Yen Ying Lim1, Paul Maruff2, Robert H Pietrzak3, Kathryn A Ellis4, David Darby5, David Ames6, Karra Harrington5, Ralph N Martins7, Colin L Masters5, Cassandra Szoeke8, Greg Savage9, Victor L Villemagne10, Christopher C Rowe11. 1. The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia; Department of Psychiatry, The University of Melbourne, Parkville, Victoria, Australia. Electronic address: yen_ying_lim@brown.edu. 2. The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia; CogState Ltd., Melbourne, Victoria, Australia. 3. Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA. 4. The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia; Academic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, Kew, Victoria, Australia; National Ageing Research Institute, Parkville, Victoria, Australia. 5. The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia. 6. Academic Unit for Psychiatry of Old Age, Department of Psychiatry, The University of Melbourne, Kew, Victoria, Australia; National Ageing Research Institute, Parkville, Victoria, Australia. 7. Centre of Excellence for Alzheimer's Disease Research and Care, School of Exercise, Biomedical, and Health Sciences, Edith Cowan University, Perth, Western Australia, Australia. 8. The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia; National Ageing Research Institute, Parkville, Victoria, Australia; CSIRO Preventative Health Flagship, Parkville, Victoria, Australia. 9. Department of Psychology and ARC Centre of Excellence in Cognition and Its Disorders, Macquarie University, Sydney, New South Wales, Australia. 10. The Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia; Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia; Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia. 11. Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia; Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia.
Abstract
BACKGROUND: High β-amyloid (Aβ) is associated with faster memory decline in healthy individuals and adults with mild cognitive impairment (MCI). However, longer prospective studies are required to determine if Aβ-related memory decline continues and whether it is associated with increased rate of disease progression. METHODS: Healthy controls (HCs; n = 177) and adults with MCI (n = 48) underwent neuroimaging for Aβ and cognitive assessment at baseline. Cognition was reassessed 18 and 36 months later. RESULTS: Compared with low-Aβ HCs, high-Aβ HC and MCI groups showed moderate decline in episodic and working memory over 36 months. Those with MCI with low Aβ did not show any cognitive decline. Rates of disease progression were increased in the high-Aβ HC and MCI groups. CONCLUSIONS: In healthy individuals, high Aβ likely indicates that Alzheimer's disease (AD)-related neurodegeneration has begun. Once commenced, the rate of decline in cognitive function remains constant across the preclinical and prodromal stages of AD.
BACKGROUND: High β-amyloid (Aβ) is associated with faster memory decline in healthy individuals and adults with mild cognitive impairment (MCI). However, longer prospective studies are required to determine if Aβ-related memory decline continues and whether it is associated with increased rate of disease progression. METHODS: Healthy controls (HCs; n = 177) and adults with MCI (n = 48) underwent neuroimaging for Aβ and cognitive assessment at baseline. Cognition was reassessed 18 and 36 months later. RESULTS: Compared with low-Aβ HCs, high-Aβ HC and MCI groups showed moderate decline in episodic and working memory over 36 months. Those with MCI with low Aβ did not show any cognitive decline. Rates of disease progression were increased in the high-Aβ HC and MCI groups. CONCLUSIONS: In healthy individuals, high Aβ likely indicates that Alzheimer's disease (AD)-related neurodegeneration has begun. Once commenced, the rate of decline in cognitive function remains constant across the preclinical and prodromal stages of AD.
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