Andrée-Ann Baril1,2, Alexa S Beiser1,2,3, Erlan Sanchez4,5, Vincent Mysliwiec6, Susan Redline7,8,9, Daniel J Gottlieb7,9,10, George T O'Connor1,11, Mitzi M Gonzales6, Dibya Himali1, Sudha Seshadri1,2,6, Jayandra J Himali1,2,3,6,12, Matthew P Pase1,13,14. 1. The Framingham Heart Study, Framingham, Massachusetts, USA. 2. Department of Neurology, Boston University School of Medicine, Boston, Massachusetts, USA. 3. Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts, USA. 4. Centre for Advanced Research in Sleep Medicine, Hôpital du Sacré-Coeur de Montréal, CIUSSS-NIM, Montreal, Québec, Canada. 5. Department of Neuroscience, Université de Montréal, Montreal, Québec, Canada. 6. Glenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases, University of Texas Health Sciences Center, San Antonio, Texas, USA. 7. Division of Sleep and Circadian Disorders, Brigham & Women's Hospital, Boston, Massachusetts, USA. 8. Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA. 9. Division of Sleep Medicine, Harvard Medical School, Boston, Massachusetts, USA. 10. VA Boston Healthcare System, Boston, Massachusetts, USA. 11. Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA. 12. Department of Population Health Sciences, University of Texas Health Science Center, San Antonio, Texas, USA. 13. School of Psychological Sciences, Turner Institute for Brain and Mental Health, Monash University, Clayton, VIC, Australia. 14. Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
Abstract
INTRODUCTION: We evaluated whether insomnia symptom severity was associated with cognitive function, and whether this relationship was modified by biomarkers associated with Alzheimer's disease risk. METHODS: We examined insomnia symptoms and neuropsychological performance 3.4 years later in 511 dementia-free Framingham Heart Study participants (62.65 ± 8.7 years, 50.9% male). Additionally, we explored insomnia symptoms combined with self-reported short habitual sleep duration and effect modification by apolipoprotein E (APOE) ε4 allele status. RESULTS: More severe insomnia symptoms were associated with lower performance on global cognition, and immediate and delayed Logical Memory recall, especially when insomnia symptoms were combined with short sleep duration. The association between insomnia symptoms and poorer memory recall was more pronounced in APOE ε4 allele carriers. DISCUSSION: Insomnia symptom severity was associated with worse subsequent global cognitive and memory performance, which was especially apparent in APOE ε4 allele carriers, suggesting that poor sleep might be particularly detrimental when the brain is already vulnerable to neurodegeneration.
INTRODUCTION: We evaluated whether insomnia symptom severity was associated with cognitive function, and whether this relationship was modified by biomarkers associated with Alzheimer's disease risk. METHODS: We examined insomnia symptoms and neuropsychological performance 3.4 years later in 511 dementia-free Framingham Heart Study participants (62.65 ± 8.7 years, 50.9% male). Additionally, we explored insomnia symptoms combined with self-reported short habitual sleep duration and effect modification by apolipoprotein E (APOE) ε4 allele status. RESULTS: More severe insomnia symptoms were associated with lower performance on global cognition, and immediate and delayed Logical Memory recall, especially when insomnia symptoms were combined with short sleep duration. The association between insomnia symptoms and poorer memory recall was more pronounced in APOE ε4 allele carriers. DISCUSSION: Insomnia symptom severity was associated with worse subsequent global cognitive and memory performance, which was especially apparent in APOE ε4 allele carriers, suggesting that poor sleep might be particularly detrimental when the brain is already vulnerable to neurodegeneration.