Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/19368
Title: Relationship Between Amyloid-β Positivity and Progression to Mild Cognitive Impairment or Dementia over 8 Years in Cognitively Normal Older Adults.
Authors: Dang, Christa;Harrington, Karra D;Lim, Yen Ying;Ames, David;Hassenstab, Jason;Laws, Simon M;Yassi, Nawaf;Hickey, Martha;Rainey-Smith, Stephanie;Robertson, Joanne;Sohrabi, Hamid R;Salvado, Olivier;Weinborn, Michael;Villemagne, Victor L;Rowe, Christopher C;Masters, Colin L;Maruff, Paul
Affiliation: CogState Ltd., Melbourne, VIC, Australia
Department of Molecular Imaging and Therapy, Centre for PET, Austin Health, Heidelberg, Victoria, Australia
Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Department of Obstetrics and Gynaecology, Melbourne Medical School, The University of Melbourne, Parkville, VIC, Australia
The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC, Australia
Cooperative Research Centre for Mental Health, Parkville, VIC, Australia
Department of Psychiatry, Academic Unit for Psychiatry of Old Age, The University of Melbourne, Parkville, VIC, Australia
National Ageing Research Institute, Parkville, VIC, Australia
Charles F. and Joanne Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA
Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA
Department of Psychological and Brain Sciences, Washington University, St. Louis, MO, USA
Collaborative Genomics Group, Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Perth, Western Australia, Australia
School of Pharmacy and Biomedical Sciences, Faculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University, Western Australia, Australia
Department of Medicine and Neurology, Royal Melbourne Hospital, Melbourne, VIC, Australia
Centre of Excellence for Alzheimer's Disease Research and Care, School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Perth, Western Australia, Australia
Australian Alzheimer's Disease Research Unit, Hollywood Private Hospital, Perth, Western Australia, Australia
School of Psychiatry and Clinical Neurosciences, University of WA, Nedlands, Western Australia, Australia
CSIRO Health and Biosecurity, the Australian eHealth Research Centre, Brisbane, QLD, Australia
School of Psychological Science, University of Western Australia, Crawley, WA, Australia
Issue Date: 22-Aug-2018
EDate: 2018-08-22
Citation: Journal of Alzheimer's disease : JAD 2018; online first: 22 August
Abstract: Preclinical Alzheimer's disease (AD) is defined by cerebral amyloid-β positivity (Aβ+) in cognitively normal (CN) older adults. To estimate the risk of progression to the symptomatic stages of AD due to PET Aβ+ and the extent that progression was influenced by other demographic, genetic, and clinical characteristics in a large prospective study. Fine-Gray subdistribution modeling was used to examine the risk of progression from CN to MCI/dementia due to Aβ+, APOEɛ4 carriage, and their interaction in the Australian Imaging, Biomarkers and Lifestyle (AIBL) flagship study of aging CN cohort (n = 599) over 8 years. 17.7% Aβ+ and 8.1% Aβ-progressed over 8 years (OR: 2.43). Risk of progression for Aβ+ was 65-104% greater than Aβ-. Aβ+ APOEɛ4 carriers were at 348% greater risk than all other participants. Significant risk factors of progression in Aβ+ were age (HR: 1.05), PET SUVR (HR: 2.49) and APOE ɛ4 carriage (HR: 2.63); only age was a significant risk factor in Aβ-(HR: 1.09). Aβ-progressors were not near the threshold for Aβ+. These relationships were not moderated by hypertension, diabetes, obesity, or stroke/TIA. Aβ+ is an important prognostic marker for progression from CN to MCI/dementia in older adults and APOEɛ4 carriage provides further predictive value in the presence of Aβ+. These data suggest that Aβ-associated clinical progression is consistent with clinical-pathological models of AD, whereas progression in the absence of elevated Aβ deposition may be the result of neuropathological processes other than AD that accumulate with age.
URI: http://ahro.austin.org.au/austinjspui/handle/1/19368
DOI: 10.3233/JAD-180507
ORCID: 0000-0003-3910-2453
PubMed URL: 30149452
Type: Journal Article
Subjects: APOEɛ4
Alzheimer’s disease
biomarkers
dementia
mild cognitive impairment
Appears in Collections:Journal articles

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