David G Bruce1, Wendy A Davis1, Sergio E Starkstein2, Timothy M Davis1. 1. School of Medicine & Pharmacology, University of Western Australia, Crawley, Western Australia, Australia. 2. School of Psychiatry & Neuroscience, University of Western Australia, Crawley, Western Australia, Australia.
Abstract
BACKGROUND: The pathway linking type 2 diabetes and cognitive disorders remains poorly understood, and there are many potential risk factors. OBJECTIVE: To conduct a longitudinal study of risk factors in middle-aged patients with type 2 diabetes. METHODS: Type 2 patients from the Fremantle Diabetes Study underwent comprehensive assessment of risk factors in 1993/1996 and cognitive assessment in 2008/2010. After a cognitive screen (Mini-Mental State Examination), the Clinical Dementia Rating was used to define cognitive impairment (rating 0.5) and dementia. The methodology was similar to a previous report in older patients from the same cohort permitting comparison with that study. RESULTS: Of 335 eligible survivors, aged 57.5 ± 9.2 years at baseline and 72.2 ± 9.1 years at cognitive assessment, 14.7 ± 1.1 years later, 276 were cognitively normal, 27 had cognitive impairment, 17 had dementia, and 15 were unclassifiable. Independent, baseline predictors of dementia were age, poorer education, and cigarette smoking. Predictors of cognitive impairment included insulin therapy and fasting glucose (negative association), while diabetic retinopathy was an additional predictor of cognitive impairment and dementia combined. CONCLUSION: This study identified diabetes-specific risk factors, insulin therapy and diabetic retinopathy, that may explain the excess risk for cognitive disorders in type 2 diabetes. These risk factors differed from a previous report in older patients and the main difference appears to be related to duration of diabetes in the respective samples. The duration of diabetes or its manifestations is an important determinant of the impact of diabetes on cognitive disorders. Smoking is another important modifiable risk factor.
BACKGROUND: The pathway linking type 2 diabetes and cognitive disorders remains poorly understood, and there are many potential risk factors. OBJECTIVE: To conduct a longitudinal study of risk factors in middle-aged patients with type 2 diabetes. METHODS: Type 2 patients from the Fremantle Diabetes Study underwent comprehensive assessment of risk factors in 1993/1996 and cognitive assessment in 2008/2010. After a cognitive screen (Mini-Mental State Examination), the Clinical Dementia Rating was used to define cognitive impairment (rating 0.5) and dementia. The methodology was similar to a previous report in older patients from the same cohort permitting comparison with that study. RESULTS: Of 335 eligible survivors, aged 57.5 ± 9.2 years at baseline and 72.2 ± 9.1 years at cognitive assessment, 14.7 ± 1.1 years later, 276 were cognitively normal, 27 had cognitive impairment, 17 had dementia, and 15 were unclassifiable. Independent, baseline predictors of dementia were age, poorer education, and cigarette smoking. Predictors of cognitive impairment included insulin therapy and fasting glucose (negative association), while diabetic retinopathy was an additional predictor of cognitive impairment and dementia combined. CONCLUSION: This study identified diabetes-specific risk factors, insulin therapy and diabetic retinopathy, that may explain the excess risk for cognitive disorders in type 2 diabetes. These risk factors differed from a previous report in older patients and the main difference appears to be related to duration of diabetes in the respective samples. The duration of diabetes or its manifestations is an important determinant of the impact of diabetes on cognitive disorders. Smoking is another important modifiable risk factor.
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