Prescreening for European Prevention of Alzheimer Dementia (EPAD) trial-ready cohort: impact of AD risk factors and recruitment settings.

Autor: Vermunt L; Department of Neurology, Alzheimer Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit, PO Box 7057, 1007 MB, Amsterdam, The Netherlands. l.vermunt@amsterdamumc.nl., Muniz-Terrera G; Centre for Dementia Prevention, University of Edinburgh, Edinburgh, Scotland., Ter Meulen L; Department of Neurology, Alzheimer Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit, PO Box 7057, 1007 MB, Amsterdam, The Netherlands., Veal C; Department of Genetics, University of Leicester, Leicester, UK., Blennow K; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden., Campbell A; Molecular Medicine Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK., Carrié I; Centre de Recherche Clinique du Gérontopôle, Toulouse University Hospital, Toulouse, France., Delrieu J; Gérontopôle de Toulouse, UMR INSERM 1027, Toulouse University Hospital, Toulouse, France., Fauria K; BarcelonaBeta Brain Research Center, Fundacio Pasqual Maragall, Barcelona, Spain., Huesa Rodríguez G; BarcelonaBeta Brain Research Center, Fundacio Pasqual Maragall, Barcelona, Spain., Ingala S; Department of Radiology and Nuclear Medicine, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit, Amsterdam, The Netherlands., Jenkins N; Centre for Dementia Prevention, University of Edinburgh, Edinburgh, Scotland., Molinuevo JL; BarcelonaBeta Brain Research Center, Fundacio Pasqual Maragall, Barcelona, Spain., Ousset PJ; Centre de Recherche Clinique du Gérontopôle, Toulouse University Hospital, Toulouse, France., Porteous D; Molecular Medicine Centre, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK., Prins ND; Department of Neurology, Alzheimer Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.; Brain Research Center, Amsterdam, The Netherlands., Solomon A; Institute of Clinical Medicine, Neurology, University of Eastern Finland, P.O. Box 1627, 70211, Kuopio, Finland.; Division of Clinical Geriatrics, NVS, Karolinska Institutet, Stockholm, Sweden., Tom BD; MRC Biostatistics Unit, University of Cambridge, Cambridge, UK., Zetterberg H; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.; Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK.; UK Dementia Research Institute at UCL, London, UK., Zwan M; Department of Neurology, Alzheimer Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit, PO Box 7057, 1007 MB, Amsterdam, The Netherlands., Ritchie CW; Centre for Dementia Prevention, University of Edinburgh, Edinburgh, Scotland., Scheltens P; Department of Neurology, Alzheimer Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit, PO Box 7057, 1007 MB, Amsterdam, The Netherlands., Luscan G; Global Innovative Pharma Business - Clinical Sciences, Pfizer, Paris, France., Brookes AJ; Department of Genetics, University of Leicester, Leicester, UK., Visser PJ; Department of Neurology, Alzheimer Center Amsterdam, Amsterdam Neuroscience, Amsterdam UMC, Vrije Universiteit, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.; Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Alzheimer Centrum Limburg, Maastricht University, Maastricht, The Netherlands.
Jazyk: angličtina
Zdroj: Alzheimer's research & therapy [Alzheimers Res Ther] 2020 Jan 06; Vol. 12 (1), pp. 8. Date of Electronic Publication: 2020 Jan 06.
DOI: 10.1186/s13195-019-0576-y
Abstrakt: Background: Recruitment is often a bottleneck in secondary prevention trials in Alzheimer disease (AD). Furthermore, screen-failure rates in these trials are typically high due to relatively low prevalence of AD pathology in individuals without dementia, especially among cognitively unimpaired. Prescreening on AD risk factors may facilitate recruitment, but the efficiency will depend on how these factors link to participation rates and AD pathology. We investigated whether common AD-related factors predict trial-ready cohort participation and amyloid status across different prescreen settings.
Methods: We monitored the prescreening in four cohorts linked to the European Prevention of Alzheimer Dementia (EPAD) Registry (n = 16,877; mean ± SD age = 64 ± 8 years). These included a clinical cohort, a research in-person cohort, a research online cohort, and a population-based cohort. Individuals were asked to participate in the EPAD longitudinal cohort study (EPAD-LCS), which serves as a trial-ready cohort for secondary prevention trials. Amyloid positivity was measured in cerebrospinal fluid as part of the EPAD-LCS assessment. We calculated participation rates and numbers needed to prescreen (NNPS) per participant that was amyloid-positive. We tested if age, sex, education level, APOE status, family history for dementia, memory complaints or memory scores, previously collected in these cohorts, could predict participation and amyloid status.
Results: A total of 2595 participants were contacted for participation in the EPAD-LCS. Participation rates varied by setting between 3 and 59%. The NNPS were 6.9 (clinical cohort), 7.5 (research in-person cohort), 8.4 (research online cohort), and 88.5 (population-based cohort). Participation in the EPAD-LCS (n = 413 (16%)) was associated with lower age (odds ratio (OR) age = 0.97 [0.95-0.99]), high education (OR = 1.64 [1.23-2.17]), male sex (OR = 1.56 [1.19-2.04]), and positive family history of dementia (OR = 1.66 [1.19-2.31]). Among participants in the EPAD-LCS, amyloid positivity (33%) was associated with higher age (OR = 1.06 [1.02-1.10]) and APOE ɛ4 allele carriership (OR = 2.99 [1.81-4.94]). These results were similar across prescreen settings.
Conclusions: Numbers needed to prescreen varied greatly between settings. Understanding how common AD risk factors link to study participation and amyloid positivity is informative for recruitment strategy of studies on secondary prevention of AD.
Databáze: MEDLINE
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