Erin L Abner1, Peter T Nelson2, Richard J Kryscio3, Frederick A Schmitt4, David W Fardo3, Randall L Woltjer5, Nigel J Cairns6, Lei Yu7, Hiroko H Dodge8, Chengjie Xiong9, Kamal Masaki10, Suzanne L Tyas11, David A Bennett7, Julie A Schneider12, Zoe Arvanitakis7. 1. Sanders-Brown Center on Aging and Alzheimer's Disease Center, University of Kentucky, Lexington, KY, USA; College of Public Health, Department of Epidemiology, University of Kentucky, Lexington, KY, USA; College of Public Health, Department of Biostatistics, University of Kentucky, Lexington, KY, USA. Electronic address: erin.abner@uky.edu. 2. Sanders-Brown Center on Aging and Alzheimer's Disease Center, University of Kentucky, Lexington, KY, USA; College of Medicine, Department of Pathology, University of Kentucky, Lexington, KY, USA. 3. Sanders-Brown Center on Aging and Alzheimer's Disease Center, University of Kentucky, Lexington, KY, USA; College of Public Health, Department of Biostatistics, University of Kentucky, Lexington, KY, USA. 4. Sanders-Brown Center on Aging and Alzheimer's Disease Center, University of Kentucky, Lexington, KY, USA; College of Medicine, Department of Neurology, University of Kentucky, Lexington, KY, USA. 5. Layton Aging and Alzheimer's Disease Center, Oregon Health & Science University, Portland, OR, USA; School of Medicine, Department of Pathology, Oregon Health & Science University, Portland, OR, USA. 6. Knight Alzheimer's Disease Research Center, Washington University, St. Louis, MO, USA; School of Medicine, Department of Neurology, Washington University, St. Louis, MO, USA. 7. Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; Rush University Medical Center, Department of Neurological Sciences, Chicago, IL, USA. 8. Layton Aging and Alzheimer's Disease Center, Oregon Health & Science University, Portland, OR, USA; School of Medicine, Department of Neurology, Oregon Health & Science University, Portland, OR, USA. 9. Knight Alzheimer's Disease Research Center, Washington University, St. Louis, MO, USA; School of Medicine, Division of Biostatistics, Washington University, St. Louis, MO, USA. 10. Kuakini Medical Center and John A. Burns School of Medicine, Department of Geriatric Medicine, University of Hawaii, Honolulu, HI, USA. 11. School of Public Health and Health Systems, Department of Psychology, University of Waterloo, Waterloo, ON, Canada. 12. Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA; Rush University Medical Center, Department of Pathology, Chicago, IL, USA.
Abstract
INTRODUCTION: The relationship of diabetes to specific neuropathologic causes of dementia is incompletely understood. METHODS: We used logistic regression to evaluate the association between diabetes and infarcts, Braak neurofibrillary tangle stage, and neuritic plaque score in 2365 autopsied persons. In a subset of >1300 persons with available cognitive data, we examined the association between diabetes and cognition using Poisson regression. RESULTS: Diabetes increased odds of brain infarcts (odds ratio [OR] = 1.57, P < .0001), specifically lacunes (OR = 1.71, P < .0001), but not Alzheimer's disease neuropathology. Diabetes plus infarcts was associated with lower cognitive scores at end of life than infarcts or diabetes alone, and diabetes plus high level of Alzheimer's neuropathologic changes was associated with lower mini-mental state examination scores than the pathology alone. DISCUSSION: This study supports the conclusions that diabetes increases the risk of cerebrovascular but not Alzheimer's disease pathology, and at least some of diabetes' relationship to cognitive impairment may be modified by neuropathology.
INTRODUCTION: The relationship of diabetes to specific neuropathologic causes of dementia is incompletely understood. METHODS: We used logistic regression to evaluate the association between diabetes and infarcts, Braak neurofibrillary tangle stage, and neuritic plaque score in 2365 autopsied persons. In a subset of >1300 persons with available cognitive data, we examined the association between diabetes and cognition using Poisson regression. RESULTS:Diabetes increased odds of brain infarcts (odds ratio [OR] = 1.57, P < .0001), specifically lacunes (OR = 1.71, P < .0001), but not Alzheimer's disease neuropathology. Diabetes plus infarcts was associated with lower cognitive scores at end of life than infarcts or diabetes alone, and diabetes plus high level of Alzheimer's neuropathologic changes was associated with lower mini-mental state examination scores than the pathology alone. DISCUSSION: This study supports the conclusions that diabetes increases the risk of cerebrovascular but not Alzheimer's disease pathology, and at least some of diabetes' relationship to cognitive impairment may be modified by neuropathology.
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