Simone Hollands1, Yen Ying Lim2, Rachel Buckley3, Robert H Pietrzak4, Peter J Snyder5, David Ames6, Kathryn A Ellis7, Karra Harrington7, Nicola Lautenschlager8, Ralph N Martins9, Colin L Masters7, Victor L Villemagne10, Christopher C Rowe11, Paul Maruff12. 1. School of Psychology, Royal Melbourne Institute of Technology, Bundoora, VIC, Australia. 2. The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia Department of Neurology, Warren Alpert School of Medicine of Brown University & Lifespan Hospital System, Providence, RI, USA. 3. The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia School of Psychology, University of Melbourne, Parkville, VIC, Australia. 4. Department of Psychiatry, Yale School of Medicine, New Haven, CT, USA. 5. Department of Neurology, Warren Alpert School of Medicine of Brown University & Lifespan Hospital System, Providence, RI, USA. 6. Academic Unit for Psychiatry of Old Age, St. Vincent's Health, The University of Melbourne, Kew, VIC, Australia National Ageing Research Institute, Parkville, VIC, Australia. 7. The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia. 8. Academic Unit for Psychiatry of Old Age, St. Vincent's Health, The University of Melbourne, Kew, VIC, Australia School of Psychiatry and Clinical Neurosciences and Western Australian Centre for Health and Aging, University of Western Australia, Perth, Australia. 9. Centre of Excellence for Alzheimer's Disease Research and Care, Edith Cowan University, Joondalup, Western Australia, Australia. 10. The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, VIC, Australia Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, VIC, Australia. 11. Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, VIC, Australia Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, VIC, Australia. 12. The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia Cogstate Ltd., Melbourne, VIC, Australia.
Abstract
BACKGROUND: The detection of early Alzheimer's disease (AD) can rely on subjective and informant reports of cognitive impairment. However, relationships between subjective cognitive impairment, objectively measured cognitive function, and amyloid-β (Aβ) biomarkers remain unclear. OBJECTIVE: To determine the extent to which impairment or decline in subjective and informant rated cognitive impairment was associated with memory in healthy older adults with high Aβ. METHODS: Healthy older adults (n = 289) enrolled in the Australian Imaging, Biomarkers and Lifestyle (AIBL) study were studied at baseline. Pittsburgh Compound B was used to determine Aβ status at baseline. At baseline and 18 months assessments, subjective memory impairment was assessed using the Memory Complaint Questionnaire and the Short Form of the Informant Questionnaire on Cognitive Decline in the Elderly. Cognition was measured using the Cogstate Brief Battery. RESULTS: At baseline, there were no differences between low and high Aβ groups in subjective or informant-rated cognitive impairment, depressive and anxiety symptoms, or cognitive function. Longitudinal analyses showed moderate decline in learning and working memory over the 18 months in the high Aβ group. However there was no change over time in subjective or informant-rated cognitive impairment, depressive and anxiety symptoms, or cognition in either Aβ group. CONCLUSIONS: Although healthy older adults with high Aβ levels show decline in learning and working memory over 18 months, subjective or informant ratings of cognitive impairment do not change over the same period suggesting subjective cognitive impairment may have limited utility for the very early identification of AD.
BACKGROUND: The detection of early Alzheimer's disease (AD) can rely on subjective and informant reports of cognitive impairment. However, relationships between subjective cognitive impairment, objectively measured cognitive function, and amyloid-β (Aβ) biomarkers remain unclear. OBJECTIVE: To determine the extent to which impairment or decline in subjective and informant rated cognitive impairment was associated with memory in healthy older adults with high Aβ. METHODS: Healthy older adults (n = 289) enrolled in the Australian Imaging, Biomarkers and Lifestyle (AIBL) study were studied at baseline. Pittsburgh Compound B was used to determine Aβ status at baseline. At baseline and 18 months assessments, subjective memory impairment was assessed using the Memory Complaint Questionnaire and the Short Form of the Informant Questionnaire on Cognitive Decline in the Elderly. Cognition was measured using the Cogstate Brief Battery. RESULTS: At baseline, there were no differences between low and high Aβ groups in subjective or informant-rated cognitive impairment, depressive and anxiety symptoms, or cognitive function. Longitudinal analyses showed moderate decline in learning and working memory over the 18 months in the high Aβ group. However there was no change over time in subjective or informant-rated cognitive impairment, depressive and anxiety symptoms, or cognition in either Aβ group. CONCLUSIONS: Although healthy older adults with high Aβ levels show decline in learning and working memory over 18 months, subjective or informant ratings of cognitive impairment do not change over the same period suggesting subjective cognitive impairment may have limited utility for the very early identification of AD.
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