Obesity impacts brain metabolism and structure independently of amyloid and tau pathology in healthy elderly

Aims/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 f...

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Published inAlzheimer's & dementia : diagnosis, assessment & disease monitoring Vol. 12; no. 1; pp. e12052 - n/a
Main Authors Pegueroles, Jordi, Pané, Adriana, Vilaplana, Eduard, Montal, Víctor, Bejanin, Alexandre, Videla, Laura, Carmona‐Iragui, María, Barroeta, Isabel, Ibarzabal, Ainitze, Casajoana, Anna, Alcolea, Daniel, Valldeneu, Silvia, Altuna, Miren, Hollanda, Ana, Vidal, Josep, Ortega, Emilio, Osorio, Ricardo, Convit, Antonio, Blesa, Rafael, Lleó, Alberto, Fortea, Juan, Jiménez, Amanda
Format Journal Article
LanguageEnglish
Published United States John Wiley & Sons, Inc 2020
John Wiley and Sons Inc
Wiley
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Summary:Aims/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.
Bibliography:Juan Fortea and Amanda Jiménez shared the senior authorship.
Jordi Pegueroles and Adriana Pané contributed equally to this work.
Data used in preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at
http://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf
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Data used in preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf.
ISSN:2352-8729
2352-8729
DOI:10.1002/dad2.12052