Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12558
Title: APOE ε4 moderates amyloid-related memory decline in preclinical Alzheimer's disease.
Austin Authors: Lim, Yen Ying;Villemagne, Victor L ;Pietrzak, Robert H;Ames, David;Ellis, Kathryn A;Harrington, Karra;Snyder, Peter J;Martins, Ralph N;Masters, Colin L ;Rowe, Christopher C ;Maruff, Paul
Institutional Author: Australian Imaging, Biomarkers and Lifestyle (AIBL) Research Group
Affiliation: Academic Unit for Psychiatry of Old Age, St. Vincent's Health, The University of Melbourne, Kew, Victoria, Australia
The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australia
Sir James McCusker Alzheimer's Disease Research Unit, Hollywood Private Hospital, Perth, Western Australia, Australia
Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA
Cogstate Ltd., Melbourne, Victoria, Australia
National Ageing Research Institute, Parkville, Victoria, Australia
Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Department of Neurology, Rhode Island Hospital, Providence, RI, USA
Department of Neurology, Warren Alpert School of Medicine, Brown University, Providence, RI, USA
Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia
Issue Date: 11-Dec-2014
Publication information: Neurobiology of Aging 2014; 36(3): 1239-44
Abstract: The apolipoprotein E (APOE) ɛ4 allele and high levels of beta-amyloid (Aβ) are associated with episodic memory decline and risk for Alzheimer's disease. However, there is debate about independent or interactive effects of ɛ4 on Aβ-related memory decline in healthy older adults. Healthy older adults with high Aβ burden (n = 84) enrolled in Australian Imaging, Biomarkers, and Lifestyle Study were included in this study. Cognition was measured using the computerized Cogstate Brief Battery at baseline, 18-, 36-, and 54-month follow-ups. Mini Mental State Examination and Clinical Dementia Rating scales were also administered at baseline and each follow-up timepoint. Relative to Aβ+ ɛ4 noncarriers (n = 36), Aβ+ ɛ4 carriers (n = 48) showed significantly faster decline on memory tasks, which was by convention, moderate in magnitude (d = 0.40-0.47). Aβ positivity coupled with APOE ɛ4 was associated with moderately increased decline in memory over a 54-month assessment period, suggesting that, in the preclinical stages of Alzheimer's disease, the manifestation of memory decline in older adults with high Aβ is exacerbated by the presence of APOE ɛ4.
URI: https://ahro.austin.org.au/austinjspui/handle/1/12558
DOI: 10.1016/j.neurobiolaging.2014.12.008
Journal: Neurobiology of aging
URL: https://pubmed.ncbi.nlm.nih.gov/25559335
Type: Journal Article
Subjects: Apolipoprotein E
Beta-amyloid
Cognitive decline
Memory
Preclinical Alzheimer's disease
Appears in Collections:Journal articles

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