Belinda M Brown1, Hamid R Sohrabi2, Kevin Taddei2, Samantha L Gardener2, Stephanie R Rainey-Smith2, Jeremiah J Peiffer3, Chengjie Xiong4, Anne M Fagan5, Tammie Benzinger6, Virginia Buckles5, Kirk I Erickson7, Roger Clarnette8, Tejal Shah9, Colin L Masters10, Michael Weiner11, Nigel Cairns12, Martin Rossor13, Neill R Graff-Radford14, Stephen Salloway15, Jonathan Vöglein16, Christoph Laske17, James Noble18, Peter R Schofield19, Randall J Bateman5, John C Morris5, Ralph N Martins2. 1. School of Psychology and Exercise Science, Murdoch University, Murdoch, Western Australia, Australia; Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia; McCusker Alzheimer's Research Foundation, Nedlands, Western Australia, Australia. Electronic address: b.brown@murdoch.edu.au. 2. Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia; McCusker Alzheimer's Research Foundation, Nedlands, Western Australia, Australia. 3. School of Psychology and Exercise Science, Murdoch University, Murdoch, Western Australia, Australia. 4. Division of Biostatistics, Washington University in St Louis, St Louis, Missouri, USA. 5. Department of Neurology, Washington University in St Louis, St Louis, Missouri, USA. 6. Department of Radiology, Washington University in St Louis, St Louis, Missouri, USA. 7. Department of Psychology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. 8. School of Medicine and Pharmacology, University of Western Australia, Crawley, Western Australia, Australia. 9. McCusker Alzheimer's Research Foundation, Nedlands, Western Australia, Australia. 10. The Florey Institute, The University of Melbourne, Parkville, Victoria, Australia. 11. Center for Imaging of Neurodegenerative Disease, San Francisco VA Medical Center, University of California, San Francisco, California, USA. 12. Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri, USA. 13. Dementia Research Centre, University College London (UCL) Institute of Neurology, London, United Kingdom. 14. Department of Neurology, Mayo Clinic Jacksonville, Jacksonville, Florida, USA. 15. Department of Neurology, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA. 16. German Center for Neurodegenerative Diseases, Munich, Germany; Department of Neurology, Ludwig-Maximilians-Universität München, Munich, Germany. 17. German Center for Neurodegenerative Diseases, Tübingen, Germany; Section for Dementia Research, Hertie Institute for Clinical Brain Research and Department of Psychiatry and Psychotherapy, University of Tübingen, Tübingen, Germany. 18. Department of Neurology, Columbia University Medical Centre, New York, New York, USA. 19. Neuroscience Research Australia, Sydney, New South Wales, Australia; School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia.
Abstract
INTRODUCTION: The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. METHODS: In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42, and CSF tau levels was evaluated using linear regression. RESULTS: No differences in brain amyloid load, CSF Aβ42, or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. DISCUSSION: Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers.
INTRODUCTION: The objective of this study was to evaluate the relationship between self-reported exercise levels and Alzheimer's disease (AD) biomarkers, in a cohort of autosomal dominant AD mutation carriers. METHODS: In 139 presymptomatic mutation carriers from the Dominantly Inherited Alzheimer Network, the relationship between self-reported exercise levels and brain amyloid load, cerebrospinal fluid (CSF) Aβ42, and CSF tau levels was evaluated using linear regression. RESULTS: No differences in brain amyloid load, CSF Aβ42, or CSF tau were observed between low and high exercise groups. Nevertheless, when examining only those already accumulating AD pathology (i.e., amyloid positive), low exercisers had higher mean levels of brain amyloid than high exercisers. Furthermore, the interaction between exercise and estimated years from expected symptom onset was a significant predictor of brain amyloid levels. DISCUSSION: Our findings indicate a relationship exists between self-reported exercise levels and brain amyloid in autosomal dominant AD mutation carriers.
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