences ,genetic structures ,mental disorders ,Pharmacology (medical) - Abstract
This is a protocol for a Cochrane Review (Diagnostic test accuracy). The objectives are as follows: Our primary objective is to determine the diagnostic accuracy of the APOE‐ε4 allele in detecting AD dementia and other types of dementia in people with MCI in a primary care setting.
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- 2018
37. Alzheimer’s disease pathology: pathways between central norepinephrine activity, memory, and neuropsychiatric symptoms
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Jacobs, Heidi I. L., primary, Riphagen, Joost M., additional, Ramakers, Inez H. G. B., additional, and Verhey, Frans R. J., additional
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- 2019
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38. Pathophysiological subtypes of Alzheimer's disease based on cerebrospinal fluid proteomics.
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Tijms, Betty M, Gobom, Johan, Reus, Lianne, Jansen, Iris, Hong, Shengjun, Dobricic, Valerija, Kilpert, Fabian, Kate, Mara ten, Barkhof, Frederik, Tsolaki, Magda, Verhey, Frans R J, Popp, Julius, Martinez-Lage, Pablo, Vandenberghe, Rik, Lleó, Alberto, Molinuevo, José Luís, Engelborghs, Sebastiaan, Bertram, Lars, Lovestone, Simon, and Streffer, Johannes
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ALZHEIMER'S disease ,CEREBROSPINAL fluid ,PROTEOMICS ,ALZHEIMER'S patients ,PATHOLOGY ,DISEASE progression ,RESEARCH ,NERVE tissue proteins ,BLOOD-brain barrier ,RESEARCH methodology ,PROTEOLYTIC enzymes ,MEDICAL cooperation ,EVALUATION research ,NEUROPSYCHOLOGICAL tests ,COMPARATIVE studies ,RESEARCH funding ,CLUSTER analysis (Statistics) ,PEPTIDES ,LONGITUDINAL method - Abstract
Alzheimer's disease is biologically heterogeneous, and detailed understanding of the processes involved in patients is critical for development of treatments. CSF contains hundreds of proteins, with concentrations reflecting ongoing (patho)physiological processes. This provides the opportunity to study many biological processes at the same time in patients. We studied whether Alzheimer's disease biological subtypes can be detected in CSF proteomics using the dual clustering technique non-negative matrix factorization. In two independent cohorts (EMIF-AD MBD and ADNI) we found that 705 (77% of 911 tested) proteins differed between Alzheimer's disease (defined as having abnormal amyloid, n = 425) and controls (defined as having normal CSF amyloid and tau and normal cognition, n = 127). Using these proteins for data-driven clustering, we identified three robust pathophysiological Alzheimer's disease subtypes within each cohort showing (i) hyperplasticity and increased BACE1 levels; (ii) innate immune activation; and (iii) blood-brain barrier dysfunction with low BACE1 levels. In both cohorts, the majority of individuals were labelled as having subtype 1 (80, 36% in EMIF-AD MBD; 117, 59% in ADNI), 71 (32%) in EMIF-AD MBD and 41 (21%) in ADNI were labelled as subtype 2, and 72 (32%) in EMIF-AD MBD and 39 (20%) individuals in ADNI were labelled as subtype 3. Genetic analyses showed that all subtypes had an excess of genetic risk for Alzheimer's disease (all P > 0.01). Additional pathological comparisons that were available for a subset in ADNI suggested that subtypes showed similar severity of Alzheimer's disease pathology, and did not differ in the frequencies of co-pathologies, providing further support that found subtypes truly reflect Alzheimer's disease heterogeneity. Compared to controls, all non-demented Alzheimer's disease individuals had increased risk of showing clinical progression (all P < 0.01). Compared to subtype 1, subtype 2 showed faster clinical progression after correcting for age, sex, level of education and tau levels (hazard ratio = 2.5; 95% confidence interval = 1.2, 5.1; P = 0.01), and subtype 3 at trend level (hazard ratio = 2.1; 95% confidence interval = 1.0, 4.4; P = 0.06). Together, these results demonstrate the value of CSF proteomics in studying the biological heterogeneity in Alzheimer's disease patients, and suggest that subtypes may require tailored therapy. [ABSTRACT FROM AUTHOR]
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- 2020
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39. Advanced Glycation End Product (AGE) Accumulation in the Skin is Associated with Depression: The Maastricht Study
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van Dooren, Fleur E. P., Pouwer, Frans, Schalkwijk, Casper G., Sep, Simone J. S., Stehouwer, Coen D. A., Henry, Ronald M. A., Dagnelie, Pieter C., Schaper, Nicolaas C., van der Kallen, Carla J. H., Koster, Annemarie, Denollet, Johan, Verhey, Frans R. J., Schram, Miranda T., Promovendi MHN, RS: CARIM - R3.01 - Vascular complications of diabetes and the metabolic syndrome, Interne Geneeskunde, MUMC+: HVC Pieken Maastricht Studie (9), MUMC+: MA Interne Geneeskunde (3), RS: CAPHRI - R5 - Optimising Patient Care, Epidemiologie, MUMC+: MA Endocrinologie (9), RS: CAPHRI - R2 - Creating Value-Based Health Care, RS: CARIM - R3.02 - Hypertension and target organ damage, Sociale Geneeskunde, RS: CAPHRI - R4 - Health Inequities and Societal Participation, MUMC+: MA Med Staf Spec Psychiatrie (9), RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience, and Psychiatrie & Neuropsychologie
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SYMPTOMS ,diabetes ,RECEPTOR ,advanced glycation end products ,INTERNATIONAL NEUROPSYCHIATRIC INTERVIEW ,TYPE-2 DIABETES-MELLITUS ,cohort ,DSM-IV ,RISK-FACTOR ,GLYCEMIC CONTROL ,depression ,OXIDATIVE STRESS ,ARTERIAL STIFFNESS ,METAANALYSIS - Abstract
BackgroundDepression is a highly prevalent disease with a high morbidity and mortality risk. Its pathophysiology is not entirely clear. However, type 2 diabetes is an important risk factor for depression. One mechanism that may explain this association may include the formation of advanced glycation end products (AGEs). We therefore investigated the association of AGEs with depressive symptoms and depressive disorder. In addition, we examined whether the potential association was present for somatic and/or cognitive symptoms of depression. MethodsCross-sectional data were used from the Maastricht Study (N = 862, mean age 59.8 8.5 years, 55% men). AGE accumulation was measured with skin autofluorescence (SAF) by use of the AGE Reader. Plasma levels of protein-bound pentosidine were measured with high-performance liquid chromatography and fluorescence detection. N epsilon-(carboxymethyl)lysine (CML) and N epsilon-(carboxyethyl)lysine (CEL) were measured with ultraperformance liquid chromatography and tandem mass spectrometry. Depressive symptoms and depressive disorder were assessed by the nine-item Patient Health Questionnaire and the Mini-International Neuropsychiatric Interview. ResultsHigher SAF was associated with depressive symptoms ( = 0.42, 95% CI 0.12-0.73, P = .007) and depressive disorder (OR = 1.42, 95% CI 1.04-1.95, P = .028) after adjustment for age, sex, type 2 diabetes, smoking, BMI, and kidney function. Plasma pentosidine, CML, and CEL were not independently associated with depressive symptoms and depressive disorder. ConclusionsThis study shows that AGE accumulation in the skin is independently associated with higher levels of depressive symptoms and depressive disorder. This association is present for both somatic and cognitive symptoms of depression. This might suggest that AGEs are involved in the development of depression.
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- 2017
40. STROKOG (stroke and cognition consortium): An international consortium to examine the epidemiology, diagnosis, and treatment of neurocognitive disorders in relation to cerebrovascular disease
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Sachdev, Perminder S, Lo, Jessica W, Bae, Hee-Joon, Linden, Thomas, Blomstrand, Christian, Fagerberg, Björn, Skoog, Ingmar, Godefroy, Olivier, Barbay, Mélanie, Roussel, Martine, Lee, Byung-Chul, Yu, Kyung-Ho, Lim, Jae-Sung, Wardlaw, Joanna, Makin, Stephen J, Doubal, Fergus N, Chappell, Francesca M, Srikanth, Velandai K, Thrift, Amanda G, Donnan, Geoffrey A, Kandiah, Nagaendran, Chander, Russell J, Lin, Xuling, Brodtmann, Amy, Cordonnier, Charlotte, Moulin, Solene, Rossi, Costanza, Sabayan, Behnam, Stott, David J, Jukema, J Wouter, Melkas, Susanna, Jokinen, Hanna, Erkinjuntti, Timo, Mok, Vincent Ct, Werden, Emilio, Wong, Adrian, Lam, Bonnie Yk, Leys, Didier, Hénon, Hilde, Bombois, Stéphanie, Sachdev, Perminder, Cumming, Toby, Köhler, Sebastian, Verhey, Frans R J, Dong, Yan-Hong, Tan, Hui Hui, Chen, Christopher, Crawford, John D, Xin, Xu, Kalaria, Raj N, Allan, Louise M, Akinyemi, Rufus O, Ogunniyi, Adesola, Klimkowicz-Mrowiec, Aleksandra, Dichgans, Martin, Wollenweber, Frank A, Zietemann, Vera, Hoffmann, Michael, Mellon, Lisa, Desmond, David W, Hickey, Anne, Williams, David, Mok, Vincent C T, Bordet, Régis, Lam, Bonnie Y K, Lipnicki, Darren M, Kochan, Nicole A, STROKOG, Mendyk, Anne-Marie, Gelé, Patrick, Deplanque, Dominique, Verhey, Frans Rj, Xu, Jing, Akinyemi, Rufus, Kalariai, Raj N, Metacohorts Consortium, Department of Chemistry, Indiana University, Indiana University [Bloomington], Indiana University System-Indiana University System, School of Civil Engineering, The University of Queensland, School of Civil Engineering, Troubles cognitifs dégénératifs et vasculaires - U 1171 - EA 1046 (TCDV), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Lille Neurosciences & Cognition - U 1172 (LilNCog), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Maastricht University Medical Centre (MUMC), Maastricht University [Maastricht], McGill University = Université McGill [Montréal, Canada], University of Ibadan, Uniwersytet Jagielloński w Krakowie = Jagiellonian University (UJ), Department of Computer Science [ETH Zürich] (D-INFK), Eidgenössische Technische Hochschule - Swiss Federal Institute of Technology [Zürich] (ETH Zürich), Institute of Neuroscience and Physiology [Göteborg], Service de neurologie [Amiens], CHU Amiens-Picardie, Laboratoire de Neurosciences Fonctionnelles et Pathologies - UR UPJV 4559 (LNFP), Université de Picardie Jules Verne (UPJV), University of Edinburgh, Harvard Medical School [Boston] (HMS), Interuniversity Cardiology Institute Netherlands, Helsinki University Central Hospital, Helsingin yliopisto = Helsingfors universitet = University of Helsinki, HUCH, Neurologian yksikkö, Clinicum, Department of Neurosciences, University of Helsinki, and HUS Neurocenter
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Gerontology ,endocrine system ,medicine.medical_specialty ,[SDV]Life Sciences [q-bio] ,education ,International consortium ,030204 cardiovascular system & hematology ,Post-stroke dementia ,Special Section: Vascular Contributions to Alzheimer's Disease ,Vascular dementia ,3124 Neurology and psychiatry ,03 medical and health sciences ,0302 clinical medicine ,Epidemiology ,medicine ,ddc:610 ,Stroke ,Data harmonization ,Post stroke dementia ,3112 Neurosciences ,Cognition ,medicine.disease ,3. Good health ,Small vessel disease ,Psychiatry and Mental health ,Vascular cognitive disorder ,Cohort studies ,Neurology (clinical) ,Psychology ,Neurocognitive ,030217 neurology & neurosurgery ,Cohort study - Abstract
Introduction: \ud \ud The Stroke and Cognition consortium (STROKOG) aims to facilitate a better understanding of the determinants of vascular contributions to cognitive disorders and help improve the diagnosis and treatment of vascular cognitive disorders (VCD).\ud \ud Methods: \ud \ud Longitudinal studies with ≥75 participants who had suffered or were at risk of stroke or TIA and which evaluated cognitive function were invited to join STROKOG. The consortium will facilitate projects investigating rates and patterns of cognitive decline, risk factors for VCD, and biomarkers of vascular dementia.\ud \ud Results: \ud \ud Currently, STROKOG includes 25 (21 published) studies, with 12,092 participants from five continents. The duration of follow-up ranges from 3 months to 21 years.\ud \ud Discussion: \ud \ud Although data harmonization will be a key challenge, STROKOG is in a unique position to reuse and combine international cohort data and fully explore patient level characteristics and outcomes. STROKOG could potentially transform our understanding of VCD and have a worldwide impact on promoting better vascular cognitive outcomes.
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- 2017
41. Emotional reactivity to daily life stress in spousal caregivers of people with dementia: An experience sampling study
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van Knippenberg, Rosalia J. M., primary, de Vugt, Marjolein E., additional, Ponds, Rudolf W., additional, Verhey, Frans R. J., additional, and Myin-Germeys, Inez, additional
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- 2018
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42. Development and feasibility of Inlife: A pilot study of an online social support intervention for informal caregivers of people with dementia
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Dam, Alieske E. H., primary, van Boxtel, Martin P. J., additional, Rozendaal, Nico, additional, Verhey, Frans R. J., additional, and de Vugt, Marjolein E., additional
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- 2017
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43. Coronary heart disease and risk for cognitive impairment or dementia: Systematic review and meta-analysis
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Deckers, Kay, primary, Schievink, Syenna H. J., additional, Rodriquez, Maria M. F., additional, van Oostenbrugge, Robert J., additional, van Boxtel, Martin P. J., additional, Verhey, Frans R. J., additional, and Köhler, Sebastian, additional
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- 2017
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44. ESTIMATED GLOMERULAR FILTRATION RATE, (MICRO) ALBUMINURIA AND COGNITIVE PERFORMANCE: THE MAASTRICHT STUDY
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Martens, Remy, Kooman, Jeroen P., Stehouwer, Coen D. A., Dagnelie, Pieter C., van der Kallen, Carla J. H., Koster, Annemarie, Kroon, Abraham A., Leunissen, Karel M. L., Nijpels, Giel, van der Sande, Frank M., Schaper, Nicolaas C., Sep, Simone J. S., Verhey, Frans R. J., van Boxtel, Martin P. J., Schram, Miranda T., Henry, Ronald M. A., RS: NUTRIM - R3 - Chronic inflammatory disease and wasting, Promovendi NTM, MUMC+: MA Nefrologie (9), Interne Geneeskunde, RS: CARIM - R3.01 - Vascular complications of diabetes and the metabolic syndrome, RS: CAPHRI School for Public Health and Primary Care, Epidemiologie, Sociale Geneeskunde, RS: CARIM - R3.02 - Hypertension and target organ damage, Psychiatrie & Neuropsychologie, and RS: FPN NPPP I
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- 2016
45. Effectiveness of an online social support intervention for caregivers of people with dementia: the study protocol of a randomised controlled trial
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Dam, Alieske E. H., primary, de Vugt, Marjolein E., additional, van Boxtel, Martin P. J., additional, and Verhey, Frans R. J., additional
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- 2017
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46. Cognitive changes in prevalent and incident cardiovascular disease: a 12-year follow-up in the Maastricht Aging Study (MAAS)
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Schievink, Syenna H J, primary, van Boxtel, Martin P J, additional, Deckers, Kay, additional, van Oostenbrugge, Robert J, additional, Verhey, Frans R J, additional, and Köhler, Sebastian, additional
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- 2017
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47. Cerebral Pathology and Cognition in Diabetes: The Merits of Multiparametric Neuroimaging
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van Bussel, Frank C. G., primary, Backes, Walter H., additional, Hofman, Paul A. M., additional, van Oostenbrugge, Robert J., additional, van Boxtel, Martin P. J., additional, Verhey, Frans R. J., additional, Steinbusch, Harry W. M., additional, Schram, Miranda T., additional, Stehouwer, Coen D. A., additional, Wildberger, Joachim E., additional, and Jansen, Jacobus F. A., additional
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- 2017
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48. Diagnostic impact of [18F]flutemetamol PET in early-onset dementia
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Zwan, Marissa D., primary, Bouwman, Femke H., additional, Konijnenberg, Elles, additional, van der Flier, Wiesje M., additional, Lammertsma, Adriaan A., additional, Verhey, Frans R. J., additional, Aalten, Pauline, additional, van Berckel, Bart N. M., additional, and Scheltens, Philip, additional
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- 2017
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49. A profile of The Clinical Course of Cognition and Comorbidity in Mild Cognitive Impairment and Dementia Study (The 4C study): two complementary longitudinal, clinical cohorts in the Netherlands
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Liao, Weiqi, primary, Hamel, Renske E. G., additional, Olde Rikkert, Marcel G. M., additional, Oosterveld, Saskia M., additional, Aalten, Pauline, additional, Verhey, Frans R. J., additional, Scheltens, Philip, additional, Sistermans, Nicole, additional, Pijnenburg, Yolande A. L., additional, van der Flier, Wiesje M., additional, Ramakers, Inez H. G. B., additional, and Melis, René J. F., additional
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- 2016
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50. Prevalence of cerebral amyloid pathology in persons without dementia
- Author
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Jansen, Willemijn J., Ossenkoppele, Rik, Knol, Dirk L., Tijms, Betty M., Scheltens, Philip, Verhey, Frans R. J., Visser, Pieter Jelle, Aalten, Pauline, Aarsland, Dag, Alcolea, Daniel, Alexander, Myriam, Roe, Catherine M., Rot, Uros, Rowe, Christopher C., Rüther, Eckart, Sabri, Osama, Sanchez-Juan, Páscual, Santana, Isabel, Sarazin, Marie, Schröder, Johannes, Schütte, Christin, Almdahl, Ina S., Seo, Sang W., Soetewey, Femke, Soininen, Hilkka, Spiru, Luiza, Struyfs, Hanne, Teunissen, Charlotte E., Tsolaki, Magda, Vandenberghe, Rik, Verbeek, Marcel M., Villemagne, Victor L., Arnold, Steven E., Vos, Stephanie J. B., van Waalwijk van Doorn, Linda J. C., Waldemar, Gunhild, Wallin, Anders, Wallin, Åsa K., Wiltfang, Jens, Wolk, David A., Zboch, Marzena, Zetterberg, Henrik, Baldeiras, Inês, Barthel, Henryk, van Berckel, Bart N. M., 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 H. G. B., Rami, Lorena, Resende de Oliveira, Catarina, Rinne, Juha O., Rodrigue, Karen M., Rodríguez-Rodríguez, Eloy, and Repositório da Universidade de Lisboa
- Abstract
Copyright © 2015 American Medical Association. All rights reserved., Importance: Cerebral 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. Objective: To 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 sources: Relevant 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 selection: Studies 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 synthesis: Individual 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 measures: Prevalence 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. Results: The 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 relevance: Among 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., The research leading to these results 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 Programme (FP7/2007-2013) and EFPIA companies’ in-kind contribution. BIOMARKAPD is an EU Joint Programme–Neurodegenerative Disease Research (JPND) project. The project is supported through national funding organizations under the aegis of JPND (http://www.jpnd.eu). In the Netherlands, this is ZonMw. 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 as part of the 6th framework programme (contract No. 37670). This research was performed within the framework of the Center for Translational Molecular Medicine (CTTM) (http://www.ctmm.nl), project LeARN (grant 02N-101). The AIBL study was funded in part by the study partners (Australian Commonwealth Scientific Industrial and Research Organization [CSIRO], Edith Cowan University [ECU], Mental Health Research Institute [MHRI], Alzheimer’s Australia [AA], National Ageing Research Institute [NARI], Austin Health, CogState, Hollywood Private Hospital, Sir Charles Gardner Hospital). The study also received support from the National Health and Medical Research Council (NHMRC) and the Dementia Collaborative Research Centres program (DCRC2), as well as ongoing funding from the Science and Industry Endowment Fund (SIEF). Data collection and sharing for this project was funded by the Alzheimer’s Disease Neuroimaging Initiative (ADNI) (National Institutes of Health grant U01 AG024904) and the US Department of Defense ADNI (W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging and the National Institute of Biomedical Imaging and Bioengineering and through generous contributions from the following: Alzheimer’s Association; Alzheimer’s Drug Discovery Foundation; BioClinica; Biogen Idec; Bristol-Myers Squibb Company; Eisai; Elan Pharmaceuticals; Eli Lilly; F. Hoffmann-La Roche and its affiliated company Genentech; GE Healthcare; Innogenetics; IXICO; Janssen Alzheimer Immunotherapy Research & Development; Johnson & Johnson Pharmaceutical Research & Development; Medpace; Merck; Meso Scale Diagnostics; NeuroRx Research; Novartis Pharmaceuticals; Pfizer; Piramal Imaging; Servier; Synarc; and Takeda Pharmaceutical. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (http://www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer’s Disease Cooperative Study at the University of California, San Diego. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California. The Dementia Competence Network (DCN) has been supported by a grant from the German Federal Ministry of Education and Research (BMBF): Kompetenznetz Demenzen (01GI0420). Additional funding related to the randomized clinical trials came from Janssen-Cilag and Merz Pharmaceuticals. The latter funds were exclusively used for personnel, pharmaceuticals, blistering and shipment of medication, and monitoring and as capitation fees for recruiting centers. Funding source for the Chandigarh study is the Indian Council of Medical Research (ICMR), India. Funding for the St Louis contribution was provided by the National Institute on Aging (P50 AG005681, P01 AG003991, and P01 AG026276); Fred Simmons and Olga Mohan, and the Charles and Joanne Knight Alzheimer’s Research Initiative of the Washington University Knight Alzheimer’s Disease Research Center. The Tours study received financial support of the French Ministry of Health grant PHRC-N 2008 1004 and the EC-FP6-project DiMI, LSHB-CT-2005-512146. The Caen study was funded by Agence Nationale de la Recherche, Programme Hospitalier de Recherche Clinique, Région Basse Normandie, and Institut National de la Santé et de la Recherche Médicale (Inserm). The research leading to the Munich contribution to the Mattsson multicenter study has received funding from the program “Investissements d’avenir” (ANR-10-IAIHU-06). The study from Pittsburgh was supported by National Institutes of Health grants (P50 AG005133, R37 AG025516, P01 AG025204). The New York contributions to the Mattsson multicenter study were in part supported by P30 AG008051, R01 AG13616, R01 AG022374, and R01 AG12101. Data from Brescia in this article were collected by Translational Outpatient Memory Clinic (TOMC) working group at IRCCS Fatebenefratelli in Brescia, Italy. Contributors to the TOMC are G. Amicucci, S. Archetti, L. Benussi, G. Binetti, L. Bocchio-Chiavetto, C. Bonvicini, E. Canu, F. Caobelli, E. Cavedo, E. Chittò, M. Cotelli, M. Gennarelli, S. Galluzzi, C. Geroldi, R. Ghidoni, R. Giubbini, U. P. Guerra, G. Kuffenschin, G. Lussignoli, D. Moretti, B. Paghera, M. Parapini, C. Porteri, M. Romano, S. Rosini, I. Villa, R. Zanardini, and O. Zanetti. The JPND Project is supported in Italy by the Italian Ministry of Health. The assembling of the TU Munich data set was supported in part by the German research foundation (Deutsche Forschungsgemeinschaft) (HE 4560/1-2, DR 445/3-1 and DR 445/4-1 to A.D.), and by a KKF grant for clinical research of the Technische Universität München (to A.D. and T.G.). The Florbetaben phase 2 study from which data were derived for this multicenter evaluation was sponsored by Bayer Healthcare/Piramal Imaging (Berlin, Germany). This work was supported by the University of Antwerp Research Fund; the Alzheimer Research Foundation (SAO-FRA); the Research Foundation Flanders (FWO); the Agency for Innovation by Science and Technology (IWT); the Belgian Science Policy Office Interuniversity Attraction Poles (IAP) program; and the Flemish Government–initiated Methusalem excellence grant.
- Published
- 2015
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