Mediterranean Diet, Alzheimer Disease Biomarkers and Brain Atrophy in Old Age.

疾病 生物标志物 神经退行性变 生理学 β淀粉样蛋白 老化
作者
Tommaso Ballarini,Debora Melo van Lent,Julia Brunner,Alina Schröder,Steffen Wolfsgruber,Slawek Altenstein,Frederic Brosseron,Katharina Buerger,Peter Dechent,Laura Dobisch,Emrah Düzel,Birgit Ertl-Wagner,Klaus Fliessbach,Silka Dawn Freiesleben,Ingo Frommann,Wenzel Glanz,Dietmar Hauser,John-Dylan Haynes,Michael T. Heneka,Daniel Janowitz,Ingo Kilimann,Christoph Laske,Franziska Maier,Coraline D. Metzger,Matthias H. J. Munk,Robert Perneczky,Oliver Peters,Josef Priller,Alfredo Ramirez,Boris-Stephan Rauchmann,Nina Roy,Klaus Scheffler,Anja Schneider,Annika Spottke,Eike Jakob Spruth,Stefan J. Teipel,Ruth Vukovich,Jens Wiltfang,Frank Jessen,Michael Wagner
出处
期刊:Neurology [Ovid Technologies (Wolters Kluwer)]
卷期号:96 (24) 被引量:15
标识
DOI:10.1212/wnl.0000000000012067
摘要

Objective To determine whether following a Mediterranean-like diet (MeDi) relates to cognitive functions and in vivo biomarkers for Alzheimer disease (AD), we analyzed cross-sectional data from the German DZNE-Longitudinal Cognitive Impairment and Dementia Study. Method The sample (n = 512, mean age 69.5 ± 5.9 years) included 169 cognitively normal participants and individuals at higher AD risk (53 with relatives with AD, 209 with subjective cognitive decline, and 81 with mild cognitive impairment). We defined MeDi adherence according to the food frequency questionnaire. Brain volume outcomes were generated via voxel-based morphometry on T1-MRI, and cognitive performance was assessed with an extensive neuropsychological battery. AD-related biomarkers (β-amyloid42/40 [Aβ42/40] ratio, phosphorylated tau 181 [pTau181]) in CSF were assessed in n = 226 individuals. We analyzed the associations between MeDi and outcomes with linear regression models controlling for several covariates. In addition, we applied hypothesis-driven mediation and moderation analysis. Results Higher MeDi adherence related to larger mediotemporal gray matter volume (p Conclusion Our findings corroborate the view of MeDi as a protective factor against memory decline and mediotemporal atrophy. They suggest that these associations might be explained by a decrease of amyloidosis and tau pathology. Longitudinal and dietary intervention studies should further examine this conjecture and its treatment implications.
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