171 results on '"Teunissen, C. E."'
Search Results
2. ASURE Clinical Trial Protocol: A Randomized, Placebo-Controlled, Proof-of-Concept Study Aiming to Evaluate Safety and Target Engagement following Administration of TW001 in Early Alzheimer’s Disease Patients
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Oosthoek, Marlies, Lili, A., Almeida, A., van Loosbroek, O., van der Geest, R., de Greef-van der Sandt, I., van Bokhoven, P., Sikkes, S. A. M., Teunissen, C. E., and Vijverberg, E. G. B.
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- 2023
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3. Serum neurofilament light release levels as marker of neurotoxicity in general anesthesia versus hypnosis: A prospective non-randomized trial.
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MESTDAGH, F., ABENE, S., BERLIERE, M., DOCQUIER, M. -A., WATREMEZ, C., ROELANTS, F., TOUIL, N., ROBU, B. C., LUPU, I.-M., ROBERT, A., MOURAD, M., BUEMI, A., TEUNISSEN, C. E., VAN REGEMORTER, V., and MOMENI, M.
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- 2024
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4. A neurologist’s perspective on serum neurofilament light in the memory clinic: a prospective implementation study
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Willemse, E. A. J., Scheltens, P., Teunissen, C. E., and Vijverberg, E. G. B.
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- 2021
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5. Characterization of symptoms and determinants of disease burden in dementia with Lewy bodies: DEvELOP design and baseline results
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van de Beek, M., van Steenoven, I., van der Zande, J. J., Porcelijn, I., Barkhof, F., Stam, C. J., Raijmakers, P. G. H. M., Scheltens, P., Teunissen, C. E., van der Flier, W. M., and Lemstra, A. W.
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- 2021
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6. Olfactory and gustatory functioning and food preferences of patients with Alzheimer’s disease and mild cognitive impairment compared to controls: the NUDAD project
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Doorduijn, A. S., de van der Schueren, M. A. E., van de Rest, O., de Leeuw, F. A., Fieldhouse, J. L. P., Kester, M. I., Teunissen, C. E., Scheltens, P., van der Flier, W. M., Visser, M., and Boesveldt, S.
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- 2020
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7. Sex-specific associations with cerebrospinal fluid biomarkers in dementia with Lewy bodies
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van de Beek, M., Babapour Mofrad, R., van Steenoven, I., Vanderstichele, H., Scheltens, P., Teunissen, C. E., Lemstra, A. W., and van der Flier, W. M.
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- 2020
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8. Systemic and intrathecal immune activation in association with cerebral and cognitive outcomes in paediatric HIV
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Blokhuis, C., Peeters, C. F. W., Cohen, S., Scherpbier, H. J., Kuijpers, T. W., Reiss, P., Kootstra, N. A., Teunissen, C. E., and Pajkrt, D.
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- 2019
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9. The role of appraisal and coping style in relation with societal participation in fatigued patients with multiple sclerosis: a cross-sectional multiple mediator analysis
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van den Akker, Lizanne Eva, Beckerman, Heleen, Collette, Emma Hubertine, Bleijenberg, Gijs, Dekker, Joost, Knoop, Hans, de Groot, Vincent, de Groot, V., Beckerman, H., Malekzadeh, A., van den Akker, L. E., Looijmans, M., Sanches, S. A., Dekker, J., Collette, E. H., van Oosten, B. W., Teunissen, C. E., Blankenstein, M. A., Eijssen, I. C. J. M., Rietberg, M., Heine, M., Verschuren, O., Kwakkel, G., Visser-Meily, J. M. A., van de Port, I. G. L., Lindeman, E., Blikman, L. J. M., van Meeteren, J., Bussmann, J. B. J., Stam, H. J., Hintzen, R. Q., Hacking, H. G. A., Hoogervorst, E. L., Frequin, S. T. F. M., Knoop, H., de Jong, B. A., de Laat, F. A. J., Verhulsdonck, M. C., van Munster, E. T. H., Oosterwijk, C. J., Aarts, G. J., and TREFAMS-ACE study group
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- 2016
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10. The role of serum and CSF levels of NfL and GFAP in predicting cognitive functioning in people with multiple sclerosis
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van Dam, M., de Jong, B. A., Willemse, E. A. J., Nauta, I. M., Huiskamp, M., Klein, M., Moraal, B., de Geus-Driessen, S., Geurts, J. J. G., Uitdehaag, B. M. J., Teunissen, C. E., Hulst, H. E., Anatomy and neurosciences, Amsterdam Neuroscience - Neuroinfection & -inflammation, Neurology, APH - Quality of Care, Clinical chemistry, Internal medicine, Medical psychology, Radiology and nuclear medicine, and Amsterdam Neuroscience - Neurodegeneration
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- 2022
11. Concomitant AD pathology affects clinical manifestation and survival in dementia with Lewy bodies
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Lemstra, A W, de Beer, M H, Teunissen, C E, Schreuder, C, Scheltens, P, van der Flier, W M, and Sikkes, S A M
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- 2017
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12. Genetics and Not Shared Environment Explains Familial Resemblance in Adult Metabolomics Data
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Pool, Rene, Hagenbeek, Fiona A., Hendriks, Anne M., van Dongen, Jenny, Willemsen, Gonneke, de Geus, Eco, van Dijk, Ko Willems, Verhoeven, Aswin, Suchiman, H. Eka, Beekman, Marian, Slagboom, P. Eline, Harms, Amy C., Hankemeier, Thomas, Boomsma, Dorret, I, Beekman, M., Suchiman, H. E. D., Amin, N., Beulens, J. W., van der Bom, J. A., Bomer, N., Demirkan, A., van Hilten, J. A., Meessen, J. M. T. A., Pool, R., Moed, M. H., Fu, J., Onderwater, G. L. J., Rutters, F., So-Osman, C., van der Flier, W. M., van der Heijden, A. A. W. A., van der Spek, A., Asselbergs, F. W., Boersma, E., Elders, P. M., Geleijnse, J. M., Ikram, M. A., Kloppenburg, M., Meulenbelt, I, Mooijaart, S. P., Nelissen, R. G. H. H., Netea, M. G., Penninx, B. W. J. H., Stehouwer, C. D. A., Teunissen, C. E., Terwindt, G. M., 't Hart, L. M., van den Maagdenberg, A. M. J. M., van der Harst, P., van der Horst, I. C. C., van der Kallen, C. J. H., van Greevenbroek, M. M. J., van Spil, W. E., Wijmenga, C., Zwinderman, A. H., Zhernikova, A., Jukema, J. W., Wolf, J. J. H. Barkey, Cats, D., Mei, H., Slofstra, M., Swertz, M., van den Akker, E. B., Deelen, J., Reinders, M. J. T., Boomsma, D., I, van Duijn, C. M., Slagboom, P. E., Interne Geneeskunde, MUMC+: MA Interne Geneeskunde (3), MUMC+: MA Med Staf Artsass Interne Geneeskunde (9), MUMC+: MA Endocrinologie (9), MUMC+: MA Maag Darm Lever (9), MUMC+: MA Hematologie (9), MUMC+: MA Medische Oncologie (9), MUMC+: MA Nefrologie (9), MUMC+: MA Reumatologie (9), RS: Carim - V01 Vascular complications of diabetes and metabolic syndrome, Groningen Institute for Gastro Intestinal Genetics and Immunology (3GI), Molecular Neuroscience and Ageing Research (MOLAR), Cardiovascular Centre (CVC), Critical care, Anesthesiology, Peri-operative and Emergency medicine (CAPE), Center for Liver, Digestive and Metabolic Diseases (CLDM), Medical Microbiology and Infection Prevention, Graduate School, Tytgat Institute for Liver and Intestinal Research, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, Obstetrics and Gynaecology, Cardiology, Public and occupational health, Gastroenterology and Hepatology, Paediatric Endocrinology, Biological Psychology, APH - Health Behaviors & Chronic Diseases, APH - Personalized Medicine, APH - Mental Health, APH - Methodology, Epidemiology and Data Science, Obstetrics and gynaecology, ACS - Diabetes & metabolism, ACS - Heart failure & arrhythmias, Anatomy and neurosciences, Anesthesiology, General practice, Internal medicine, Psychiatry, Amsterdam Neuroscience - Complex Trait Genetics, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, Laboratory Medicine, Amsterdam Neuroscience - Neurodegeneration, Amsterdam Neuroscience - Neuroinfection & -inflammation, Amsterdam Reproduction & Development (AR&D), AMS - Musculoskeletal Health, AMS - Tissue Function & Regeneration, Rheumatology, Gastroenterology and hepatology, APH - Aging & Later Life, and APH - Digital Health
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Male ,Netherlands Twin Register (NTR) ,0301 basic medicine ,Shared environment ,Metabolite ,lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4] ,Genome-wide association study ,heritability ,METABOLITES ,Keywords: Classical twin design ,chemistry.chemical_compound ,0302 clinical medicine ,metabolite classes ,Twins, Dizygotic ,EPIDEMIOLOGY ,Classical twin design ,Genetics (clinical) ,Genetics ,HERITABILITY ,shared environment ,Obstetrics and Gynecology ,Phenotype ,Quartile ,Metabolome ,Female ,Adult ,Dizygotic twin ,POWER ,TWIN ,Environment ,Biology ,enrichment analysis ,03 medical and health sciences ,All institutes and research themes of the Radboud University Medical Center ,Metabolomics ,AGE ,Diseases in Twins ,Humans ,Family ,GENOME-WIDE ASSOCIATION ,Classical twin design [Keywords] ,Twins, Monozygotic ,PROFILES ,Heritability ,Diet ,Metabolomics data ,030104 developmental biology ,chemistry ,Pediatrics, Perinatology and Child Health ,Gene-Environment Interaction ,030217 neurology & neurosurgery - Abstract
Metabolites are small molecules involved in cellular metabolism where they act as reaction substrates or products. The term ‘metabolomics’ refers to the comprehensive study of these molecules. The concentrations of metabolites in biological tissues are under genetic control, but this is limited by environmental factors such as diet. In adult mono- and dizygotic twin pairs, we estimated the contribution of genetic and shared environmental influences on metabolite levels by structural equation modeling and tested whether the familial resemblance for metabolite levels is mainly explained by genetic or by environmental factors that are shared by family members. Metabolites were measured across three platforms: two based on proton nuclear magnetic resonance techniques and one employing mass spectrometry. These three platforms comprised 237 single metabolic traits of several chemical classes. For the three platforms, metabolites were assessed in 1407, 1037 and 1116 twin pairs, respectively. We carried out power calculations to establish what percentage of shared environmental variance could be detected given these sample sizes. Our study did not find evidence for a systematic contribution of shared environment, defined as the influence of growing up together in the same household, on metabolites assessed in adulthood. Significant heritability was observed for nearly all 237 metabolites; significant contribution of the shared environment was limited to 6 metabolites. The top quartile of the heritability distribution was populated by 5 of the 11 investigated chemical classes. In this quartile, metabolites of the class lipoprotein were significantly overrepresented, whereas metabolites of classes glycerophospholipids and glycerolipids were significantly underrepresented.
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- 2020
13. Impact of white matter hyperintensity location on depressive symptoms in memory-clinic patients
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Leeuwis, Anna E., Weaver, Nick A., Biesbroek, J. Matthijs, Exalto, L. G., Kuijf, Hugo J., Hooghiemstra, Astrid M., Prins, Niels D., Scheltens, Philip, Barkhof, Frederik, van der Flier, Wiesje M., Biessels, Geert Jan, Benedictus, M. R., Bremer, J., Leijenaar, J., Scheltens, P., Tijms, B. M., Wattjes, M. P., Teunissen, C. E., Koene, T., van den Berg, E., van den Brink, H., Boomsma, J. M. F., Ferro, D. A., Frijns, C. J. M., Groeneveld, O., Heinen, R., Heringa, S. M., Kappelle, L. J., Reijmer, Y. D., Verwer, J., de Bresser, J., Koek, H. L., Boss, H. M., Weinstein, H. C., Neurology, Amsterdam Neuroscience - Neurodegeneration, Radiology and nuclear medicine, APH - Personalized Medicine, APH - Methodology, Immunology, and Pediatrics
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Male ,medicine.medical_specialty ,Population ,Pyramidal Tracts ,Neuroimaging ,Comorbidity ,computer.software_genre ,Cohort Studies ,White matter ,03 medical and health sciences ,0302 clinical medicine ,Voxel ,Internal medicine ,medicine ,Journal Article ,Humans ,Dementia ,Cognitive Dysfunction ,Pharmacology (medical) ,Cognitive decline ,education ,Geriatric Assessment ,Biological Psychiatry ,Aged ,Psychiatric Status Rating Scales ,education.field_of_study ,030214 geriatrics ,Depression ,business.industry ,Middle Aged ,medicine.disease ,Magnetic Resonance Imaging ,White Matter ,Cerebrovascular Disorders ,Psychiatry and Mental health ,medicine.anatomical_structure ,Corticospinal tract ,Female ,Geriatric Depression Scale ,Biological psychiatry ,business ,computer ,030217 neurology & neurosurgery ,Research Paper - Abstract
Background: We investigated the association between white matter hyperintensity location and depressive symptoms in a memoryclinic population using lesion–symptom mapping.Methods: We included 680 patients with vascular brain injury from the TRACE-VCI cohort (mean age ± standard deviation: 67 ± 8 years; 52% female): 168 patients with subjective cognitive decline, 164 with mild cognitive impairment and 348 with dementia. We assessed depressive symptoms using the Geriatric Depression Scale. We applied assumptionfree voxel-based lesion–symptom mapping, adjusted for age, sex, total white matter hyperintensity volume and multiple testing. Next, we applied exploratory region-of-interest linear regression analyses of major white matter tracts, with additional adjustment for diagnosis.Results: Voxel-based lesion–symptom mapping identified voxel clusters related to the Geriatric Depression Scale in the left corticospinal tract. Region-of-interest analyses showed no relation between white matter hyperintensity volume and the Geriatric Depression Scale, but revealed an interaction with diagnosis in the forceps minor, where larger regional white matter hyperintensity volume was associated with more depressive symptoms in subjective cognitive decline (β = 0.26, p < 0.05), but not in mild cognitive impairment or dementia.Limitations: We observed a lack of convergence of findings between voxel-based lesion–symptom mapping and region-of-interest analyses, which may have been due to small effect sizes and limited lesion coverage despite the large sample size. This warrants replication of our findings and further investigation in other cohorts.Conclusion: This lesion–symptom mapping study in depressive symptoms indicates the corticospinal tract and forceps minor as strategic tracts in which white matter hyperintensity is associated with depressive symptoms in memory-clinic patients with vascular brain injury. The impact of white matter hyperintensity on depressive symptoms is modest, but it appears to depend on the location of white matter hyperintensity and disease severity.
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- 2019
14. Clinical relevance of acute cerebral microinfarcts in vascular cognitive impairment
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Ferro, Doeschka A., van den Brink, Hilde, Exalto, Lieza G., Boomsma, Jooske M. F., Barkhof, Frederik, Prins, Niels D., van der Flier, Wiesje M., Biessels, Geert Jan, Benedictus, M. R., Bremer, J., Leijenaar, J., Tijms, B. M., Wattjes, M. P., Heringa, S. M., Kappelle, L. J., Reijmer, Y. D., Hamaker, M., Faaij, R., Pleizier, M., Vriens, E., Boss, H. M., Weinstein, H. C., Scheltens, P., Teunissen, C. E., van den Berg, E., Groeneveld, O., Heinen, R., Verwer, J., de Bresser, J., Kuijf, H. J., Koek, H. L., Neurology, Radiology and nuclear medicine, Amsterdam Neuroscience - Neurodegeneration, APH - Personalized Medicine, APH - Methodology, Pediatrics, Erasmus MC other, and Immunology
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medicine.medical_specialty ,medicine.diagnostic_test ,business.industry ,Memory clinic ,Magnetic resonance imaging ,Odds ratio ,medicine.disease ,Hyperintensity ,Internal medicine ,medicine ,Cardiology ,Dementia ,Clinical significance ,Neurology (clinical) ,Vascular dementia ,business ,Stroke - Abstract
ObjectiveTo determine the occurrence of acute cerebral microinfarcts (ACMIs) in memory clinic patients and relate their presence to vascular risk and cognitive profile, CSF and neuroimaging markers, and clinical outcome.MethodsThe TRACE-VCI study is a memory clinic cohort of patients with vascular brain injury on MRI (i.e., possible vascular cognitive impairment [VCI]). We included 783 patients (mean age 67.6 ± 8.5, 46% female) with available 3T diffusion-weighted imaging (DWI). ACMIs were defined as supratentorial DWI hyperintensities ResultsA total of 23 ACMIs were found in 16 of the 783 patients (2.0%). Patients with ACMIs did not differ in vascular risk or cognitive profile, but were more often diagnosed with vascular dementia (odds ratio [OR] 5.1; 95% confidence interval [CI] 1.4–18.9, p = 0.014). ACMI presence was associated with lower levels of β-amyloid (p < 0.004) and with vascular imaging markers (lacunar infarcts: OR 3.5, CI 1.3–9.6, p = 0.015; nonlacunar infarcts: OR 4.1, CI 1.4–12.5, p = 0.012; severe white matter hyperintensities: OR 4.8, CI 1.7–13.8, p = 0.004; microbleeds: OR 18.9, CI 2.5–144.0, p = 0.0001). After a median follow-up of 2.1 years, the risk of poor clinical outcome (composite of marked cognitive decline, major vascular event, death, and institutionalization) was increased among patients with ACMIs (hazard ratio 3.0; 1.4–6.0, p = 0.005).ConclusionIn patients with possible VCI, ACMI presence was associated with a high burden of cerebrovascular disease of both small and large vessel etiology and poor clinical outcome. ACMIs may thus be a novel marker of active vascular brain injury in these patients.
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- 2019
15. Author Correction: Heritability estimates for 361 blood metabolites across 40 genome-wide association studies (Nature Communications, (2020), 11, 1, (39), 10.1038/s41467-019-13770-6)
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Hagenbeek, Fiona A., Pool, René, van Dongen, Jenny, Draisma, H. M., Jan Hottenga, Jouke, Willemsen, Gonneke, Abdellaoui, Abdel, Fedko, Iryna O., den Braber, Anouk, Visser, Pieter Jelle, de Geus, Eco J.C.N., Willems van Dijk, Ko, Verhoeven, Aswin, Suchiman, H. Eka, Beekman, Marian, Slagboom, P. Eline, van Duijn, Cornelia M., Barkey Wolf, J. J.H., Cats, D., Amin, N., Beulens, J. W., van der Bom, J. A., Bomer, N., Demirkan, A., van Hilten, J. A., Meessen, J. M.T.A., Moed, M. H., Fu, J., Onderwater, G. L.J., Rutters, F., So-Osman, C., van der Flier, W. M., van der Heijden, A. A.W.A., van der Spek, A., Asselbergs, F. W., Boersma, E., Elders, P. M., Geleijnse, J. M., Ikram, M. A., Kloppenburg, M., Meulenbelt, I., Mooijaart, S. P., Nelissen, R. G.H.H., Netea, M. G., Penninx, B. W.J.H., Stehouwer, C. D.A., Teunissen, C. E., Terwindt, G. M., ‘t Hart, L. M., van den Maagdenberg, A. M.J.M., van der Harst, P., van der Horst, I. C.C., van der Kallen, C. J.H., van Greevenbroek, M. M.J., van Spil, W. E., Wijmenga, C., Zwinderman, A. H., Zhernikova, A., Jukema, J. W., Mei, H., Slofstra, M., Swertz, M., van den Akker, E. B., Deelen, J., Reinders, M. J.T., Harms, Amy C., Hankemeier, Thomas, Bartels, Meike, Nivard, Michel G., Boomsma, Dorret I., Neurology, APH - Health Behaviors & Chronic Diseases, ACS - Heart failure & arrhythmias, Epidemiology and Data Science, General practice, APH - Methodology, APH - Mental Health, Psychiatry, Clinical chemistry, APH - Aging & Later Life, APH - Personalized Medicine, APH - Digital Health, and ACS - Diabetes & metabolism
- Abstract
The original version of the Supplementary Information associated with this Article included an incorrect Supplementary Data 1 file, in which additional delimiters were included in the first column for a number of rows, resulting in column shifts for some of these rows. The HTML has been updated to include a corrected version of Supplementary Data 1; the original incorrect version of Supplementary Data 1 can be found as Supplementary Information associated with this Correction. In addition, the original version of this Article contained an error in the author affiliations. An affiliation of Abdel Abdellaoui with Department of Psychiatry, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands was inadvertently omitted. This has now been corrected in both the PDF and HTML versions of the Article.
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- 2020
16. Mild cognitive impairment with suspected non AD pathology (SNAP): prediction of progression to dementia: OS1103
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Caroli, A., Prestia, A., Galluzzi, S., Ferrari, C., van der Flier, W. M., Ossenkoppele, R., Van Berckel, B., Barkhof, F., Teunissen, C. E., Wall, A., Carter, S. F., Scholl, M., Choo, I. H., Grimmer, T., Nordberg, A., Scheltens, P., Drzezga, A., and Frisoni, G. B.
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- 2014
17. Multi-tracer model for staging cortical amyloid deposition using PET imaging
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Collij, L. E., Markiewicz, P., Golla, S. S. V., Wottschel, V., Wink, A. M., Visser, P. J., Teunissen, C. E., Lammertsma, A. A., Scheltens, P., van der Flier, W. M., Boellaard, R., Heeman, F., van Berckel, B. N. M., Molinuevo, J. L., Gispert, J. D., Schmidt, M. E., Bsarkhof, F., Alves, I. L., ALFA Study for the Alzheimer’s Disease Neuroimaging Initiative, Salvadó, G., Ingala, S., Altomare, D., Wilde, A., Konijnenberg, E., van Buchem, M., and Yaqub, M.
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mental disorders - Abstract
OBJECTIVE: To develop and evaluate a model for staging cortical amyloid deposition using PET with high generalizability. METHODS: 3027 subjects (1763 Cognitively Unimpaired (CU), 658 Impaired, 467 Alzheimer's disease (AD) dementia, 111 non-AD dementia, and 28 with missing diagnosis) from six cohorts (EMIF-AD, ALFA, ABIDE, ADC, OASIS-3, ADNI) who underwent amyloid PET were retrospectively included; 1049 subjects had follow-up scans. Applying dataset-specific cut-offs to global Standard Uptake Value ratio (SUVr) values from 27 regions, single-tracer and pooled multi-tracer regional rankings were constructed from the frequency of abnormality across 400 CU subjects (100 per tracer). The pooled multi-tracer ranking was used to create a staging model consisting of four clusters of regions as it displayed a high and consistent correlation with each single-tracer ranking. Relationships between amyloid stage, clinical variables and longitudinal cognitive decline were investigated. RESULTS: SUVr abnormality was most frequently observed in cingulate, followed by orbitofrontal, precuneal, and insular cortices, then the associative, temporal and occipital regions. Abnormal amyloid levels based on binary global SUVr classification were observed in 1.0%, 5.5%, 17.9%, 90.0%, and 100.0% of stage 0-4 subjects, respectively. Baseline stage predicted decline in MMSE (ADNI: N=867, F=67.37, p3000 subjects across cohorts and radiotracers, and detects pre-global amyloid burden and distinct risk profiles of cognitive decline within globally amyloid-positive subjects.
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- 2020
18. Selection of memory clinic patients for CSF biomarker assessment can be restricted to a quarter of cases by using computerized decision support, without compromising diagnostic accuracy
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Rhodius-Meester, H. F. (Hanneke F. M.), van Maurik, I. S. (Ingrid S.), Koikkalainen, J. (Juha), Tolonen, A. (Antti), Frederiksen, K. S. (Kristian S.), Hasselbalch, S. G. (Steen G.), Soininen, H. (Hilkka), Herukka, S.-K. (Sanna-Kaisa), Remes, A. M. (Anne M.), Teunissen, C. E. (Charlotte E.), Barkhof, F. (Frederik), Pijnenburg, Y. A. (Yolande A. L.), Scheltens, P. (Philip), Lötjönen, J. (Jyrki), and van der Flier, W. M. (Wiesje M.)
- Abstract
Introduction: An accurate and timely diagnosis for Alzheimer’s disease (AD) is important, both for care and research. The current diagnostic criteria allow the use of CSF biomarkers to provide pathophysiological support for the diagnosis of AD. How these criteria should be operationalized by clinicians is unclear. Tools that guide in selecting patients in which CSF biomarkers have clinical utility are needed. We evaluated computerized decision support to select patients for CSF biomarker determination. Methods: We included 535 subjects (139 controls, 286 Alzheimer’s disease dementia, 82 frontotemporal dementia and 28 vascular dementia) from three clinical cohorts. Positive (AD like) and negative (normal) CSF biomarker profiles were simulated to estimate whether knowledge of CSF biomarkers would impact (confidence in) diagnosis. We applied these simulated CSF values and combined them with demographic, neuropsychology and MRI data to initiate CSF testing (computerized decision support approach). We compared proportion of CSF measurements and patients diagnosed with sufficient confidence (probability of correct class ≥0.80) based on an algorithm with scenarios without CSF (only neuropsychology, MRI and APOE), CSF according to the appropriate use criteria (AUC) and CSF for all patients. Results: The computerized decision support approach recommended CSF testing in 140 (26%) patients, which yielded a diagnosis with sufficient confidence in 379 (71%) of all patients. This approach was more efficient than CSF in none (0% CSF, 308 (58%) diagnosed), CSF selected based on AUC (295 (55%) CSF, 350 (65%) diagnosed) or CSF in all (100% CSF, 348 (65%) diagnosed). Conclusions: We used a computerized decision support with simulated CSF results in controls and patients with different types of dementia. This approach can support clinicians in making a balanced decision in ordering additional biomarker testing. Computer-supported prediction restricts CSF testing to only 26% of cases, without compromising diagnostic accuracy.
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- 2020
19. Cerebral amyloid burden is associated with white matter hyperintensity location in specific posterior white matter regions
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Weaver, Nick A., Doeven, Thomas, Barkhof, Frederik, Biesbroek, J. Matthijs, Groeneveld, Onno N., Kuijf, H. J., Prins, N. D., Scheltens, Philip, Teunissen, Charlotte E., van der Flier, W. M., Biessels, G. J., Benedictus, M. R., Bremer, J., Leijenaar, J., Scheltens, P., Tijms, B. M., Barkhof, F., Wattjes, M. P., Teunissen, C. E., Koene, T., van den Berg, E., van den Brink, H., Exalto, L. G., Ferro, D. A., Groeneveld, O., Heinen, R., Heringa, S. M., Kappelle, L. J., Reijmer, Y. D., Verwer, J., de Bresser, J., Koek, H. L., Hamaker, M., Faaij, R., Pleizier, M., Vriens, E., Boomsma, J. M. F., Boss, H. M., Weinstein, H. C., Radiology and nuclear medicine, Amsterdam Neuroscience - Neurodegeneration, Neurology, Laboratory Medicine, APH - Personalized Medicine, APH - Methodology, Epidemiology and Data Science, Immunology, Pediatrics, and Erasmus MC other
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0301 basic medicine ,Aging ,Pathology ,medicine.medical_specialty ,Lesion mapping ,Amyloid ,Amyloid beta ,Neuroscience(all) ,Clinical Neurology ,Splenium ,tau Proteins ,Corpus callosum ,White matter ,03 medical and health sciences ,0302 clinical medicine ,Cerebrospinal fluid ,Magnetic resonance imaging ,Alzheimer Disease ,mental disorders ,medicine ,White matter hyperintensities ,Journal Article ,Humans ,Amyloid beta-Peptides ,medicine.diagnostic_test ,biology ,business.industry ,General Neuroscience ,Alzheimer's disease ,White Matter ,Peptide Fragments ,Hyperintensity ,Ageing ,030104 developmental biology ,medicine.anatomical_structure ,biology.protein ,Neurology (clinical) ,Amyloid-beta ,Tau ,Geriatrics and Gerontology ,business ,030217 neurology & neurosurgery ,Developmental Biology - Abstract
White matter hyperintensities (WMHs) are a common manifestation of cerebral small vessel disease. WMHs are also frequently observed in patients with familial and sporadic Alzheimer's disease, often with a particular posterior predominance. Whether amyloid and tau pathologies are linked to WMH occurrence is still debated. We examined whether cerebral amyloid and tau burden, reflected in cerebrospinal fluid amyloid-beta 1-42 (A beta-42) and phosphorylated tau (p-tau), are related to WMH location in a cohort of 517 memory clinic patients. Two lesion mapping techniques were performed: voxel-based analyses and region of interest-based linear regression. Voxelwise associations were found between lower (A beta-42) and parieto-occipital periventricular WMHs. Regression analyses demonstrated that lower A beta-42 correlated with larger WMH volumes in the splenium of the corpus callosum and posterior thalamic radiation, also after controlling for markers of vascular disease. P-tau was not consistently related to WMH occurrence. Our findings indicate that cerebral amyloid burden is associated with WMHs located in specific posterior white matter regions, possibly reflecting region-specific effects of amyloid pathology on the white matter. (C) 2019 The Authors. Published by Elsevier Inc.
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- 2019
20. Performance of five automated white matter hyperintensity segmentation methods in a multicenter dataset
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Heinen, Rutger, Steenwijk, Martijn D., Barkhof, Frederik, Biesbroek, J. Matthijs, van der Flier, Wiesje M., Kuijf, H. J., Prins, N. D., Vrenken, Hugo, Biessels, Geert Jan, de Bresser, Jeroen, van den Berg, E., Boomsma, J. M. F., Exalto, L. G., Ferro, D. A., Frijns, C. J. M., Groeneveld, O. N., van Kalsbeek, N. M., Verwer, J. H., de Bresser, J., Emmelot-Vonk, M. E., Koek, H. L., Benedictus, M. R., Bremer, J., Leeuwis, A. E., Leijenaar, J., Scheltens, P., Tijms, B. M., Wattjes, M. P., Teunissen, C. E., Koene, T., Weinstein, H. C., Hamaker, M., Faaij, R., Pleizier, M., Prins, M., Vriens, E., Anatomy and neurosciences, Radiology and nuclear medicine, Amsterdam Neuroscience - Neurodegeneration, Neurology, APH - Personalized Medicine, APH - Methodology, Other Research, Clinical chemistry, CCA - Imaging and biomarkers, Immunology, Erasmus MC other, and Public Health
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Male ,Computer science ,lcsh:Medicine ,Article ,030218 nuclear medicine & medical imaging ,03 medical and health sciences ,0302 clinical medicine ,Image Interpretation, Computer-Assisted ,medicine ,Journal Article ,Humans ,Multicenter Studies as Topic ,Segmentation ,lcsh:Science ,General ,Aged ,Automation, Laboratory ,Multidisciplinary ,medicine.diagnostic_test ,business.industry ,lcsh:R ,Magnetic resonance imaging ,Pattern recognition ,Middle Aged ,Magnetic Resonance Imaging ,White Matter ,Hyperintensity ,Stroke ,White matter hyperintensity ,Female ,lcsh:Q ,Artificial intelligence ,Small vessel ,business ,Algorithms ,030217 neurology & neurosurgery - Abstract
White matter hyperintensities (WMHs) are a common manifestation of cerebral small vessel disease, that is increasingly studied with large, pooled multicenter datasets. This data pooling increases statistical power, but poses challenges for automated WMH segmentation. Although there is extensive literature on the evaluation of automated WMH segmentation methods, such evaluations in a multicenter setting are lacking. We performed WMH segmentations in sixty patients scanned on six different magnetic resonance imaging (MRI) scanners (10 patients per scanner) using five freely available and fully-automated WMH segmentation methods (Cascade, kNN-TTP, Lesion-TOADS, LST-LGA and LST-LPA). Different MRI scanner vendors and field strengths were included. We compared these automated WMH segmentations with manual WMH segmentations as a reference. Performance of each method both within and across scanners was assessed using spatial and volumetric correspondence with the reference segmentations by Dice’s similarity coefficient (DSC) and intra-class correlation coefficient (ICC) respectively. We found the best performance, both within and across scanners, for kNN-TTP, followed by LST-LPA and LST-LGA, with worse performance for Lesion-TOADS and Cascade. Our findings can serve as a guide for choosing a method and also highlight the importance to further improve and evaluate consistency of methods in a multicenter setting.
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- 2019
21. Elevated Lipoprotein(a) in Perinatally HIV-Infected Children Compared with Healthy Ethnicity-Matched Controls
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Van Den Hof, Malon, Haneveld, Mirthe J.Klein, Blokhuis, Charlotte, Scherpbier, Henriette J., Jansen, Hans P.G., Kootstra, N. A., Dallinga-Thie, Geesje M., Van Deventer, Sander J.H., Tsimikas, Sotirios, Pajkrt, Dasja, Van Den Hof, M., Blokhuis, C., Cohen, S., Pajkrt, D., Kuijpers, T. W., Van Der Plas, A., Weijsenfeld, A., Ter Stege, J. S., Caan, M. W.A., Mutsaerts, H. J.M.M., Majoie, C. B.L.M., Demirkaya, N., Verbraak, F. D., Schmand, B., Geurtsen, G., Mathot, R. A.A., Wit, F. W.N.M., Reiss, P., Teunissen, C. E., Kuhle, J., Meijer, J. C.M., Pediatric surgery, Amsterdam Reproduction & Development (AR&D), APH - Aging & Later Life, Ophthalmology, Clinical chemistry, and ACS - Atherosclerosis & ischemic syndromes
- Subjects
lipids (amino acids, peptides, and proteins) - Abstract
Background: HIV-associated cardiovascular disease (CVD) risk in combination antiretroviral therapy (cART)-treated perinatally HIV-infected patients (PHIV+) remains unknown due to the young age of this population. Lipoprotein(a) (Lp(a)) has been established as an independent causal risk factor for CVD in the general population but has not been well established in the population of PHIV+. Methods: We cross-sectionally compared lipid profiles, including nonfasting Lp(a), together with total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides between 35 cART-treated PHIV+ children aged 8-18 years and 37 controls who were matched for age, sex, ethnicity, and socioeconomic status. We explored associations between Lp(a) and disease-and treatment-related factors (inflammation, monocyte activation, and vascular), biomarkers, and neuroimaging outcomes using linear regression models. Results: PHIV+ children had significantly higher levels of Lp(a) compared with controls (median, 43.6 [21.6-82.4] vs 21.8 [16.8-46.6] mg/dL; P =. 033). Other lipid levels were comparable between groups. Additional assessment of apolipoprotein B, apolipoprotein CIII, apolipoprotein E, and APOE genotype revealed no significant differences. Higher Lp(a) levels were associated with higher plasma apoB levels and with lower monocyte chemoattractant protein-1 and TG levels in PHIV+ children. Lp(a) was not associated with HIV-or cART-related variables or with neuroimaging outcomes. Conclusions: cART-treated PHIV+ children appear to have higher levels of Lp(a) compared with ethnicity-matched controls, which may implicate higher CVD risk in this population. Future research should focus on the association between Lp(a) and (sub)clinical CVD measurements in cART-treated PHIV+ patients. Dutch Trial Register number: NRT4074.
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- 2019
22. Antioxidants and polyunsaturated fatty acids in multiple sclerosis
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van Meeteren, M E, Teunissen, C E, Dijkstra, C D, and van Tol, E A F
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- 2005
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23. Concentrations of Different Sterols in the Striatum and Serum of 3-Nitropropionic Acid-Treated Wistar and Lewis Rats
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Teunissen, C. E., Mulder, M., de Vente, J., von Bergmann, K., De Bruijn, C., Steinbusch, H. W. M., and Lütjohann, D.
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- 2001
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24. Brain-specific fatty acid-binding protein is elevated in serum of patients with dementia-related diseases
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Teunissen, C. E., Veerhuis, R., De Vente, J., Verhey, F. R. J., Vreeling, F., van Boxtel, M. P. J., Glatz, J. F. C., and Pelsers, M. A. L.
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- 2011
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25. Olfactory and gustatory functioning and food preferences of patients with Alzheimer’s disease and mild cognitive impairment compared to controls: the NUDAD project
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Doorduijn, A. S., primary, de van der Schueren, M. A. E., additional, van de Rest, O., additional, de Leeuw, F. A., additional, Fieldhouse, J. L. P., additional, Kester, M. I., additional, Teunissen, C. E., additional, Scheltens, P., additional, van der Flier, W. M., additional, Visser, M., additional, and Boesveldt, S., additional
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- 2019
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26. Cerebrospinal fluid anti-myelin antibodies are related to magnetic resonance measures of disease activity in multiple sclerosis
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Vogt, M H J, Teunissen, C E, Iacobaeus, E, Heijnen, D A M, Breij, E C W, Olsson, T, Brundin, L, Killestein, J, and Dijkstra, Christine D
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- 2009
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27. An In Vitro Model for De- and Remyelination Using Lysophosphatidyl Choline in Rodent Whole Brain Spheroid Cultures
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Vereyken, E. J. F., Fluitsma, D. M., Bolijn, M. J., Dijkstra, C. D., and Teunissen, C. E.
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- 2009
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28. Serum homocysteine levels in relation to clinical progression in multiple sclerosis
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Teunissen, C E, Killestein, J, Kragt, J J, Polman, C H, Dijkstra, C D, and Blom, H J
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- 2008
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29. Serum neurofilaments as candidate biomarkers of natalizumab-associated PML
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Loonstra, F. C., Verberk, I. M. W., Wijburg, M. T., Wattjes, M. P., Teunissen, C. E., van Oosten, B. W., Uitdehaag, B. M. J., Killestein, J., van Kempen, Z. L. E., Neurology, Clinical chemistry, Other Research, Amsterdam Neuroscience - Neuroinfection & -inflammation, Amsterdam Neuroscience - Neurodegeneration, and AII - Inflammatory diseases
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- 2019
30. Assay stability and preanalytics of neurofilament determinations
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Willemse, E., Teunissen, C. E., Clinical chemistry, Amsterdam Neuroscience - Neurodegeneration, Amsterdam Neuroscience - Neuroinfection & -inflammation, CCA - Imaging and biomarkers, and Amsterdam Reproduction & Development
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- 2019
31. Three distinct physical behavior types in fatigued patients with multiple sclerosis
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Braakhuis, H. E. M., Berger, M. A. M., van der Stok, G. A., van Meeteren, J., de Groot, V., Beckerman, H., Bussmann, J. B. J., Malekzadeh, A., van den Akker, L. E., Looijmans, M., Sanches, S. A., Dekker, J., Collette, E. H., van Oosten, B. W., Teunissen, C. E., Blankenstein, M. A., Eijssen, I. C. J. M., Rietberg, M., Heine, M., Verschuren, O., Kwakkel, G., Visser-Meily, J. M. A., van de Port, I. G. L., Lindeman, E., Blikman, L. J. M., Stam, H. J., Hintzen, R. Q., Hacking, H. G. A., Hoogervorst, E. L., Frequin, S. T. F. M., Knoop, H., de Jong, B. A., Bleijenberg, G., de Laat, F. A. J., Verhulsdonck, M. C., van Munster, E. Th L., Oosterwijk, C. J., Aarts, G. J., Academic Medical Center, Rehabilitation Medicine, Neurology, Pediatrics, Urology, Immunology, Gastroenterology & Hepatology, Erasmus School of Health Policy & Management, APH - Societal Participation & Health, APH - Methodology, APH - Mental Health, APH - Aging & Later Life, AMS - Rehabilitation & Development, MOVE Research Institute, Amsterdam Movement Sciences - Restoration and Development, APH - Quality of Care, and APH - Health Behaviors & Chronic Diseases
- Subjects
Adult ,Male ,030506 rehabilitation ,medicine.medical_specialty ,Neurology ,Evening ,Multiple Sclerosis ,Adolescent ,medicine.medical_treatment ,Psychological intervention ,Health Informatics ,multiple sclerose ,hoofdcomponentenanalyse ,lcsh:RC321-571 ,03 medical and health sciences ,clusteranalyse ,Young Adult ,Cluster analysis ,Accelerometry ,medicine ,Humans ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,Fatigue ,Aged ,Behavior ,Principal Component Analysis ,Rehabilitation ,business.industry ,Multiple sclerosis ,Research ,Middle Aged ,medicine.disease ,Checklist ,Clinical trial ,Cross-Sectional Studies ,Ambulatory ,Physical therapy ,lichamelijk gedrag ,Female ,0305 other medical science ,business ,Physical behavior - Abstract
Background Multiple sclerosis often leads to fatigue and changes in physical behavior (PB). Changes in PB are often assumed as a consequence of fatigue, but effects of interventions that aim to reduce fatigue by improving PB are not sufficient. Since the heterogeneous nature of MS related symptoms, levels of PB of fatigued patients at the start of interventions might vary substantially. Better understanding of the variability by identification of PB subtypes in fatigued patients may help to develop more effective personalized rehabilitation programs in the future. This study aimed to identify PB subtypes in fatigued patients with multiple sclerosis based on multidimensional PB outcome measures. Methods Baseline accelerometer (Actigraph) data, demographics and clinical characteristics of the TREFAMS-ACE participants (n = 212) were used for secondary analysis. All patients were ambulatory and diagnosed with severe fatigue based on a score of ≥35 on the fatigue subscale of the Checklist Individual Strength (CIS20r). Fifteen PB measures were used derived from 7 day measurements with an accelerometer. Principal component analysis was performed to define key outcome measures for PB and two-step cluster analysis was used to identify PB types. Results Analysis revealed five key outcome measures: percentage sedentary behavior, total time in prolonged moderate-to-vigorous physical activity, number of sedentary bouts, and two types of change scores between day parts (morning, afternoon and evening). Based on these outcomes three valid PB clusters were derived. Conclusions Patients with severe MS-related fatigue show three distinct and homogeneous PB subtypes. These PB subtypes, based on a unique set of PB outcome measures, may offer an opportunity to design more individually-tailored interventions in rehabilitation. Trial registration Clinical trial registration no ISRCTN 82353628, ISRCTN 69520623 and ISRCTN 58583714. Electronic supplementary material The online version of this article (10.1186/s12984-019-0573-1) contains supplementary material, which is available to authorized users.
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- 2019
32. The Clinical Phenotype of Vascular Cognitive Impairment in Patients with Type 2 Diabetes Mellitus
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Groeneveld, Onno N., Moneti, Costanza, Heinen, Rutger, de Bresser, Jeroen, Kuijf, Hugo J., Exalto, Lieza G., Boomsma, Jooske M. F., Kappelle, L. Jaap, Barkhof, Frederik, Prins, Niels D., Scheltens, Philip, van der Flier, Wiesje M., Biessels, Geert Jan, Benedictus, M. R., Bremer, J., Goos, J., Leeuwis, A. E., Leijenaar, J., Tijms, B. M., Vrenken, H., Teunissen, C. E., van den Berg, E., Ferro, D. A., Frijns, C. J. M., Groeneveld, O. N., van Kalsbeek, N. M., Verwer, J. H., Koek, H. L., Boss, H. M., Weinstein, H. C., Neurology, Surgery, Plastic and Reconstructive Surgery and Hand Surgery, Immunology, Radiology and nuclear medicine, Amsterdam Neuroscience - Neurodegeneration, APH - Personalized Medicine, APH - Methodology, and Epidemiology and Data Science
- Subjects
0301 basic medicine ,Male ,medicine.medical_specialty ,endocrine system diseases ,type 2 diabetes mellitus ,Neuroscience(all) ,Cohort Studies ,03 medical and health sciences ,0302 clinical medicine ,Atrophy ,SDG 3 - Good Health and Well-being ,Internal medicine ,Journal Article ,medicine ,magnetic resonance imaging ,Humans ,Cognitive Dysfunction ,Prospective Studies ,Cognitive decline ,Prospective cohort study ,Stroke ,Aged ,vascular brain injury ,business.industry ,General Neuroscience ,Memory clinic ,nutritional and metabolic diseases ,Type 2 Diabetes Mellitus ,Cognition ,General Medicine ,Middle Aged ,medicine.disease ,Psychiatry and Mental health ,Clinical Psychology ,030104 developmental biology ,Cerebrospinal fluid ,Phenotype ,Diabetes Mellitus, Type 2 ,Etiology ,Female ,prognosis ,Geriatrics and Gerontology ,business ,030217 neurology & neurosurgery ,Follow-Up Studies - Abstract
Background: Type 2 diabetes mellitus (T2DM) increases the risk of vascular cognitive impairment (VCI). It is unknown which type of vascular lesions and co-morbid etiologies, in particular Alzheimer's disease pathology, are associated with T2DM in patients with VCI, and how this relates to cognition and prognosis.Objective: To compare brain MRI and cerebrospinal fluid (CSF) markers, cognition, and prognosis in patients with possible VCI with and without T2DM.Methods: We included 851 memory clinic patients with vascular brain injury on MRI (i.e., possible VCI) from a prospective cohort study (T2DM: n = 147, 68.4 +/- 7.9 years, 63% men; no T2DM: n = 704, 67.6 +/- 8.5 years, 52% men). At baseline, we assessed between-group differences in brain MRI abnormalities, CSF markers of Alzheimer's disease, and cognitive profile. After two years follow-up, we compared occurrence of cognitive decline, stroke, and death.Results: The distribution of clinical diagnoses did not differ between patients with and without T2DM. T2DM patients had more pronounced brain atrophy (total and white matter volume), and more lacunar infarcts, whereas microbleeds were less common (all p < 0.05). CSF amyloid-beta levels were similar between the groups. T2DM patients performed worse on working memory (effect size: -0.17, p = 0.03) than those without, whereas performance on other domains was similar. During follow-up, risk of further cognitive decline was not increased in T2DM.Conclusion: In patients with possible VCI, presence of T2DM is related to more pronounced brain atrophy and a higher burden of lacunar infarcts, but T2DM does not have a major impact on cognitive profile or prognosis.
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- 2019
33. Energy Conservation Management for People With Multiple Sclerosis-Related Fatigue: Who Benefits?
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Blikman, L. J. M., van Meeteren, J., Twisk, Jos W. R., de laat, Fred A. J., de Groot, Vincent, Beckerman, Heleen, Stam, Henk J., Bussmann, Johannes B. J., Malekzadeh, A., van den Akker, L. E., Looijmans, M., Sanches, S. A., Dekker, J., Collette, E. H., van Oosten, B. W., Teunissen, C. E., Blankenstein, M. A., Eijssen, I. C. J. M., Rietberg, M., Heine, M., Verschuren, O., Kwakkel, G., Visser-Meily, J. M. A., van de Port, I. G. L., Lindeman, E., Bussmann, J. B. J., Stam, H. J., Hintzen, R. Q., Hacking, H. G. A., Hoogervorst, E. L., Frequin, S. T. F. M., Knoop, H., de Jong, B. A., Bleijenberg, G., Verhulsdonck, M. C., van Munster, E. T. H. L., Oosterwijk, C. J., Aarts, G. J., Rehabilitation Medicine, Erasmus School of Law, Neurology, Pediatrics, Urology, Immunology, Gastroenterology & Hepatology, Public Health, Erasmus School of Health Policy & Management, Academic Medical Center, Epidemiology and Data Science, Rehabilitation medicine, Amsterdam Movement Sciences - Rehabilitation & Development, Amsterdam Neuroscience - Systems & Network Neuroscience, APH - Methodology, APH - Societal Participation & Health, Amsterdam Movement Sciences - Restoration and Development, and ACS - Atherosclerosis & ischemic syndromes
- Subjects
medicine.medical_specialty ,Multiple Sclerosis ,media_common.quotation_subject ,MEDLINE ,Disease ,Logistic regression ,law.invention ,03 medical and health sciences ,Social support ,0302 clinical medicine ,Occupational Therapy ,Randomized controlled trial ,law ,Perception ,Medicine ,Humans ,Single-Blind Method ,030212 general & internal medicine ,SDG 7 - Affordable and Clean Energy ,Fatigue ,Research Articles ,media_common ,business.industry ,Checklist ,Ambulatory ,Physical therapy ,Fatigue/physiopathology ,business ,030217 neurology & neurosurgery - Abstract
OBJECTIVE. We investigated whether demographic, disease-related, or personal baseline determinants can predict a positive response to energy conservation management (ECM). METHOD. We conducted a secondary analysis of a single-blind, two-parallel-arms randomized controlled trial that included ambulatory adults with severe MS-related fatigue. Therapy responders and nonresponders were categorized by Checklist Individual Strength fatigue change scores between baseline and end of treatment. Logistic regression analyses were used to assess the determinants of response. RESULTS. Sixty-nine participants were included (ECM group, n = 34; control group, n = 35). In the ECM group, fatigue severity, perception of fatigue, illness cognitions about MS, and social support discrepancies were related to the probability of being a responder. CONCLUSION. The results suggest that people with MS-related fatigue who had a less negative perception of fatigue and who perceived fewer disease benefits and a higher discrepancy in social support had the best response to ECM treatment.
- Published
- 2019
34. Erratum to:α-Synuclein species as potential cerebrospinal fluid biomarkers for dementia with lewy bodies: CSF α-Synuclein species as biomarkers for DLB (Movement Disorders, (2018), 33, 11, (1724-1733), 10.1002/mds.111)
- Author
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van Steenoven, I, Majbour, N. K., Vaikath, N. N., Berendse, H. W., van der Flier, W. M., van de Berg, W. D. J., Teunissen, C. E., Lemstra, A. W., and El-Agnaf, O. M. A.
- Abstract
In the published article referenced below, an error occurred regarding reference number 47. The correct reference citation is: 47Reesink FE, Lemstra AW, van Dijk KD, et al. CSF alpha-synuclein does not discriminate dementia with Lewy bodies from Alzheimer's disease. J Alzheimers Disord 2010;22:87-95. We apologize for the oversight and any inconvenience this has caused.
- Published
- 2019
35. BRAIN-SPECIFIC FATTY ACID BINDING PROTEIN IS DETECTABLE IN SERUM OF PATIENTS WITH DEMENTIA
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Pelsers, M. M.A.L., De Vente, J., Dijkstra, C. D., Verhey, F., Vreeling, F., Glatz, J. F.C., van Boxtel, M. P.J., and Teunissen, C. E.
- Published
- 2007
36. Growth-associated protein 43 in lesions and cerebrospinal fluid in multiple sclerosis
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Teunissen, C. E., Dijkstra, C. D., Jasperse, B., Barkhof, F., Vanderstichele, H., Vanmechelen, E., Polman, C. H., and Bö, L.
- Published
- 2006
37. Cerebrospinal fluid mtDNA concentration is elevated in multiple sclerosis disease and responds to treatment
- Author
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Ministerio de Economía y Competitividad (España), Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (España), Leurs, Cyra E., Podlesniy, Petar, Trullas, Ramón, Balk, Lisanne, Steenwijk, Martijn D., Malekzadeh, Arjan, Fredrik Piehl, Uitdehaag, Bernard M. J., Killestein, Joep, Horssen, Jack van, Teunissen, C. E., Ministerio de Economía y Competitividad (España), Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (España), Leurs, Cyra E., Podlesniy, Petar, Trullas, Ramón, Balk, Lisanne, Steenwijk, Martijn D., Malekzadeh, Arjan, Fredrik Piehl, Uitdehaag, Bernard M. J., Killestein, Joep, Horssen, Jack van, and Teunissen, C. E.
- Abstract
[Background] Mitochondrial dysfunction is increasingly recognized as an important feature of multiple sclerosis (MS) pathology and may be relevant for clinical disease progression. However, it is unknown whether mitochondrial DNA (mtDNA) levels in the cerebrospinal fluid (CSF) associate with disease progression and therapeutic response. [Objectives] To evaluate whether CSF concentrations of mtDNA in MS patients can serve as a marker of ongoing neuropathology and may be helpful to differentiate between MS disease subtypes. To explore the effect of disease-modifying therapies on mtDNA levels in the CSF. [Methods] CSF mtDNA was measured using a digital polymerase chain reaction (PCR) CSF mtDNA in two independent MS cohorts. The cohorts included 92 relapsing-remitting multiple sclerosis (RRMS) patients, 40 progressive multiple sclerosis (PMS) patients (27 secondary progressive and 13 primary progressive), 50 various neurologic disease controls, and 5 healthy controls. [Results] Patients with PMS showed a significant increase in CSF mtDNA compared to non-inflammatory neurologic disease controls. Patients with higher T2 lesion volumes and lower normalized brain volumes showed increased concentration of mtDNA. Patients treated with fingolimod had significantly lower mtDNA copy levels at follow-up compared to baseline. [Conclusion] Our results showed a non-specific elevation of concentration of mtDNA in PMS patients. mtDNA concentrations respond to fingolimod and may be used to monitor biological effect of this treatment
- Published
- 2018
38. Brain endothelial cell expression of SPARCL-1 is specific to chronic multiple sclerosis lesions and is regulated by inflammatory mediators in vitro
- Author
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Bridel, C., primary, Koel-Simmelink, M. J. A., additional, Peferoen, L., additional, Derada Troletti, C., additional, Durieux, S., additional, Gorter, R., additional, Nutma, E., additional, Gami, P., additional, Iacobaeus, E., additional, Brundin, L., additional, Kuhle, J., additional, Vrenken, H., additional, Killestein, J., additional, Piersma, S. R., additional, Pham, T. V., additional, De Vries, H. E., additional, Amor, S., additional, Jimenez, C. R., additional, and Teunissen, C. E., additional
- Published
- 2017
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39. Concomitant AD pathology affects clinical manifestation and survival in dementia with Lewy bodies
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Lemstra, A W, primary, de Beer, M H, additional, Teunissen, C E, additional, Schreuder, C, additional, Scheltens, P, additional, van der Flier, W M, additional, and Sikkes, S A M, additional
- Published
- 2016
- Full Text
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40. Brain endothelial cell expression of SPARCL-1 is specific to chronic multiple sclerosis lesions and is regulated by inflammatory mediators in vitro.
- Author
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Bridel, C., Koel‐Simmelink, M. J. A., Peferoen, L., Derada Troletti, C., Durieux, S., Gorter, R., Nutma, E., Gami, P., Iacobaeus, E., Brundin, L., Kuhle, J., Vrenken, H., Killestein, J., Piersma, S. R., Pham, T. V., De Vries, H. E., Amor, S., Jimenez, C. R., and Teunissen, C. E.
- Subjects
ENDOTHELIAL cells ,PROTEIN expression ,MULTIPLE sclerosis ,INFLAMMATORY mediators ,BIOLOGICAL tags ,CELL culture - Abstract
Aims: Cell matrix modulating protein SPARCL-1 is highly expressed by astrocytes during CNS development and following acute CNS damage. Applying NanoLC-MS/MS to CSF of RRMS and SPMS patients, we identified SPARCL-1 as differentially expressed between these two stages of MS, suggesting a potential as CSF biomarker to differentiate RRMS from SPMS and a role in MS pathogenesis. Methods: This study examines the potential of SPARCL-1 as CSF biomarker discriminating RRMS from SPMS in three independent cohorts (n = 249), analyses its expression pattern in MS lesions (n = 26), and studies its regulation in cultured human brain microvasculature endothelial cells (BEC) after exposure to MS-relevant inflammatory mediators. Results: SPARCL-1 expression in CSF was significantly higher in SPMS compared to RRMS in a Dutch cohort of 76 patients. This finding was not replicated in 2 additional cohorts of MS patients from Sweden (n = 81) and Switzerland (n = 92). In chronic MS lesions, but not active lesions or NAWM, a vessel expression pattern of SPARCL-1 was observed in addition to the expression by astrocytes. EC were found to express SPARCL-1 in chronic MS lesions, and SPARCL-1 expression was regulated by MS-relevant inflammatory mediators in cultured human BEC. Conclusions: Conflicting results of SPARCL-10s differential expression in CSF of three independent cohorts of RRMS and SPMS patients precludes its use as biomarker for disease progression. The expression of SPARCL-1 by BEC in chronic MS lesions together with its regulation by inflammatory mediators in vitro suggest a role for SPARCL-1 in MS neuropathology, possibly at the brain vascular level. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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41. Cerebrospinal fluid mtDNA concentration is elevated in multiple sclerosis disease and responds to treatment.
- Author
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Leurs, Cyra E., Podlesniy, Petar, Trullas, Ramon, Balk, Lisanne, Steenwijk, Martijn D., Malekzadeh, Arjan, Piehl, Fredrik, Uitdehaag, Bernard M. J., Killestein, Joep, van Horssen, Jack, and Teunissen, C. E.
- Subjects
MULTIPLE sclerosis ,MITOCHONDRIAL DNA ,CEREBROSPINAL fluid ,POLYMERASE chain reaction ,CENTRAL nervous system diseases - Abstract
Background: Mitochondrial dysfunction is increasingly recognized as an important feature of multiple sclerosis (MS) pathology and may be relevant for clinical disease progression. However, it is unknown whether mitochondrial DNA (mtDNA) levels in the cerebrospinal fluid (CSF) associate with disease progression and therapeutic response. Objectives: To evaluate whether CSF concentrations of mtDNA in MS patients can serve as a marker of ongoing neuropathology and may be helpful to differentiate between MS disease subtypes. To explore the effect of disease-modifying therapies on mtDNA levels in the CSF. Methods: CSF mtDNA was measured using a digital polymerase chain reaction (PCR) CSF mtDNA in two independent MS cohorts. The cohorts included 92 relapsing-remitting multiple sclerosis (RRMS) patients, 40 progressive multiple sclerosis (PMS) patients (27 secondary progressive and 13 primary progressive), 50 various neurologic disease controls, and 5 healthy controls. Results: Patients with PMS showed a significant increase in CSF mtDNA compared to non-inflammatory neurologic disease controls. Patients with higher T2 lesion volumes and lower normalized brain volumes showed increased concentration of mtDNA. Patients treated with fingolimod had significantly lower mtDNA copy levels at follow-up compared to baseline. Conclusion: Our results showed a non-specific elevation of concentration of mtDNA in PMS patients. mtDNA concentrations respond to fingolimod and may be used to monitor biological effect of this treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
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42. Inflammation and axonal damage biomarkers in Multiple Sclerosis: new perspective on their role
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Trentini, Alessandro, Manfrinato, Maria Cristina, Castellazzi, Massimiliano, Fainardi, Enrico, Bellini, Tiziana, Koel Simmelink, M., and Teunissen, C. E.
- Published
- 2011
43. Mild cognitive impairment with suspected non AD pathology (SNAP) : prediction of progression to dementia
- Author
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Caroli, A., Prestia, A., Galluzzi, S., Ferrari, C., van der Flier, W. M., Ossenkoppele, R., Van Berckel, B., Barkhof, F., Teunissen, C. E., Wall, Anders, Carter, S. F., Scholl, M., Choo, I. H., Grimmer, T., Nordberg, A., Scheltens, P., Drzezga, A., Frisoni, G. B., Caroli, A., Prestia, A., Galluzzi, S., Ferrari, C., van der Flier, W. M., Ossenkoppele, R., Van Berckel, B., Barkhof, F., Teunissen, C. E., Wall, Anders, Carter, S. F., Scholl, M., Choo, I. H., Grimmer, T., Nordberg, A., Scheltens, P., Drzezga, A., and Frisoni, G. B.
- Published
- 2014
44. BRI2 ectodomain affects Aβ42 fibrillation and tau truncation in human neuroblastoma cells
- Author
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Del Campo, M., primary, Oliveira, C. R., additional, Scheper, W., additional, Zwart, R., additional, Korth, C., additional, Müller-Schiffmann, A., additional, Kostallas, G., additional, Biverstal, H., additional, Presto, J., additional, Johansson, J., additional, Hoozemans, J. J., additional, Pereira, C. F., additional, and Teunissen, C. E., additional
- Published
- 2014
- Full Text
- View/download PDF
45. P29-M Sample Preparation for Body Fluid Profiling using Magnetic Bead Technology
- Author
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Gillooly, D., Knol, J., Teunissen, C. E., Simmelink, M., and Jimenez, C. R.
- Subjects
Poster Abstracts: Biomarkers - Abstract
Peptide profiling of biological samples using MALDI-TOF mass spectrometry (MS) is an increasingly popular approach used for the discovery of biomarkers and as a means to detect and diagnose disease and allow the assessment of disease severity, progression, and the effectiveness of treatments.
- Published
- 2007
46. Homocysteine: A marker for cognitive performance? A longitudinal follow-up study
- Author
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Teunissen, C. E., Blom, A. Henk J., Van Boxtel, M. P.J., Bosma, H., De Bruijn, C., Jolles, J., Wauters, B. A., Steinbusch, H. W.M., De Vente, J., Laboratory Medicine, Amsterdam Neuroscience - Neurodegeneration, Amsterdam Neuroscience - Neuroinfection & -inflammation, and Amsterdam Reproduction & Development (AR&D)
- Abstract
The present prospective study investigated whether elevated total serum homocysteine concentration is a risk factor for cognitive decline. The outcomes were compared to the possible relation between cognition and vitamin B 12 or folic acid. Cognitive performance of 144 normal aging individuals (aged 30-80 years) was tested at baseline and after six years of follow-up. Domains of cognitive function addressed were cognitive speed (Letter-Digit Coding test), attention and information processing (Stroop test) and verbal learning and memory (Word Learning Test Total; Delayed Recall). Serum concentrations of homocysteine, folic acid and vitamin B12 were determined. Serum concentrations of homocysteine correlated negatively with cognitive performance on the Word Learning tests at baseline, independent of age, sex, education level or folic acid concentration. Homocysteine concentration at baseline correlated negatively with cognitive performance on the Stroop and Word Learning tests during the whole six-year follow-up period. The folic acid concentration correlated to the Delayed Recall test at baseline only and no correlations were observed for vitamin B12. Thus, while a relation between vitamin B12 or folic acid and cognition was almost absent, elevated homocysteine concentrations were associated with prolonged lower cognitive performance in this normal aging population.
- Published
- 2003
47. Serum markers in relation to cognitive functioning in an aging population:Results of the Maastricht Aging Study (MAAS)
- Author
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Teunissen, C. E., Van Boxtel, M. P.J., Bosma, H., Jolles, J., Lütjohann, D., Von Bergmann, K., Wauters, A., Bosmans, E., Maes, M., Delanghe, J., De Bruijn, C., Steinbusch, H. W.M., Blom, H. J., De Vente, J., Neurocognitie, Laboratory Medicine, Amsterdam Neuroscience - Neurodegeneration, Amsterdam Neuroscience - Neuroinfection & -inflammation, and Amsterdam Reproduction & Development (AR&D)
- Abstract
Little is known of the biochemical processes of cognitive decline during 'healthy' aging. Biological markers in body fluids, such as blood, could provide insight in those processes. In the present studies serum concentrations of different markers have been correlated to cognitive functioning of cognitively healthy aging individuals over a period of six years (mean age 57 years, SD 11, n=93). Markers were related to mechanisms known to be involved in Alzheimer's disease, including inflammation, cholesterol homeostasis and homocysteine homeostasis. Domains of cognitive function addressed were cognitive speed (Letter-Digit Coding test), attention and information processing (Stroop test), and memory (Word Learning test: Total Words and Delayed Recall). Baseline concentrations of haptoglobine, homocysteine, lathosterol and lanosterol were negatively correlated with cognitive functioning on the Stroop test over the whole follow-up period of six years. Concentrations of all markers, i.e. haptoglobine, C-reactive protein, homocysteine, lathosterol and lanosterol, were also negatively correlated with functioning on the Word Learning test (Delayed Recall and for some markers also with the Total Words) over the whole six-years follow-up period. In conclusion, concentrations of serum markers related to inflammation, homocysteine and cholesterol homeostasis are not only associated with Alzheimer's disease, but also with cognitive functioning in the cognitively healthy aging population.
- Published
- 2003
48. Homocysteine:A marker for cognitive performance? A longitudinal follow-up study
- Author
-
Teunissen, C. E., Blom, A. Henk J., Van Boxtel, M. P.J., Bosma, H., De Bruijn, C., Jolles, J., Wauters, B. A., Steinbusch, H. W.M., and De Vente, J.
- Abstract
The present prospective study investigated whether elevated total serum homocysteine concentration is a risk factor for cognitive decline. The outcomes were compared to the possible relation between cognition and vitamin B 12 or folic acid. Cognitive performance of 144 normal aging individuals (aged 30-80 years) was tested at baseline and after six years of follow-up. Domains of cognitive function addressed were cognitive speed (Letter-Digit Coding test), attention and information processing (Stroop test) and verbal learning and memory (Word Learning Test Total; Delayed Recall). Serum concentrations of homocysteine, folic acid and vitamin B12 were determined. Serum concentrations of homocysteine correlated negatively with cognitive performance on the Word Learning tests at baseline, independent of age, sex, education level or folic acid concentration. Homocysteine concentration at baseline correlated negatively with cognitive performance on the Stroop and Word Learning tests during the whole six-year follow-up period. The folic acid concentration correlated to the Delayed Recall test at baseline only and no correlations were observed for vitamin B12. Thus, while a relation between vitamin B12 or folic acid and cognition was almost absent, elevated homocysteine concentrations were associated with prolonged lower cognitive performance in this normal aging population.
- Published
- 2003
49. A consensus protocol for the standardization of cerebrospinal fluid collection and biobanking.
- Author
-
UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, UCL - (SLuc) Service de neurologie, UCL - MD/MNOP - Département de morphologie normale et pathologique, Teunissen, C E, Petzold, A, Bennett, J L, Berven, F S, Brundin, L, Comabella, M, Franciotta, D, Frederiksen, J L, Fleming, J O, Furlan, R, Hintzen, R Q, Hughes, S G, Johnson, M H, Krasulova, E, Kuhle, J, Magnone, M C, Rajda, C, Rejdak, K, Schmidt, H K, Van Pesch, Vincent, Waubant, E, Wolf, C, Giovannoni, G, Hemmer, B, Tumani, H, Deisenhammer, F, UCL - SSS/IONS/CEMO - Pôle Cellulaire et moléculaire, UCL - (SLuc) Service de neurologie, UCL - MD/MNOP - Département de morphologie normale et pathologique, Teunissen, C E, Petzold, A, Bennett, J L, Berven, F S, Brundin, L, Comabella, M, Franciotta, D, Frederiksen, J L, Fleming, J O, Furlan, R, Hintzen, R Q, Hughes, S G, Johnson, M H, Krasulova, E, Kuhle, J, Magnone, M C, Rajda, C, Rejdak, K, Schmidt, H K, Van Pesch, Vincent, Waubant, E, Wolf, C, Giovannoni, G, Hemmer, B, Tumani, H, and Deisenhammer, F
- Abstract
There is a long history of research into body fluid biomarkers in neurodegenerative and neuroinflammatory diseases. However, only a few biomarkers in CSF are being used in clinical practice. One of the most critical factors in CSF biomarker research is the inadequate powering of studies because of the lack of sufficient samples that can be obtained in single-center studies. Therefore, collaboration between investigators is needed to establish large biobanks of well-defined samples. Standardized protocols for biobanking are a prerequisite to ensure that the statistical power gained by increasing the numbers of CSF samples is not compromised by preanalytical factors. Here, a consensus report on recommendations for CSF collection and biobanking is presented, formed by the BioMS-eu network for CSF biomarker research in multiple sclerosis. We focus on CSF collection procedures, preanalytical factors, and high-quality clinical and paraclinical information. The biobanking protocols are applicable for CSF biobanks for research targeting any neurologic disease.
- Published
- 2009
50. A consensus protocol for the standardization of cerebrospinal fluid collection and biobanking
- Author
-
Teunissen, C E, Petzold, A, Bennett, J L, Berven, F S, Brundin, L, Comabella, M, Franciotta, D, Frederiksen, J L, Fleming, J O, Furlan, R, Hintzen, R Q, Hughes, S G, Johnson, M H, Krasulova, E, Kuhle, J, Magnone, M C, Rajda, C, Rejdak, K, Schmidt, H K, van Pesch, V, Waubant, E, Wolf, C, Giovannoni, G, Hemmer, B, Tumani, H, Deisenhammer, F, Teunissen, C E, Petzold, A, Bennett, J L, Berven, F S, Brundin, L, Comabella, M, Franciotta, D, Frederiksen, J L, Fleming, J O, Furlan, R, Hintzen, R Q, Hughes, S G, Johnson, M H, Krasulova, E, Kuhle, J, Magnone, M C, Rajda, C, Rejdak, K, Schmidt, H K, van Pesch, V, Waubant, E, Wolf, C, Giovannoni, G, Hemmer, B, Tumani, H, and Deisenhammer, F
- Abstract
Udgivelsesdato: 2009-Dec, There is a long history of research into body fluid biomarkers in neurodegenerative and neuroinflammatory diseases. However, only a few biomarkers in CSF are being used in clinical practice. One of the most critical factors in CSF biomarker research is the inadequate powering of studies because of the lack of sufficient samples that can be obtained in single-center studies. Therefore, collaboration between investigators is needed to establish large biobanks of well-defined samples. Standardized protocols for biobanking are a prerequisite to ensure that the statistical power gained by increasing the numbers of CSF samples is not compromised by preanalytical factors. Here, a consensus report on recommendations for CSF collection and biobanking is presented, formed by the BioMS-eu network for CSF biomarker research in multiple sclerosis. We focus on CSF collection procedures, preanalytical factors, and high-quality clinical and paraclinical information. The biobanking protocols are applicable for CSF biobanks for research targeting any neurologic disease.
- Published
- 2009
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