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Ntanasi, Eva

0000-0001-9311-0994

Mayo Clinic

Harokopio University of Athens

Citations 2

Associations of lifestyle factors with amyloid pathology in persons without dementia
Oomens, Julie Elisabeth , Vos, Stephanie J. B. , Maserejian, Nancy N., Didic, Mira , Engelborghs, Sebastiaan , Fladby, Tormod, Fröhlich, Lutz, Gill, Kiran Dip, Grimmer, Timo, Itoh, Yoshiaki , Landau, Susan, Lleó, Alberto, Meyer, Philipp T. , Pardini, Matteo , Rami, Lorena , Reiman, Eric M. , Rinne, Juha O. , Sánchez‐Juan, Pascual, Scarmeas, Nikolaos , Villeneuve, Sylvia , Waldemar, Gunhild , Alcolea, Daniel, Altomare, Daniele , Baldeiras, Inês , Blennow, Kaj , Cerman, Jiří , Chipi, Elena , Day, Gregory S. , Förster, Stefan , Frings, Lars , Guedj, Éric , Habeck, Christian , Hausner, Lucrezia , Jiménez‐Bonilla, J., Juaristi, Arantxa, Kern, Silke , Kirsebom, Bjørn‐Eivind , Legdeur, Nienke , Xiong, Chengjie , Maier, W., Marquié, Marta, Minatani, Shinobu, Prabhakar, Sudesh, Ramakers, Inez H.G.B. , Rodríguez‐Rodríguez, Eloy , Ruiz, Agustín, Rüther, E., Sakhardande, Jayant, Selnes, Per, Spiru, Luiza , Vermunt, Lisa , Wallin, Åsa K., Zettergren, Anna , (ADNI), for the Alzheimer's Disease Neuroimaging Initiative, group, A4 Study, (DIAN), Dominantly Inherited Alzheimer Network, (KBASE), Japan Alzheimer's Disease Neuroimaging Initiative (J-ADNI), Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer's Disease, Ossenkoppele, Rik, Verhey, Frans RJ, Visser, Pieter Jelle, Jansen, Willemijn J, Marquié, Marta , Selnes, Per , Day, Gregory S , Xiong, Chengjie , Oomens, Julie E , Boada, Merçé , Fladby, Tormod , Flier, Wiesje M. van der , Frisoni, Giovanni B. , Fröhlich, Lutz, Grimmer, Timo , Hort, Jakub , Iwatsubo, Takeshi , Klimkowicz‐Mrowiec, Aleksandra , Lee, Dong Young , Lleó, Alberto , Martínez‐Lage, Pablo , Mendonça, Alexandre de , Parchi, Piero , Parnetti, Lucilla , Popp, Julius , Rodrigue, Karen M. , Santana, Isabel , Scheltens, Philip , Skoog, Ingmar , Sperling, Reisa Anne , Stern, Yaakov , Wiltfang, Jens , Zetterberg, Henrik , Alcolea, Daniel , Allegri, Ricardo , Bateman, Randall J. , Baiardi, Simone , Braber, Anouk den , Buchem, Mark A. van , Byun, Min Soo , Chen, Kewei , Drzezga, Alexander E. , Ekblad, Laura L. , Fortea, Juan , Freund‐Levi, Yvonne , Handels, Ron , Hellwig, Sabine , Kandimalla, Ramesh , Kornhuber, Johannes , Morbelli, Silvia , Mroczko, Barbara , Ntanasi, Eva , Oliveira, Catarina Resende , Orellana, Adelina , Peters, Oliver , Ruiz, Agustı́n , Silva, Dina , Soininen, Hilkka S. , Takeda, Akitoshi , Teunissen, Charlotte E. , Tijms, Betty M. , Wiels, Wietse A. , Yannakoulia, Mary , Yi, Dahyun , (ADNI), for the Alzheimer's Disease Neuroimaging Initiative, group, A4 Study, (DIAN), Dominantly Inherited Alzheimer Network, (KBASE), Japan Alzheimer's Disease Neuroimaging Initiative (J-ADNI), Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer's Disease, Ossenkoppele, Rik, Verhey, Frans R.J. , Visser, Pieter Jelle , Jansen, Willemijn J.

Journal of Alzheimer’s Disease | November 14, 2025 | Volume: 108 | Issue: 3 | Pages: 1043-1059

10.1177/13872877251379083 Get It

Background The association between lifestyle factors and Alzheimer's disease (AD) pathophysiology remains incompletely understood. Objective The aim of this study was to assess the association of alcohol consumption, smoking behavior, sleep quality and physical, cognitive, and social activity with cerebral amyloid pathology. Methods For this cross-sectional study, we selected participants from the Amyloid Biomarker Study data pooling initiative. We used generalized estimating equations to assess associations of dichotomized lifestyle measures with amyloid pathology. Results We included 9171 participants with normal cognition (NC) and 2555 participants with mild cognitive impairment (MCI) from the Amyloid Biomarker Study. Of participants with NC, 58% were women, 34% were APOE ε4 carrier, and 27% had amyloid pathology. Of participants with MCI, 48% were women, 47% were APOE ε4 carrier, and 57% had amyloid pathology. In NC, cognitively active participants were less likely to have amyloid pathology (OR = 0.77, 95%CI 0.66–0.89, p < 0.001). In MCI, participants who had ever smoked or had sleep problems were less likely to have amyloid pathology (OR = 0.85, 95%CI 0.73–0.99, p = 0.029; OR = 0.62, 95%CI 0.45–0.86, p = 0.004). Conclusions In NC, cognitive activity was associated with a lower frequency of amyloid pathology. In MCI, favorable lifestyle behaviors were not associated with a lower frequency of amyloid pathology. The results of the current study contribute to the broader evidence base on lifestyle and AD by further characterizing the role of lifestyle behaviors in AD pathology across different clinical stages.
Depressive Symptoms and Amyloid Pathology
Oomens, Julie Elisabeth , Engelborghs, Sebastiaan , Arnim, Christine A. F. Von , Boada, Merçé , Didic, Mira , Dubois, Bruno, Fröhlich, Lutz, Gill, Kiran Dip, Grimmer, Timo, Hildebrandt, Helmut , Itoh, Yoshiaki , Lee, Dong Young , Lleó, Alberto, Meyer, Philipp T. , Kapaki, Elisabeth, Pardini, Matteo , Popp, Julius , Rami, Lorena , Reiman, Eric M. , Rinne, Juha O. , Sánchez‐Juan, Pascual, Sarazin, Marie , Scarmeas, Nikolaos , Villeneuve, Sylvia , Wallin, Anders, Vos, Stephanie J. B. , Jansen, Willemijn J. , group, Amyloid Biomarker Study, Altomare, Daniele , Baldeiras, Inês , Blennow, Kaj, Braber, Anouk den , Cerman, Jiří , Chipi, Elena , Eckerström, Marie , Ekblad, Laura L. , Förster, Stefan , Guedj, Éric , Hausner, Lucrezia , Huey, Edward D. , Jiménez‐Bonilla, J., Johnson, Keith A. , Juaristi, Arantxa, Kern, Silke , Kirsebom, Bjørn‐Eivind , Landau, Susan , Legdeur, Nienke , Guerra, Jorge J. Llibre, Maserejian, Nancy N., Marquié, Marta , Minatani, Shinobu, Olivieri, Pauline , Perrin, Richard J., Peters, Oliver , Prabhakar, Sudesh, Ramakers, Inez H., Rodríguez‐Rodríguez, Eloy , Ruiz, Agustín, Rüther, E., Selnes, Per , Spiru, Luiza , Takeda, Akitoshi , Teichmann, Marc , Thompson, Loisa I., Vogelgsangs, Jonathan, Wallin, Åsa K., Zettergren, Anna , Frisoni, Giovanni B. , Boada, Merce , Oomens, Julie E , Bottlaender, Michel , Wiels, Wietse A. , Baeken, Chris , Dubois, Bruno , Fladby, Tormod , Flier, Wiesje M. van der , Frisoni, Giovanni B. , Fröhlich, Lutz, Grimmer, Timo , Hort, Jakub , Iwatsubo, Takeshi , Klimkowicz‐Mrowiec, Aleksandra , Lleó, Alberto , Martínez‐Lage, Pablo , Mendonça, Alexandre de , Parchi, Piero , Parnetti, Lucilla , Rodrigue, Karen M. , Santana, Isabel , Skoog, Ingmar , Snyder, Peter J. , Sperling, Reisa Anne , Wiltfang, Jens , Zetterberg, Henrik , Ossenkoppele, Rik , Verhey, Frans R.J. , Visser, Pieter Jelle , Alcolea, Daniel , Baiardi, Simone , Bateman, Randall J. , Blennow, Kaj , Buchem, Mark A. van , Byun, Min Soo , Chen, Kewei , Day, Gregory S. , Drzezga, Alexander E. , Epelbaum, Stéphane , Fortea, Juan , Freund‐Levi, Yvonne , Frings, Lars , Hellwig, Sabine , Kandimalla, Ramesh , Paraskevas, George P. , Kornhuber, Johannes , Lagarde, Julien , Morbelli, Silvia , Mroczko, Barbara , Ntanasi, Eva , Oliveira, Catarina Resende , Olivieri, Pauline , Orellana, Adelina , Ruiz, Agustı́n , Silva, Dina , Soininen, Hilkka S. , Tijms, Betty M. , Teunissen, Charlotte E. , Vöglein, Jonathan , Waldemar, Gunhild , Yannakoulia, Mary , Yi, Dahyun

JAMA Psychiatry | January 22, 2025 | Volume: 82 | Issue: 3 | Pages: 296

10.1001/jamapsychiatry.2024.4305 Get It

Importance Depressive symptoms are associated with cognitive decline in older individuals. Uncertainty about underlying mechanisms hampers diagnostic and therapeutic efforts. This large-scale study aimed to elucidate the association between depressive symptoms and amyloid pathology. Objective To examine the association between depressive symptoms and amyloid pathology and its dependency on age, sex, education, and APOE genotype in older individuals without dementia. Design, Setting, and Participants Cross-sectional analyses were performed using data from the Amyloid Biomarker Study data pooling initiative. Data from 49 research, population-based, and memory clinic studies were pooled and harmonized. The Amyloid Biomarker Study has been collecting data since 2012 and data collection is ongoing. At the time of analysis, 95 centers were included in the Amyloid Biomarker Study. The study included 9746 individuals with normal cognition (NC) and 3023 participants with mild cognitive impairment (MCI) aged between 34 and 100 years for whom data on amyloid biomarkers, presence of depressive symptoms, and age were available. Data were analyzed from December 2022 to February 2024. Main Outcomes and Measures Amyloid-β1-42 levels in cerebrospinal fluid or amyloid positron emission tomography scans were used to determine presence or absence of amyloid pathology. Presence of depressive symptoms was determined on the basis of validated depression rating scale scores, evidence of a current clinical diagnosis of depression, or self-reported depressive symptoms. Results In individuals with NC (mean [SD] age, 68.6 [8.9] years; 5664 [58.2%] female; 3002 [34.0%] APOE ε4 carriers; 937 [9.6%] had depressive symptoms; 2648 [27.2%] had amyloid pathology), the presence of depressive symptoms was not associated with amyloid pathology (odds ratio [OR], 1.13; 95% CI, 0.90-1.40; P = .29). In individuals with MCI (mean [SD] age, 70.2 [8.7] years; 1481 [49.0%] female; 1046 [44.8%] APOE ε4 carriers; 824 [27.3%] had depressive symptoms; 1668 [55.8%] had amyloid pathology), the presence of depressive symptoms was associated with a lower likelihood of amyloid pathology (OR, 0.73; 95% CI 0.61-0.89; P = .001). When considering subgroup effects, in individuals with NC, the presence of depressive symptoms was associated with a higher frequency of amyloid pathology in APOE ε4 noncarriers (mean difference, 5.0%; 95% CI 1.0-9.0; P = .02) but not in APOE ε4 carriers. This was not the case in individuals with MCI. Conclusions and Relevance Depressive symptoms were not consistently associated with a higher frequency of amyloid pathology in participants with NC and were associated with a lower likelihood of amyloid pathology in participants with MCI. These findings were not influenced by age, sex, or education level. Mechanisms other than amyloid accumulation may commonly underlie depressive symptoms in late life.