Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/19211
Title: Aβ-related memory decline in APOE ε4 noncarriers: Implications for Alzheimer disease.
Austin Authors: Lim, Yen Ying;Laws, Simon M;Villemagne, Victor L ;Pietrzak, Robert H;Porter, Tenielle;Ames, David;Fowler, Christopher;Rainey-Smith, Stephanie R;Snyder, Peter J;Martins, Ralph N;Salvado, Olivier;Bourgeat, Pierrick;Rowe, Christopher C ;Masters, Colin L ;Maruff, Paul
Affiliation: Department of Medicine, Austin Health, Heidelberg, Victoria, Australia
Department of Neurology, Warren Alpert Medical School of Brown University, Providence, RI
CogState Ltd., Melbourne, Australia
Sir James McCusker Alzheimer's Disease Research Unit, Hollywood Private Hospital, Perth
Co-operative Research Centre for Mental Health, Carlton South
From The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville
Centre of Excellence for Alzheimer's Disease Research and Care, Edith Cowan University, Joondalup, Australia
Department of Psychiatry, Yale University School of Medicine, New Haven, CT
Academic Unit for Psychiatry of Old Age, St. Vincent's Health, The University of Melbourne, Kew
National Ageing Research Institute, Parkville, Australia
Commonwealth Scientific Industrial Research Organization (CSIRO) Preventative Health National Research Flagship, Australian e-Health Research Centre-BiaMedIA, Brisbane
Department of Nephrology, Austin Health, Heidelberg, Victoria, Australia
Issue Date: 2016
Date: 2016
Publication information: Neurology 2016; 86(17): 1635-42
Abstract: As the absence of Aβ-related memory decline in APOE ε4 noncarriers may be due to the relative brevity of previous studies, we aimed to characterize Aβ-related cognitive decline over 72 months in APOE ε4 carriers and noncarriers who were cognitively normal (CN). CN older adults (n = 423) underwent Aβ imaging and APOE genotyping. Participants completed comprehensive neuropsychological testing at baseline 18-, 36-, 54-, and 72-month assessments. Relative to Aβ- CN ε4 noncarriers, both Aβ+ CN ε4 carriers and noncarriers showed significantly increased decline in measures of memory, language, and executive function as well as higher rates of progression to a clinical classification of mild cognitive impairment. Memory decline was greater in Aβ+ CN ε4 carriers than in Aβ+ CN ε4 noncarriers. No cognitive decline was evident in Aβ- CN ε4 carriers. In CN older adults, Aβ+ is associated with memory decline in ε4 noncarriers; however, the rate of this decline is much slower than that observed in ε4 carriers. These data indicate that the processes by which ε4 carriage increases the rate of Aβ-related cognitive decline occur in the preclinical stage of Alzheimer disease.
URI: https://ahro.austin.org.au/austinjspui/handle/1/19211
DOI: 10.1212/WNL.0000000000002604
ORCID: 0000-0003-3910-2453
Journal: Neurology
PubMed URL: 27029632
Type: Journal Article
Appears in Collections:Journal articles

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