Rachel F Buckley1, Elizabeth C Mormino2, Rebecca E Amariglio3, Michael J Properzi4, Jennifer S Rabin5, Yen Ying Lim6, Kathryn V Papp3, Heidi I L Jacobs7, Samantha Burnham8, Bernard J Hanseeuw9, Vincent Doré10, Annette Dobson11, Colin L Masters6, Michael Waller11, Christopher C Rowe12, Paul Maruff13, Michael C Donohue14, Dorene M Rentz3, Dylan Kirn3, Trey Hedden15, Jasmeer Chhatwal4, Aaron P Schultz3, Keith A Johnson15, Victor L Villemagne12, Reisa A Sperling3. 1. The Florey Institute, The University of Melbourne, Victoria, Australia; Melbourne School of Psychological Science, University of Melbourne, Victoria, Australia; Harvard Aging Brain Study, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. Electronic address: rfbuckley@mgh.harvard.edu. 2. Department of Neurology, Stanford University, CA, USA. 3. Harvard Aging Brain Study, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA. 4. Harvard Aging Brain Study, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 5. Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 6. The Florey Institute, The University of Melbourne, Victoria, Australia. 7. Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA; Faculty of Health, Medicine and Life Sciences, School for Mental Health and Neuroscience, Alzheimer Centre Limburg, Maastricht University, Maastricht, The Netherlands. 8. The Australian eHealth Research Centre, CSIRO Health & Biosecurity, Victoria, Australia. 9. Harvard Aging Brain Study, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Center for Alzheimer Research and Treatment, Department of Neurology, Brigham and Women's Hospital, Boston, MA, USA; Department of Neurology, Cliniques Universitaires Saint-Luc, Institute of Neuroscience, Université Catholique de Louvain, Brussels, Belgium. 10. The Australian eHealth Research Centre, CSIRO Health & Biosecurity, Queensland, Australia. 11. The University of Queensland, School of Public Health, Faculty of Medicine, Queensland, Australia. 12. Department of Nuclear Medicine and Centre for PET, Austin Health, Victoria, Australia; Department of Medicine, Austin Health, The University of Melbourne, Victoria, Australia. 13. Cogstate, Ltd., Australia. 14. Department of Neurology, University of Southern California, San Diego, CA, USA. 15. Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Massachusetts General Hospital/Harvard Medical School, Boston, MA, USA.
Abstract
INTRODUCTION: Our objective was to investigate the effect of sex on cognitive decline within the context of amyloid β (Aβ) burden and apolipoprotein E genotype. METHODS: We analyzed sex-specific effects on Aβ-positron emission tomography, apolipoprotein, and rates of change on the Preclinical Alzheimer Cognitive Composite-5 across three cohorts, such as the Alzheimer's Disease Neuroimaging Initiative, Australian Imaging, Biomarker and Lifestyle, and Harvard Aging Brain Study (n = 755; clinical dementia rating = 0; age (standard deviation) = 73.6 (6.5); female = 55%). Mixed-effects models of cognitive change by sex, Aβ-positron emission tomography, and apolipoprotein ε4 were examined with quadratic time effects over a median of 4 years of follow-up. RESULTS: Apolipoprotein ε4 prevalence and Aβ burden did not differ by sex. Sex did not directly influence cognitive decline. Females with higher Aβ exhibited faster decline than males. Post hoc contrasts suggested that females who were Aβ and apolipoprotein ε4 positive declined faster than their male counterparts. DISCUSSION: Although Aβ did not differ by sex, cognitive decline was greater in females with higher Aβ. Our findings suggest that sex may play a modifying role on risk of Alzheimer's disease-related cognitive decline.
INTRODUCTION: Our objective was to investigate the effect of sex on cognitive decline within the context of amyloid β (Aβ) burden and apolipoprotein E genotype. METHODS: We analyzed sex-specific effects on Aβ-positron emission tomography, apolipoprotein, and rates of change on the Preclinical Alzheimer Cognitive Composite-5 across three cohorts, such as the Alzheimer's Disease Neuroimaging Initiative, Australian Imaging, Biomarker and Lifestyle, and Harvard Aging Brain Study (n = 755; clinical dementia rating = 0; age (standard deviation) = 73.6 (6.5); female = 55%). Mixed-effects models of cognitive change by sex, Aβ-positron emission tomography, and apolipoprotein ε4 were examined with quadratic time effects over a median of 4 years of follow-up. RESULTS:Apolipoprotein ε4 prevalence and Aβ burden did not differ by sex. Sex did not directly influence cognitive decline. Females with higher Aβ exhibited faster decline than males. Post hoc contrasts suggested that females who were Aβ and apolipoprotein ε4 positive declined faster than their male counterparts. DISCUSSION: Although Aβ did not differ by sex, cognitive decline was greater in females with higher Aβ. Our findings suggest that sex may play a modifying role on risk of Alzheimer's disease-related cognitive decline.
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