Tommaso Ballarini1, Debora Melo van Lent2,3, Julia Brunner2, Alina Schröder2, Steffen Wolfsgruber2,4, Slawek Altenstein5,6, Frederic Brosseron2,4, Katharina Buerger7,8, Peter Dechent9, Laura Dobisch10,11, Emrah Duzel10,11, Birgit Ertl-Wagner12, Klaus Fliessbach2,4, Silka Dawn Freiesleben13, Ingo Frommann2, Wenzel Glanz10, Dietmar Hauser13, John Dylan Haynes14, Michael T Heneka2,4, Daniel Janowitz15, Ingo Kilimann16,17, Christoph Laske18,19, Franziska Maier20, Coraline Danielle Metzger10,11, Matthias Munk18,19, Robert Perneczky7,21,22,23, Oliver Peters5,13, Josef Priller5,6, Alfredo Ramirez20, Boris Rauchmann21, Nina Roy2, Klaus Scheffler24, Anja Schneider2,4, Annika Spottke2,25, Eike Jakob Spruth5,6, Stefan J Teipel16,17, Ruth Vukovich26, Jens Wiltfang26,27,28,29, Frank Jessen2,20,30, Michael Wagner2,4. 1. German Center for Neurodegenerative Diseases (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany tommaso.ballarini@dzne.de. 2. German Center for Neurodegenerative Diseases (DZNE), Bonn, Venusberg-Campus 1, 53127 Bonn, Germany. 3. University of Texas Health Science Center at San Antonio: San Antonio, TX, US. 4. Department of Neurodegeneration and Geriatric Psychiatry, University Hospital Bonn, Venusberg-Campus 1, 53127 Bonn, Germany. 5. German Center for Neurodegenerative Diseases (DZNE), Berlin, Germany. 6. Department of Psychiatry and Psychotherapy, Charité, Charitéplatz 1, 10117 Berlin, Germany. 7. German Center for Neurodegenerative Diseases (DZNE, Munich), Feodor-Lynen-Strasse 17, 81377 Munich, Germany. 8. Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Feodor-LynenStrasse 17, 81377 Munich, Germany. 9. MR-Research in Neurology and Psychiatry, Georg-AugustUniversity Göttingen, Germany. 10. German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany. 11. Institute of Cognitive Neurology and Dementia Research (IKND), Otto-von-Guericke University, Magdeburg, Germany. 12. Institute for Clinical Radiology, Ludwig-MaximiliansUniversity, Marchioninistr. 15, 81377 Munich. 13. Charité Universitätsmedizin Berlin, Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin, Hindenburgdamm 30, 12203 Berlin, Germany. 14. Bernstein Center for Computational Neuroscience, Charité Universitätsmedizin, Berlin, Germany. 15. Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Feodor-Lynen-Strasse 17, 81377 Munich, Germany. 16. German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany. 17. Department of Psychosomatic Medicine, Rostock University Medical Center, Gehlsheimer Str. 20, 18147 Rostock. 18. German Center for Neurodegenerative Diseases (DZNE), Tübingen, Germany. 19. Section for Dementia Research, Hertie Institute for Clinical Brain Research and Department of Psychiatry and Psychotherapy, University of Tübingen, Tübingen, Germany. 20. Department of Psychiatry, University of Cologne, Medical Faculty, Kerpener Strasse 62, 50924 Cologne, Germany. 21. Department of Psychiatry and Psychotherapy, University Hospital, LMU Munich, Munich, Germany. 22. Munich Cluster for Systems Neurology (SyNergy) Munich, Munich, Germany. 23. Ageing Epidemiology Research Unit (AGE), School of Public Health, Imperial College London, London, UK. 24. Department for Biomedical Magnetic Resonance, University of Tübingen, 72076 Tübingen, Germany. 25. Department of Neurology, University of Bonn, Venusberg-Campus 1, 53127 Bonn, Germany. 26. Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, University of Goettingen, Von-Siebold-Str. 5, 37075 Goettingen. 27. German Center for Neurodegenerative Diseases (DZNE), Goettingen, Germany. 28. Neurosciences and Signaling Group, Institute of Biomedicine (iBiMED). 29. Department of Medical Sciences, University of Aveiro, Aveiro, Portugal. 30. Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann-Strasse 26, 50931Köln, Germany.
Abstract
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.
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.
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