| dc.identifier.citation |
Oomens JE, Vos SJ, Maserejian NN, Boada M, Didic M, Engelborghs S, Fladby T, van der Flier WM, Frisoni GB, Fröhlich L, Gill KD, Grimmer T, Hort J, Itoh Y, Iwatsubo T, Klimkowicz-Mrowiec A, Landau SM, Lee DY, Lleó A, Martinez-Lage P, de Mendonça A, Meyer PT, Parchi P, Pardini M, Parnetti L, Popp J, Rami L, Reiman EM, Rinne JO, Rodrigue KM, Sánchez-Juan P, Santana I, Scarmeas N, Scheltens P, Skoog I, Sperling RA, Stern Y, Villeneuve S, Waldemar G, Wiltfang J, Zetterberg H, Alcolea D, Allegri RF, Altomare D, Bateman RJ, Baiardi S, Baldeiras I, Blennow K, Braber AD, van Buchem MA, Byun MS, Cerman J, Chen K, Chipi E, Day GS, Drzezga A, Ekblad LL, Förster S, Fortea J, Freund-Levi Y, Frings L, Guedj E, Habeck CG, Handels R, Hausner L, Hellwig S, Jiménez-Bonilla JF, Juaristi AI, Kandimalla R, Kern S, Bordewick Kirsebom BS, Kornhuber J, Legdeur N, Levin J, Maier W, Marquié M, Minatani S, Morbelli SD, Mroczko B, Ntanasi E, de Oliveira CR, Orellana A, Peters O, Prabhakar S, Ramakers IH, Rodríguez-Rodriguez E, Ruiz A, Rüther E, Sakhardande J, Selnes P, Silva D, Soininen H, Spiru L, Takeda A, Teunissen CE, Tijms BM, Vermunt L, Wallin ÅK, Wiels W, Yannakoulia M, Yi D, Zettergren A; Alzheimer's Disease Neuroimaging Initiative (ADNI); A4 Study group; Dominantly Inherited Alzheimer Network (DIAN); European Prevention of Alzheimer's Dementia (EPAD) consortium, Fundació ACE Healthy Brain Initiative (FACEHBI); Japan Alzheimer's Disease Neuroimaging Initiative (J-ADNI), Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer's Disease (KBASE); Presymptomatic Evaluation of Experimental or Novel Treatments for Alzheimer's Disease (PREVENT-AD) research group; Ossenkoppele R, Verhey FR, Visser PJ, Jansen WJ. Associations of lifestyle factors with amyloid pathology in persons without dementia. J Alzheimers Dis. 2025 Dec;108(3):1043-1059. doi: 10.1177/13872877251379083. Epub 2025 Nov 13. |
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| dc.description.abstract |
BackgroundThe association between lifestyle factors and Alzheimer's disease (AD) pathophysiology remains incompletely understood.ObjectiveThe 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.MethodsFor 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.ResultsWe 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).ConclusionsIn 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. |
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