Nina Kemppainen1, Jarkko Johansson2, Jarmo Teuho2, Riitta Parkkola2, Juho Joutsa2, Tiia Ngandu2, Alina Solomon2, Ruth Stephen2, Yawu Liu2, Tuomo Hänninen2, Teemu Paajanen2, Tiina Laatikainen2, Hilkka Soininen2, Antti Jula2, Johanna Rokka2, Eero Rissanen2, Tero Vahlberg2, Julia Peltoniemi2, Miia Kivipelto2, Juha O Rinne2. 1. From the Turku PET Centre (N.K., J. Johansson, J.T., J. Joutsa, J.R., E.R., J.P., J.O.R.), University of Turku; Division of Clinical Neurosciences (N.K., J. Joutsa, E.R., J.O.R.), Turku University Hospital; Department of Radiology (R.P.), Turku University Hospital and University of Turku, Finland; Athinoula A. Martinos Center for Biomedical Imaging (J. Joutsa), Massachusetts General Hospital and Harvard Medical School, Charlestown; Berenson-Allen Center for Noninvasive Brain Stimulation (J. Joutsa), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; Department of Public Health Solutions (T.N., T.L., M.K.), Chronic Disease Prevention Unit, National Institute for Health and Welfare, Helsinki, Finland; Division of Clinical Geriatrics (T.N., A.S., M.K.), Center for Alzheimer Research, NVS, and Aging Research Center (A.S., M.K.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (A.S., R.S., Y.L., H.S., M.K.), Institute of Clinical Medicine, and Institute of Public Health and Clinical Nutrition (T.L.), University of Eastern Finland, Kuopio; Department of Neurology (T.H., H.S.), Kuopio University Hospital; Research and Service Centre for Occupational Health (T.P.), Finnish Institute of Occupational Health, Helsinki; Joint Municipal Authority for North Karelia Social and Health Services (T.L.), Joensuu; National Institute for Health and Welfare (A.J.); and Department of Biostatistics (T.V.), University of Turku and Turku University Hospital, Turku, Finland. nina.kemppainen@tyks.fi. 2. From the Turku PET Centre (N.K., J. Johansson, J.T., J. Joutsa, J.R., E.R., J.P., J.O.R.), University of Turku; Division of Clinical Neurosciences (N.K., J. Joutsa, E.R., J.O.R.), Turku University Hospital; Department of Radiology (R.P.), Turku University Hospital and University of Turku, Finland; Athinoula A. Martinos Center for Biomedical Imaging (J. Joutsa), Massachusetts General Hospital and Harvard Medical School, Charlestown; Berenson-Allen Center for Noninvasive Brain Stimulation (J. Joutsa), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; Department of Public Health Solutions (T.N., T.L., M.K.), Chronic Disease Prevention Unit, National Institute for Health and Welfare, Helsinki, Finland; Division of Clinical Geriatrics (T.N., A.S., M.K.), Center for Alzheimer Research, NVS, and Aging Research Center (A.S., M.K.), Karolinska Institutet, Stockholm, Sweden; Department of Neurology (A.S., R.S., Y.L., H.S., M.K.), Institute of Clinical Medicine, and Institute of Public Health and Clinical Nutrition (T.L.), University of Eastern Finland, Kuopio; Department of Neurology (T.H., H.S.), Kuopio University Hospital; Research and Service Centre for Occupational Health (T.P.), Finnish Institute of Occupational Health, Helsinki; Joint Municipal Authority for North Karelia Social and Health Services (T.L.), Joensuu; National Institute for Health and Welfare (A.J.); and Department of Biostatistics (T.V.), University of Turku and Turku University Hospital, Turku, Finland.
Abstract
OBJECTIVE: To investigate brain amyloid pathology in a dementia-risk population defined as cardiovascular risk factors, aging, and dementia risk (CAIDE) score of at least 6 but with normal cognition and to examine associations between brain amyloid load and cognitive performance and vascular risk factors. METHODS: A subgroup of 48 individuals from the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) main study participated in brain 11C-Pittsburgh compound B (PiB)-PET imaging, brain MRI, and neuropsychological assessment at the beginning of the study. Lifestyle/vascular risk factors were determined as body mass index, blood pressure, total and low-density lipoprotein cholesterol, and glucose homeostasis model assessment. White matter lesions were visually rated from MRIs by a semiquantitative Fazekas score. RESULTS: Twenty participants (42%) had a positive PiB-PET on visual analysis. The PiB-positive group performed worse in executive functioning tests, included more participants with APOE ε4 allele (50%), and showed slightly better glucose homeostasis compared to PiB-negative participants. PiB-positive and -negative participants did not differ significantly in other cognitive domain scores or other vascular risk factors. There was no significant difference in Fazekas score between the PiB groups. CONCLUSIONS: The high percentage of PiB-positive participants provides evidence of a successful recruitment process of the at-risk population in the main FINGER intervention trial. The results suggest a possible association between early brain amyloid accumulation and decline in executive functions. APOE ε4 was clearly associated with amyloid positivity, but no other risk factor was found to be associated with positive PiB-PET.
OBJECTIVE: To investigate brain amyloid pathology in a dementia-risk population defined as cardiovascular risk factors, aging, and dementia risk (CAIDE) score of at least 6 but with normal cognition and to examine associations between brain amyloid load and cognitive performance and vascular risk factors. METHODS: A subgroup of 48 individuals from the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) main study participated in brain 11C-Pittsburgh compound B (PiB)-PET imaging, brain MRI, and neuropsychological assessment at the beginning of the study. Lifestyle/vascular risk factors were determined as body mass index, blood pressure, total and low-density lipoprotein cholesterol, and glucose homeostasis model assessment. White matter lesions were visually rated from MRIs by a semiquantitative Fazekas score. RESULTS: Twenty participants (42%) had a positive PiB-PET on visual analysis. The PiB-positive group performed worse in executive functioning tests, included more participants with APOE ε4 allele (50%), and showed slightly better glucose homeostasis compared to PiB-negative participants. PiB-positive and -negative participants did not differ significantly in other cognitive domain scores or other vascular risk factors. There was no significant difference in Fazekas score between the PiB groups. CONCLUSIONS: The high percentage of PiB-positive participants provides evidence of a successful recruitment process of the at-risk population in the main FINGER intervention trial. The results suggest a possible association between early brain amyloid accumulation and decline in executive functions. APOE ε4 was clearly associated with amyloid positivity, but no other risk factor was found to be associated with positive PiB-PET.
Authors: Samuel N Lockhart; Christopher L Schaich; Suzanne Craft; Bonnie C Sachs; Stephen R Rapp; Youngkyoo Jung; Christopher T Whitlow; Kiran Kumar Solingapuram Sai; Maryjo Cleveland; Benjamin J Williams; Gregory L Burke; Alain Bertoni; Kathleen M Hayden; Timothy M Hughes Journal: Alzheimers Dement Date: 2021-09-05 Impact factor: 16.655
Authors: Emily Rosenich; Lisa Bransby; Nawaf Yassi; Jurgen Fripp; Simon M Laws; Ralph N Martins; Christopher Fowler; Stephanie R Rainey-Smith; Christopher C Rowe; Colin L Masters; Paul Maruff; Yen Ying Lim Journal: Neurology Date: 2022-02-15 Impact factor: 11.800
Authors: Isabelle Bos; Stephanie J B Vos; Suzanne E Schindler; Jason Hassenstab; Chengjie Xiong; Elizabeth Grant; Frans Verhey; John C Morris; Pieter Jelle Visser; Anne M Fagan Journal: Alzheimers Dement Date: 2019-08-01 Impact factor: 21.566