Pegueroles, JordiPané, AdrianaVilaplana, EduardMontal, VictorBejanin, AlexandreVidela, LauraCarmona Iragui, MaríaBarroeta, IsabelIbarzabal, AinitzeCasajoana, AnnaAlcolea, DanielValldeneu, SilviaAltuna, MirenHollanda Ramírez, Ana M. deVidal i Cortada, JosepOrtega Martínez de Victoria, EmilioOsorio, RicardoConvit, AntonioBlesa González, RafaelLleó Bisa, AlbertoFortea Ormaechea, JuanJiménez Pineda, AmandaAlzheimer's Disease Neuroimaging Initiative2021-11-042021-11-042020-01-012352-8729https://hdl.handle.net/2445/181054Aims/hypothesis: Midlife obesity is a risk factor for dementia. We investigated the impact of obesity on brain structure, metabolism, and cerebrospinal fluid (CSF) core Alzheimer's disease (AD) biomarkers in healthy elderly. Methods: We selected controls from ADNI2 with CSF AD biomarkers and/or fluorodeoxyglucose positron emission tomography (FDG-PET) and 3T-MRI. We measured cortical thickness, FDG uptake, and CSF amyloid beta (Aβ)1-42, p-tau, and t-tau levels. We performed regression analyses between these biomarkers and body mass index (BMI). Results: We included 201 individuals (mean age 73.5 years, mean BMI 27.4 kg/m2). Higher BMI was related to less cortical thickness and higher metabolism in brain areas typically not involved in AD (family-wise error [FWE] <0.05), but not to AD CSF biomarkers. It is notable that the impact of obesity on brain metabolism and structure was also found in amyloid negative individuals. Conclusions/interpretation: In the cognitively unimpaired elderly, obesity has differential effects on brain metabolism and structure independent of an underlying AD pathophysiology.9 p.application/pdfengcc by-nc-nd (c) Pegueroles, Jordi et al, 2020http://creativecommons.org/licenses/by-nc-nd/3.0/es/ObesitatDemènciaObesityDementiainfo:eu-repo/semantics/article2021-11-04info:eu-repo/semantics/openAccess32743041