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Title: Plasma Cortisol, Brain Amyloid-β, and Cognitive Decline in Preclinical Alzheimer's Disease: A 6-Year Prospective Cohort Study.
Austin Authors: Pietrzak, Robert H;Laws, Simon M;Lim, Yen Ying;Bender, Sophie J;Porter, Tenielle;Doecke, James;Ames, David;Fowler, Christopher;Masters, Colin L ;Milicic, Lidija;Rainey-Smith, Stephanie R;Villemagne, Victor L ;Rowe, Christopher C ;Martins, Ralph N;Maruff, Paul
Affiliation: National Ageing Research Institute, Parkville, Victoria
Co-operative Research Centre for Mental Health..
U.S. Department of Veterans Affairs National Center for Posttraumatic Stress Disorder, Clinical Neurosciences Division, VA Connecticut Healthcare System, West Haven
Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut
The Florey Institute, The University of Melbourne, Parkville, Victoria
Sir James McCusker Alzheimer's Disease Research Unit, Hollywood Private Hospital, Perth, Western Australia
Academic Unit for Psychiatry of Old Age, St. Vincent's Health, Department of Psychiatry, The University of Melbourne, Kew
Centre of Excellence for Alzheimer's Disease Research and Care, Edith Cowan University, Joondalup, Western Australia
The Florey Institute, The University of Melbourne, Parkville, Victoria
School of Health Sciences, University of Notre Dame Australia, Fremantle, Western Australia
Sir James McCusker Alzheimer's Disease Research Unit, Hollywood Private Hospital, Perth, Western Australia
Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia
The Florey Institute, The University of Melbourne, Parkville, Victoria
The Commonwealth Scientific and Industrial Research Organization, Canberra..
Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Cogstate Ltd., Melbourne, Victoria, Australia
Issue Date: Jan-2017 2016-09-07
Publication information: Biological psychiatry. Cognitive neuroscience and neuroimaging 2017; 2(1): 45-52
Abstract: Hypothalamic-pituitary-adrenal axis dysregulation, which is typically assessed by measuring cortisol levels, is associated with cognitive dysfunction, hippocampal atrophy, and increased risk for mild cognitive impairment and Alzheimer's disease (AD). However, little is known about the role of hypothalamic-pituitary-adrenal axis dysregulation in moderating the effect of high levels of amyloid-β (Aβ+) on cognitive decline in the preclinical phase of AD, which is often protracted, and thus offers opportunities for prevention and early intervention. Using data from a 6-year multicenter prospective cohort study, we evaluated the relation between Aβ level, plasma cortisol level, and cognitive decline in 416 cognitively normal older adults. Results revealed that Aβ+ older adults experienced faster decline than Aβ- older adults in all cognitive domains (Cohen's d at 6-year assessment = 0.37-0.65). They further indicated a significant interaction between Aβ and cortisol levels for global cognition (d = 0.32), episodic memory (d = 0.50), and executive function (d = 0.59) scores, with Aβ+ older adults with high cortisol levels having significantly faster decline in these domains compared with Aβ+ older adults with low cortisol levels. These effects were independent of age, sex, APOE genotype, anxiety symptoms, and radiotracer type. In cognitively healthy older adults, Aβ+ is associated with greater cognitive decline and high plasma cortisol levels may accelerate the effect of Aβ+ on decline in global cognition, episodic memory, and executive function. These results suggest that therapies targeted toward lowering plasma cortisol and Aβ levels may be helpful in mitigating cognitive decline in the preclinical phase of AD.
DOI: 10.1016/j.bpsc.2016.08.006
ORCID: 0000-0003-3910-2453
PubMed URL: 29560886
Type: Journal Article
Subjects: Aging
Appears in Collections:Journal articles

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