Sophie E Holmes1, Irina Esterlis2, Carolyn M Mazure2, Yen Ying Lim3, David Ames4, Stephanie Rainey-Smith5, Ralph N Martins6, Olivier Salvado7, Vincent Dore8, Victor L Villemagne9, Christopher C Rowe10, Simon M Laws11, Colin L Masters3, Paul Maruff12, Robert H Pietrzak13. 1. Department of Psychiatry, Yale University School of Medicine, New Haven, CT. Electronic address: sophie.holmes@yale.edu. 2. Department of Psychiatry, Yale University School of Medicine, New Haven, CT. 3. The Florey Institute, The University of Melbourne, Parkville, Victoria, Australia. 4. Academic Unit for Psychiatry of Old Age, St. Vincent's Health, Department of Psychiatry, The University of Melbourne, Kew, Victoria, Australia; National Ageing Research Institute, Parkville, Victoria, Australia. 5. Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia. 6. Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia; Sir James McCusker Alzheimer's Disease Research Unit, Hollywood Private Hospital, Perth, Western Australia, Australia. 7. The Commonwealth Scientific and Industrial Research Organization, Canberra, Australia. 8. The Commonwealth Scientific and Industrial Research Organization, Canberra, Australia; Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia. 9. The Florey Institute, The University of Melbourne, Parkville, Victoria, Australia; Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia. 10. Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia. 11. Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia; School of Biomedical Sciences, Faculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australia. 12. The Florey Institute, The University of Melbourne, Parkville, Victoria, Australia; Cogstate Ltd., Melbourne, Victoria, Australia. 13. Department of Psychiatry, Yale University School of Medicine, New Haven, CT; U.S. Department of Veterans Affairs National Center for Posttraumatic Stress Disorder, Clinical Neurosciences Division, VA Connecticut Healthcare System, West Haven, CT.
Abstract
OBJECTIVE: To examine how β-amyloid (Aβ), APOE and BDNF genotypes, and cortisol relate to depressive and anxiety symptoms in cognitively normal older women and men. METHODS: Cross-sectional data were analyzed from 423 older adults from the Australian Imaging Biomarkers and Lifestyle study. Analyses of covariance evaluated associations between Aβ, APOE and BDNF genotype, and cortisol in relation to severity of depressive and anxiety symptoms. RESULTS: Among Aβ+ older adults, APOE ε4 carriage was associated with greater severity of anxiety symptoms (d = 0.55); and in the full sample, APOE ε4 carriage was linked to greater severity of depressive (d = 0.26) and anxiety (d = 0.21) symptoms. Among Aβ+ women, ε4 carriers reported greater anxiety symptoms than non-ε4 carriers (d = 0.83), and female BDNF rs6265 Val66 Met allele carriers reported greater depressive symptoms (d = 0.29). CONCLUSION: Sex moderated the relationship between Aβ, APOE genotype, and BDNF genotype in predicting severity of anxiety and depressive symptoms in cognitively normal older adults. Copyright Â
OBJECTIVE: To examine how β-amyloid (Aβ), APOE and BDNF genotypes, and cortisol relate to depressive and anxiety symptoms in cognitively normal older women and men. METHODS: Cross-sectional data were analyzed from 423 older adults from the Australian Imaging Biomarkers and Lifestyle study. Analyses of covariance evaluated associations between Aβ, APOE and BDNF genotype, and cortisol in relation to severity of depressive and anxiety symptoms. RESULTS: Among Aβ+ older adults, APOE ε4 carriage was associated with greater severity of anxiety symptoms (d = 0.55); and in the full sample, APOE ε4 carriage was linked to greater severity of depressive (d = 0.26) and anxiety (d = 0.21) symptoms. Among Aβ+ women, ε4 carriers reported greater anxiety symptoms than non-ε4 carriers (d = 0.83), and female BDNF rs6265 Val66 Met allele carriers reported greater depressive symptoms (d = 0.29). CONCLUSION: Sex moderated the relationship between Aβ, APOE genotype, and BDNF genotype in predicting severity of anxiety and depressive symptoms in cognitively normal older adults. Copyright Â
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