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12 results on '"Vos, S.J.B."'

1. Prevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum

Author

Jansen, W.J., Janssen, O., Tijms, B.M., Vos, S.J.B., Ossenkoppele, R., Visser, P.J., Group, A.B.S., Aarsland, D., Alcolea, D., Altomare, D., Arnim, C. von, Baiardi, S., Baldeiras, I., Barthel, H., Bateman, R.J., Berckel, B. Van, Binette, A.P., Blennow, K., Boada, M., Boecker, H., Bottlaender, M., Braber, A., Brooks, D.J., Buchem, M.A. van, Camus, V., Carill, J.M., Cerman, J., Chen, K., Chételat, G., Chipi, E., Cohen, A.D., Daniels, A., Delarue, M., Didic, M., Drzezga, A., Dubois, B., Eckerström, M., Ekblad, L.L., Engelborghs, S., Epelbaum, S., Fagan, A.M., Fan, Y., Fladby, T., Fleisher, A.S., Flier, W.M. van der, Förster, S., Fortea, J., Frederiksen, K.S., Freund-Levi, Y., Frings, L., Frisoni, G.B., Fröhlich, L., Gabryelewicz, T., Gertz, H.J., Gill, K.D., Gkatzima, O., Gómez-Tortosa, E., Grimmer, T., Guedj, E., Habeck, C.G., Hampel, H., Handels, R., Hansson, O., Hausner, L., Hellwig, S., Heneka, M.T., Herukka, S.K., Hildebrandt, H., Hodges, J., Hort, J., Huang, C.C., Iriondo, A.J., Itoh, Y., Ivanoiu, A., Jagust, W.J., Jessen, F., Johannsen, P., Johnson, K.A., Kandimalla, R., Kapaki, E.N., Kern, S., Kilander, L., Klimkowicz-Mrowiec, A., Klunk, W.E., Koglin, N., Kornhuber, J., Kramberger, M.G., Kuo, H.C., Laere, K. Van, Landau, S.M., Landeau, B., Lee, Dyantha I. van der, Leon, M., Leyton, C.E., Lin, K.J., Lleó, A., Löwenmark, M., Madsen, K., Maier, W., Marcusson, J., Olde Rikkert, M.G.M., Verbeek, M.M., Zboch, M., Zetterberg, H., Jansen, W.J., Janssen, O., Tijms, B.M., Vos, S.J.B., Ossenkoppele, R., Visser, P.J., Group, A.B.S., Aarsland, D., Alcolea, D., Altomare, D., Arnim, C. von, Baiardi, S., Baldeiras, I., Barthel, H., Bateman, R.J., Berckel, B. Van, Binette, A.P., Blennow, K., Boada, M., Boecker, H., Bottlaender, M., Braber, A., Brooks, D.J., Buchem, M.A. van, Camus, V., Carill, J.M., Cerman, J., Chen, K., Chételat, G., Chipi, E., Cohen, A.D., Daniels, A., Delarue, M., Didic, M., Drzezga, A., Dubois, B., Eckerström, M., Ekblad, L.L., Engelborghs, S., Epelbaum, S., Fagan, A.M., Fan, Y., Fladby, T., Fleisher, A.S., Flier, W.M. van der, Förster, S., Fortea, J., Frederiksen, K.S., Freund-Levi, Y., Frings, L., Frisoni, G.B., Fröhlich, L., Gabryelewicz, T., Gertz, H.J., Gill, K.D., Gkatzima, O., Gómez-Tortosa, E., Grimmer, T., Guedj, E., Habeck, C.G., Hampel, H., Handels, R., Hansson, O., Hausner, L., Hellwig, S., Heneka, M.T., Herukka, S.K., Hildebrandt, H., Hodges, J., Hort, J., Huang, C.C., Iriondo, A.J., Itoh, Y., Ivanoiu, A., Jagust, W.J., Jessen, F., Johannsen, P., Johnson, K.A., Kandimalla, R., Kapaki, E.N., Kern, S., Kilander, L., Klimkowicz-Mrowiec, A., Klunk, W.E., Koglin, N., Kornhuber, J., Kramberger, M.G., Kuo, H.C., Laere, K. Van, Landau, S.M., Landeau, B., Lee, Dyantha I. van der, Leon, M., Leyton, C.E., Lin, K.J., Lleó, A., Löwenmark, M., Madsen, K., Maier, W., Marcusson, J., Olde Rikkert, M.G.M., Verbeek, M.M., Zboch, M., and Zetterberg, H.

Abstract

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Published
2022

2. The link between cognition and somatic conditions related to insulin resistance in the UK Biobank study cohort: a systematic review

Author

Fanelli, G., Roth Mota, N., Salas-Salvadó, J., Bulló, M., Fernandez-Aranda, F., Camacho-Barcia, L., Testa, G., Jiménez-Murcia, S., Bertaina-Anglade, V., Franke, B., Poelmans, G.J.V., Gils, V. van, Jansen, W.J., Vos, S.J.B., Wimberley, T., Dalsgaard, S., Barta, C., Serretti, A., Fabbri, C., Bralten, J.B., Fanelli, G., Roth Mota, N., Salas-Salvadó, J., Bulló, M., Fernandez-Aranda, F., Camacho-Barcia, L., Testa, G., Jiménez-Murcia, S., Bertaina-Anglade, V., Franke, B., Poelmans, G.J.V., Gils, V. van, Jansen, W.J., Vos, S.J.B., Wimberley, T., Dalsgaard, S., Barta, C., Serretti, A., Fabbri, C., and Bralten, J.B.

Abstract

Item does not contain fulltext, Clinical and genomic studies have shown an overlap between neuropsychiatric disorders and insulin resistance (IR)-related somatic conditions, including obesity, type 2 diabetes, and cardiovascular diseases. Impaired cognition is often observed among neuropsychiatric disorders, where multiple cognitive domains may be affected. In this review, we aimed to summarise previous evidence on the relationship between IR-related diseases/traits and cognitive performance in the large UK Biobank study cohort. Electronic searches were conducted on PubMed, Scopus, and Web of Science until April 2022. Eighteen articles met the inclusion criteria and were qualitatively reviewed. Overall, there is substantial evidence for an association between IR-related cardio-metabolic diseases/traits and worse performance on various cognitive domains, which is largely independent of possible confoundings. The most consistent findings referred to IR-related associations with poorer verbal and numerical reasoning ability, as well as slower processing speed. The observed associations might be mediated by alterations in immune-inflammation, brain integrity/connectivity, and/or comorbid somatic or psychiatric diseases/traits. Our findings provide impetus for further research into the underlying neurobiology and possible new therapeutic targets.

Published
2022

3. Subjective cognitive decline and rates of incident Alzheimer's disease and non–Alzheimer's disease dementia

Author

Slot, R.E.R. Sikkes, S.A.M. Berkhof, J. Brodaty, H. Buckley, R. Cavedo, E. Dardiotis, E. Guillo-Benarous, F. Hampel, H. Kochan, N.A. Lista, S. Luck, T. Maruff, P. Molinuevo, J.L. Kornhuber, J. Reisberg, B. Riedel-Heller, S.G. Risacher, S.L. Roehr, S. Sachdev, P.S. Scarmeas, N. Scheltens, P. Shulman, M.B. Saykin, A.J. Verfaillie, S.C.J. Visser, P.J. Vos, S.J.B. Wagner, M. Wolfsgruber, S. Jessen, F. Boada, M. de Deyn, P.P. Jones, R. Frisoni, G. Spiru, L. Nobili, F. Freund-Levi, Y. Soininen, H. Verhey, F. Wallin, Å.K. Touchon, J. Rikkert, M.O. Rigaud, A.-S. Bullock, R. Tsolaki, M. Vellas, B. Wilcock, G. Froelich, L. Bakardjian, H. Benali, H. Bertin, H. Bonheur, J. Boukadida, L. Boukerrou, N. Chiesa, P. Colliot, O. Dubois, B. Dubois, M. Epelbaum, S. Gagliardi, G. Genthon, R. Habert, M.-O. Houot, M. Kas, A. Lamari, F. Levy, M. Metzinger, C. Mochel, F. Nyasse, F. Poisson, C. Potier, M.-C. Revillon, M. Santos, A. Andrade, K.S. Sole, M. Surtee, M. Thiebaud de Schotten, M. Vergallo, A. Younsi, N. van der Flier, W.M. Alzheimer's Disease Neuroimaging Initiative DESCRIPA working group INSIGHT-preAD study group SCD-I working group

Abstract

Introduction: In this multicenter study on subjective cognitive decline (SCD) in community-based and memory clinic settings, we assessed the (1) incidence of Alzheimer's disease (AD) and non-AD dementia and (2) determinants of progression to dementia. Methods: Eleven cohorts provided 2978 participants with SCD and 1391 controls. We estimated dementia incidence and identified risk factors using Cox proportional hazards models. Results: In SCD, incidence of dementia was 17.7 (95% Poisson confidence interval 15.2-20.3)/1000 person-years (AD: 11.5 [9.6-13.7], non-AD: 6.1 [4.7-7.7]), compared with 14.2 (11.3-17.6) in controls (AD: 10.1 [7.7-13.0], non-AD: 4.1 [2.6-6.0]). The risk of dementia was strongly increased in SCD in a memory clinic setting but less so in a community-based setting. In addition, higher age (hazard ratio 1.1 [95% confidence interval 1.1-1.1]), lower Mini–Mental State Examination (0.7 [0.66-0.8]), and apolipoprotein E ε4 (1.8 [1.3-2.5]) increased the risk of dementia. Discussion: SCD can precede both AD and non-AD dementia. Despite their younger age, individuals with SCD in a memory clinic setting have a higher risk of dementia than those in community-based cohorts. © 2018 The Authors

Published
2019

5. Association of cerebral amyloid-β Aggregation with cognitive functioning in persons without dementia

Author

Jansen, W.J. Ossenkoppele, R. Tijms, B.M. Fagan, A.M. Hansson, O. Klunk, W.E. Van Der Flier, W.M. Villemagne, V.L. Frisoni, G.B. Fleisher, A.S. Lleó, A. Mintun, M.A. Wallin, A. Engelborghs, S. Na, D.L. Chételat, G. Molinuevo, J.L. Landau, S.M. Mattsson, N. Kornhuber, J. Sabri, O. Rowe, C.C. Parnetti, L. Popp, J. Fladby, T. Jagust, W.J. Aalten, P. Lee, D.Y. Vandenberghe, R. De Oliveira, C.R. Kapaki, E. Froelich, L. Ivanoiu, A. Gabryelewicz, T. Verbeek, M.M. Sanchez-Juan, P. Hildebrandt, H. Camus, V. Zboch, M. Brooks, D.J. Drzezga, A. Rinne, J.O. Newberg, A. De Mendonça, A. Sarazin, M. Rabinovici, G.D. Madsen, K. Kramberger, M.G. Nordberg, A. Mok, V. Mroczko, B. Wolk, D.A. Meyer, P.T. Tsolaki, M. Scheltens, P. Verhey, F.R.J. Visser, P.J. Aarsland, D. Alcolea, D. Alexander, M. Almdahl, I.S. Arnold, S.E. Baldeiras, I. Barthel, H. Van Berckel, B.N.M. Blennow, K. Van Buchem, M.A. Cavedo, E. Chen, K. Chipi, E. Cohen, A.D. Förster, S. Fortea, J. Frederiksen, K.S. Freund-Levi, Y. Gkatzima, O. Gordon, M.F. Grimmer, T. Hampel, H. Hausner, L. Hellwig, S. Herukka, S.-K. Johannsen, P. Klimkowicz-Mrowiec, A. Köhler, S. Koglin, N. Van Laere, K. De Leon, M. Lisetti, V. Maier, W. Marcusson, J. Meulenbroek, O. Møllergård, H.M. Morris, J.C. Nordlund, A. Novak, G.P. Paraskevas, G.P. Perera, G. Peters, O. Ramakers, I.H.G.B. Rami, L. Rodríguez-Rodríguez, E. Roe, C.M. Rot, U. Rüther, E. Santana, I. Schröder, J. Seo, S.W. Sorininen, H. Spiru, L. Stomrud, E. Struyfs, H. Teunissen, C.E. Vos, S.J.B. Van Waalwijk Van Doorn, L.J.C. Waldemar, G. Wallin, Å.K. Wiltfang, J. Zetterberg, H. Amyloid Biomarker Study Group

Subjects
mental disorders
Abstract

IMPORTANCE Cerebral amyloid-β aggregation is an early event in Alzheimer disease (AD). Understanding the association between amyloid aggregation and cognitive manifestation in persons without dementia is important for a better understanding of the course of AD and for the design of prevention trials. OBJECTIVE To investigate whether amyloid-β aggregation is associated with cognitive functioning in persons without dementia. DESIGN, SETTING, AND PARTICIPANTS This cross-sectional study included 2908 participants with normal cognition and 4133 with mild cognitive impairment (MCI) from 53 studies in the multicenter Amyloid Biomarker Study. Normal cognition was defined as having no cognitive concerns for which medical help was sought and scores within the normal range on cognitive tests. Mild cognitive impairment was diagnosed according to published criteria. Study inclusion began in 2013 and is ongoing. Data analysis was performed in January 2017. MAIN OUTCOMES AND MEASURES Global cognitive performance as assessed by the Mini-Mental State Examination (MMSE) and episodic memory performance as assessed by a verbal word learning test. Amyloid aggregation was measured with positron emission tomography or cerebrospinal fluid biomarkers and dichotomized as negative (normal) or positive (abnormal) according to study-specific cutoffs. Generalized estimating equations were used to examine the association between amyloid aggregation and low cognitive scores (MMSE score≤27 or memory z score≤-1.28) and to assess whether this association was moderated by age, sex, educational level, or apolipoprotein E genotype. RESULTS Among 2908 persons with normal cognition (mean [SD] age, 67.4 [12.8] years), amyloid positivity was associated with low memory scores after age 70 years (mean difference in amyloid positive vs negative, 4%[95%CI, 0%-7%] at 72 years and 21% [95%CI, 10%-33%] at 90 years) but was not associated with low MMSE scores (mean difference, 3%[95%CI, -1%to 6%], P = .16). Among 4133 patients with MCI (mean [SD] age, 70.2 [8.5] years), amyloid positivity was associated with low memory (mean difference, 16%[95%CI, 12%-20%], P < .001) and low MMSE (mean difference, 14%[95%CI, 12%-17%], P < .001) scores, and this association decreased with age. Low cognitive scores had limited utility for screening of amyloid positivity in persons with normal cognition and those with MCI. In persons with normal cognition, the age-related increase in low memory score paralleled the age-related increase in amyloid positivity with an intervening period of 10 to 15 years. CONCLUSIONS AND RELEVANCE Although low memory scores are an early marker of amyloid positivity, their value as a screening measure for early AD among persons without dementia is limited.

Published
2018

6. Prevalence of the apolipoprotein E epsilon4 allele in amyloid beta positive subjects across the spectrum of Alzheimer's disease

Author

Mattsson, N., Groot, C. de, Jansen, W.J., Landau, S.M., Villemagne, V.L., Engelborghs, S., Mintun, M.M., Lleo, A., Molinuevo, J.L., Jagust, W.J., Frisoni, G.B., Ivanoiu, A., Chetelat, G., Oliveira, C. de, Rodrigue, K.M., Kornhuber, J., Wallin, A., Klimkowicz-Mrowiec, A., Kandimalla, R., Popp, J., Aalten, P.P., Aarsland, D., Alcolea, D., Almdahl, I.S., Baldeiras, I., Buchem, M.A. van, Cavedo, E., Chen, K., Cohen, A.D., Forster, S., Fortea, J., Frederiksen, K.S., Freund-Levi, Y., Gill, K.D., Gkatzima, O., Grimmer, T., Hampel, H., Herukka, S.K., Johannsen, P., Laere, K. Van, Leon, M.J. de, Maier, W., Marcusson, J., Meulenbroek, O.V., Mollergard, H.M., Morris, J.C., Mroczko, B., Nordlund, A., Prabhakar, S., Peters, O., Rami, L., Rodriguez-Rodriguez, E., Roe, C.M., Ruther, E., Santana, I., Schroder, J., Seo, S.W., Soininen, H., Spiru, L., Stomrud, E., Struyfs, H., Teunissen, C.E., Verhey, F.R.J., Vos, S.J.B., Waalwijk van Doorn, L.L.C. van, Waldemar, G., Wallin, A.K., Wiltfang, J., Vandenberghe, R., Brooks, D.J., Fladby, T., Rowe, C.C., Drzezga, A., Verbeek, M.M., Sarazin, M., Wolk, D.A., Fleisher, A.S., Klunk, W.E., Na, D.L., Sanchez-Juan, P., Lee, D.Y., Nordberg, A., Tsolaki, M., Camus, V., Rinne, J.O., Fagan, A.M., Zetterberg, H., Blennow, K., Rabinovici, G.D., Hansson, O., Berckel, B.N. van, Flier, W.M. van der, Scheltens, P., Visser, P.J., Ossenkoppele, R., Mattsson, N., Groot, C. de, Jansen, W.J., Landau, S.M., Villemagne, V.L., Engelborghs, S., Mintun, M.M., Lleo, A., Molinuevo, J.L., Jagust, W.J., Frisoni, G.B., Ivanoiu, A., Chetelat, G., Oliveira, C. de, Rodrigue, K.M., Kornhuber, J., Wallin, A., Klimkowicz-Mrowiec, A., Kandimalla, R., Popp, J., Aalten, P.P., Aarsland, D., Alcolea, D., Almdahl, I.S., Baldeiras, I., Buchem, M.A. van, Cavedo, E., Chen, K., Cohen, A.D., Forster, S., Fortea, J., Frederiksen, K.S., Freund-Levi, Y., Gill, K.D., Gkatzima, O., Grimmer, T., Hampel, H., Herukka, S.K., Johannsen, P., Laere, K. Van, Leon, M.J. de, Maier, W., Marcusson, J., Meulenbroek, O.V., Mollergard, H.M., Morris, J.C., Mroczko, B., Nordlund, A., Prabhakar, S., Peters, O., Rami, L., Rodriguez-Rodriguez, E., Roe, C.M., Ruther, E., Santana, I., Schroder, J., Seo, S.W., Soininen, H., Spiru, L., Stomrud, E., Struyfs, H., Teunissen, C.E., Verhey, F.R.J., Vos, S.J.B., Waalwijk van Doorn, L.L.C. van, Waldemar, G., Wallin, A.K., Wiltfang, J., Vandenberghe, R., Brooks, D.J., Fladby, T., Rowe, C.C., Drzezga, A., Verbeek, M.M., Sarazin, M., Wolk, D.A., Fleisher, A.S., Klunk, W.E., Na, D.L., Sanchez-Juan, P., Lee, D.Y., Nordberg, A., Tsolaki, M., Camus, V., Rinne, J.O., Fagan, A.M., Zetterberg, H., Blennow, K., Rabinovici, G.D., Hansson, O., Berckel, B.N. van, Flier, W.M. van der, Scheltens, P., Visser, P.J., and Ossenkoppele, R.

Abstract

Item does not contain fulltext, INTRODUCTION: Apolipoprotein E (APOE) epsilon4 is the major genetic risk factor for Alzheimer's disease (AD), but its prevalence is unclear because earlier studies did not require biomarker evidence of amyloid beta (Abeta) pathology. METHODS: We included 3451 Abeta+ subjects (853 AD-type dementia, 1810 mild cognitive impairment, and 788 cognitively normal). Generalized estimating equation models were used to assess APOE epsilon4 prevalence in relation to age, sex, education, and geographical location. RESULTS: The APOE epsilon4 prevalence was 66% in AD-type dementia, 64% in mild cognitive impairment, and 51% in cognitively normal, and it decreased with advancing age in Abeta+ cognitively normal and Abeta+ mild cognitive impairment (P < .05) but not in Abeta+ AD dementia (P = .66). The prevalence was highest in Northern Europe but did not vary by sex or education. DISCUSSION: The APOE epsilon4 prevalence in AD was higher than that in previous studies, which did not require presence of Abeta pathology. Furthermore, our results highlight disease heterogeneity related to age and geographical location.

Published
2018

8. Discovery and validation of multimodal biomarker signatures relating to Alzheimer's disease pathology and progression

Author

Westwood, S., Hye, A., Lleó, A., Nevado-Holgado, A.J., Baird, A.L., Wallin, A., Leslie, A., Jimenez, B., Liu, B.Y., Legido-Quigley, C., Dima, D., Ruvolo, D., Holmes, E., D'Hondt, E., Westman, E., Barkhof, F., Frisoni, G.B., Zetterberg, H., Bos, I., Pearce, J., Streffer, J., Molinuevo, J.L., Popp, J., Bertram, L., Whiley, L., Maslen, L., Gómez-Romero, M., David, M., Lewis, M., Kurbatova, N., Ashton, N.J., Voyle, N., Kowalczyk, O., Martinez-Lage, P., Proitsi, P., Scheltens, P., Visser, P.J., Dobson, R.J.B., Vandenberghe, R., Engelborghs, S., Vos, S.J.B., Snowden, S.G., Athersuch, T., Ashby, T., Kimhofer, T., Verachtert, W., Lovestone, S., Westwood, S., Hye, A., Lleó, A., Nevado-Holgado, A.J., Baird, A.L., Wallin, A., Leslie, A., Jimenez, B., Liu, B.Y., Legido-Quigley, C., Dima, D., Ruvolo, D., Holmes, E., D'Hondt, E., Westman, E., Barkhof, F., Frisoni, G.B., Zetterberg, H., Bos, I., Pearce, J., Streffer, J., Molinuevo, J.L., Popp, J., Bertram, L., Whiley, L., Maslen, L., Gómez-Romero, M., David, M., Lewis, M., Kurbatova, N., Ashton, N.J., Voyle, N., Kowalczyk, O., Martinez-Lage, P., Proitsi, P., Scheltens, P., Visser, P.J., Dobson, R.J.B., Vandenberghe, R., Engelborghs, S., Vos, S.J.B., Snowden, S.G., Athersuch, T., Ashby, T., Kimhofer, T., Verachtert, W., and Lovestone, S.

Abstract

Background Biomarkers of Alzheimer’s disease (AD) pathology and progression have now been identified across various modalities. The aims of the two studies presented (ANM-MMB and EMIF-AD biomarker discovery) are to discover and replicate previously identified biomarkers of disease pathology and progression, and moreover to determine whether a multimodal biomarker signature may add value in comparison to a biomarker of a single modality. Methods The ANM-MMB cohort is comprised of 718 AD, MCI converters and non-converters, and control subjects selected from the AddNeuroMed, Alzheimer’s research trust and Dementia case register cohorts. Cognitive measures, serum and urine metabolomics, structural MRI, genomics, whole blood transcriptomics and plasma proteomics data was available. The EMIF-AD biomarker discovery cohort consists of 1221 AD, MCI and control subjects, selected from the EMIF catalogue. All subjects had existing amyloid measures (CSF Aβ or amyloid-PET), structural MRI and clinical data, and furthermore plasma proteomics (targeted and untargeted), CSF proteomics (targeted), metabolomics, genomics and epigenetics data were generated. For both studies univariate and multivariate statistics were utilised to identify candidate biomarkers of AD pathology (neurodegeneration and/or brain amyloid burden), rates of cognitive decline, and MCI progression to dementia. pQTL-eQTL-mQTL analyses, network/pathway analysis, and multimodal classifiers were employed to detect multimodal signatures. Results Initial analyses indicate that in the ANM-MMB study a serum and urine derived 15 metabolite classifier predicts MCI progression to AD with 72% accuracy, and the biological significance of the metabolites included in the biomarker panel was identified. Further analyses will examine whether a multimodal classifier is able to predict with even greater accuracy. We will then seek to replicate this in the EMIF-AD biomarker discovery study. Further analyses will also examine single

Published
2017

9. Prevalence of cerebral amyloid pathology in persons without dementia: A meta-analysis

Author

Jansen, W.J. Ossenkoppele, R. Knol, D.L. Tijms, B.M. Scheltens, P. Verhey, F.R.J. Visser, P.J. Aalten, P. Aarsland, D. Alcolea, D. Alexander, M. Almdahl, I.S. Arnold, S.E. Baldeiras, I. Barthel, H. Van Berckel, B.N.M. Bibeau, K. Blennow, K. Brooks, D.J. Van Buchem, M.A. Camus, V. Cavedo, E. Chen, K. Chetelat, G. Cohen, A.D. Drzezga, A. Engelborghs, S. Fagan, A.M. Fladby, T. Fleisher, A.S. Van Der Flier, W.M. Ford, L. Forster, S. Fortea, J. Foskett, N. Frederiksen, K.S. Freund-Levi, Y. Frisoni, G.B. Froelich, L. Gabryelewicz, T. Gill, K.D. Gkatzima, O. Gomez-Tortosa, E. Gordon, M.F. Grimmer, T. Hampel, H. Hausner, L. Hellwig, S. Herukka, S.-K. Hildebrandt, H. Ishihara, L. Ivanoiu, A. Jagust, W.J. Johannsen, P. Kandimalla, R. Kapaki, E. Klimkowicz-Mrowiec, A. Klunk, W.E. Kohler, S. Koglin, N. Kornhuber, J. Kramberger, M.G. Van Laere, K. Landau, S.M. Lee, D.Y. De Leon, M. Lisetti, V. Lleo, A. Madsen, K. Maier, W. Marcusson, J. Mattsson, N. De Mendonca, A. Meulenbroek, O. Meyer, P.T. Mintun, M.A. Mok, V. Molinuevo, J.L. Mollergard, H.M. Morris, J.C. Mroczko, B. Van Der Mussele, S. Na, D.L. Newberg, A. Nordberg, A. Nordlund, A. Novak, G.P. Paraskevas, G.P. Parnetti, L. Perera, G. Peters, O. Popp, J. Prabhakar, S. Rabinovici, G.D. Ramakers, I.H.G.B. Rami, L. De Oliveira, C.R. Rinne, J.O. Rodrigue, K.M. Rodriguez-Rodriguez, E. Roe, C.M. Rot, U. Rowe, C.C. Ruther, E. Sabri, O. Sanchez-Juan, P. Santana, I. Sarazin, M. Schroder, J. Schutte, C. Seo, S.W. Soetewey, F. Soininen, H. Spiru, L. Struyfs, H. Teunissen, C.E. Tsolaki, M. Vandenberghe, R. Verbeek, M.M. Villemagne, V.L. Vos, S.J.B. Van Waalwijk Van Doorn, L.J.C. Waldemar, G. Wallin, A. Wallin, A.K. Wiltfang, J. Wolk, D.A. Zboch, M. Zetterberg, H. the Amyloid Biomarker Study Group

Subjects
mental disorders
Abstract

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 andWeb 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 recordswere 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. Copyright 2015 American Medical Association. All rights reserved.

Published
2015

11. Injury markers predict time to dementia in subjects with MCI and amyloid pathology

Author

van Rossum, I.A., Vos, S.J.B., Burns, L., Knol, D.L., Scheltens, P., Soininen, H., Wahlund, L.O., Hampel, H., Tsolaki, M., Minthon, L., L'Italien, G., van der Flier, W.M., Teunissen, C.E., Blennow, K., Barkhof, F., Rueckert, D., Wolz, R., Verhey, F., Visser, P.J., van Rossum, I.A., Vos, S.J.B., Burns, L., Knol, D.L., Scheltens, P., Soininen, H., Wahlund, L.O., Hampel, H., Tsolaki, M., Minthon, L., L'Italien, G., van der Flier, W.M., Teunissen, C.E., Blennow, K., Barkhof, F., Rueckert, D., Wolz, R., Verhey, F., and Visser, P.J.

Abstract

Objectives: Alzheimer disease (AD) can now be diagnosed in subjects with mild cognitive impairment (MCI) using biomarkers. However, little is known about the rate of decline in those subjects. In this cohort study, we aimed to assess the conversion rate to dementia and identify prognostic markers in subjects with MCI and evidence of amyloid pathology. Methods: We pooled subjects from the VU University Medical Center Alzheimer Center and the Development of Screening Guidelines and Criteria for Predementia Alzheimer's Disease (DESCRIPA) study. We included subjects with MCI, an abnormal level of β-amyloid

Published
2012
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