Karra D Harrington1,2,3, Emma Gould1, Yen Ying Lim2, David Ames3,4, Robert H Pietrzak5,6, Alan Rembach2, Stephanie Rainey-Smith7,8, Ralph N Martins7,8, Olivier Salvado9, Victor L Villemagne2,10,11, Christopher C Rowe10,11, Colin L Masters2, Paul Maruff2,12. 1. School of Psychology, Deakin University, Geelong, Victoria, Australia. 2. Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australia. 3. Academic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, Parkville, Victoria, Australia. 4. National Ageing Research Institute, Parkville, Victoria, Australia. 5. United States Department of Veterans Affairs, National Center for Posttraumatic Stress Disorder, Clinical Neurosciences Division, VA Connecticut Healthcare System, West Haven, CT, USA. 6. Department of Psychiatry, Yale School of Medicine, New Haven, CT, USA. 7. Centre of Excellence for Alzheimer's Disease Research and Care, School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Perth, WA, Australia. 8. Sir James McCusker Alzheimer's Disease Research Unit, Hollywood Private Hospital, Nedlands, Western Australia, Australia. 9. CSIRO Preventative Health National Research Flagship, The Australian e-Health Research Centre-BioMedIA, Herston, Queensland, Australia. 10. Department of Nuclear Medicine, Centre for PET, Austin Health, Heidelberg, VIC, Australia. 11. Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia. 12. CogState Ltd., Melbourne, Victoria, Australia.
Abstract
OBJECTIVE: Several studies have reported that non-demented older adults with clinical depression show changes in amyloid-β (Aβ) levels in blood, cerebrospinal fluid and on neuroimaging that are consistent with those observed in patients with Alzheimer's disease. These findings suggest that Aβ may be one of the mechanisms underlying the relation between the two conditions. We sought to determine the relation between elevated cerebral Aβ and the presence of depression across a 54-month prospective observation period. METHODS: Cognitively normal older adults from the Australian Imaging Biomarkers and Lifestyle study who were not depressed and had undergone a positron emission tomography scan to classify them as either high Aβ (n = 81) or low Aβ (n = 278) participated. Depressive symptoms were assessed using the Geriatric Depression Scale - Short Form at 18-month intervals over 54 months. RESULTS: Whilst there was no difference in probable depression between groups at baseline, incidence was 4.5 (95% confidence interval [CI] 1.3-16.4) times greater within the high Aβ group (9%) than the low Aβ group (2%) by the 54-month assessment. CONCLUSIONS: Results of this study suggest that elevated Aβ levels are associated with a 4.5-fold increased likelihood of developing clinically significant depressive symptoms on follow-up in preclinical Alzheimer's disease. This underscores the importance of assessing, monitoring and treating depressive symptoms in older adults with elevated Aβ.
OBJECTIVE: Several studies have reported that non-demented older adults with clinical depression show changes in amyloid-β (Aβ) levels in blood, cerebrospinal fluid and on neuroimaging that are consistent with those observed in patients with Alzheimer's disease. These findings suggest that Aβ may be one of the mechanisms underlying the relation between the two conditions. We sought to determine the relation between elevated cerebral Aβ and the presence of depression across a 54-month prospective observation period. METHODS: Cognitively normal older adults from the Australian Imaging Biomarkers and Lifestyle study who were not depressed and had undergone a positron emission tomography scan to classify them as either high Aβ (n = 81) or low Aβ (n = 278) participated. Depressive symptoms were assessed using the Geriatric Depression Scale - Short Form at 18-month intervals over 54 months. RESULTS: Whilst there was no difference in probable depression between groups at baseline, incidence was 4.5 (95% confidence interval [CI] 1.3-16.4) times greater within the high Aβ group (9%) than the low Aβ group (2%) by the 54-month assessment. CONCLUSIONS: Results of this study suggest that elevated Aβ levels are associated with a 4.5-fold increased likelihood of developing clinically significant depressive symptoms on follow-up in preclinical Alzheimer's disease. This underscores the importance of assessing, monitoring and treating depressive symptoms in older adults with elevated Aβ.
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