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




Tommaso Ballarini, Debora Melo van Lent, Julia Brunner, Alina Schröder, Steffen Wolfsgruber, Slawek Altenstein, View ORCID ProfileFrederic Brosseron, Katharina Buerger, Peter Dechent, Laura Dobisch, Emrah Duzel, Birgit Ertl-Wagner, Klaus Fliessbach, Silka Dawn Freiesleben, View ORCID ProfileIngo Frommann, Wenzel Glanz, Dietmar Hauser, John Dylan Haynes, Michael T. Heneka, Daniel Janowitz, Ingo Kilimann, Christoph Laske, Franziska Maier, Coraline Danielle Metzger, Matthias Munk, View ORCID ProfileRobert Perneczky, Oliver Peters, Josef Priller, View ORCID ProfileAlfredo Ramirez, Boris Rauchmann, Nina Roy, View ORCID ProfileKlaus Scheffler, Anja Schneider, Annika Spottke, Eike Jakob Spruth, Stefan J. Teipel, Ruth Vukovich, Jens Wiltfang, Frank Jessen, View ORCID ProfileMichael Wagner, DELCODE study group


Objective: To determine if following a Mediterranean-like diet (MeDi) relates to cognitive functions and in vivo biomarkers for Alzheimer’s disease (AD), we analyzed cross-sectional data from the German Longitudinal Cognitive Impairment and Dementia Study

Method: The sample (n=512, mean age: 69.5±5.9 years) included 169 cognitively normal participants and subjects at higher AD risk (53 AD relatives, 209 SCD and 81 MCI). We defined MeDi adherence based on the Food Frequency Questionnaire. Brain volume outcomes were generated via voxel-based morphometry on T1-MRI and cognitive performance with an extensive neuropsychological battery. AD-related biomarkers (Aβ42/40 ratio, pTau181) in cerebrospinal fluid were assessed in n=226 individuals. We analyzed the associations between MeDi and the outcomes with linear regression models controlling for several covariates. Additionally, we applied hypothesis-driven mediation and moderation analysis.

Results: Higher MeDi adherence related to larger mediotemporal gray matter volume (p < 0.05 FWE corrected), better memory (β±SE = 0.03 ± 0.02; p=0.038), and less amyloid (Aβ42/40 ratio, β±SE = 0.003 ± 0.001; p=0.008) and pTau181 pathology (β±SE = -1.96±0.68; p=0.004). Mediotemporal volume mediated the association between MeDi and memory (40% indirect mediation). Finally, MeDi favorably moderated the associations between Aβ42/40 ratio, pTau181 and mediotemporal atrophy. Results were consistent correcting for ApoE-ε4 status.

Conclusion: Our findings corroborate the view of MeDi as a protective factor against memory decline and mediotemporal atrophy. Importantly, 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.


May 5, 2021

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