Introduction: Type 2 diabetes is a dementia risk factor and is associated with brain atrophy. We investigated the impact of glucose disorders on cognition and brain volumes in the elderly, examining the contribution of inflammatory, oxidative and genetic factors.
Methods: Longitudinal study of an elderly cohort with neuropsychological testing (n=880) and brain MRI (n=312) with assessment at baseline and two years. Participants were categorized as normal or impaired fasting glucose (at both assessments), diabetes (at baseline), and incident glucose disorders (normal at baseline and IFG or diabetes at wave 2). Covariates were age, sex, hyperlipidemia, hypertension, education, and mood. Potential contributors to cognitive outcomes included inflammatory markers (VCAM, IL-6, IL-12p70, SAA, byproducts of oxidative metabolism (urate, malondialdehyde and homocysteine) and apolipoprotein E genotype.
Results: Diabetes at baseline was associated with greater decline in global cognition, executive function and visuospatial function. Incident glucose disorders were also associated with greater decline in global cognition and visuospatial function. Homocysteine was an independent predictor of the observed effect of diabetes on executive function. Apolipoprotein E genotype did not influence the observed effects on cognition. Impaired fasting glucose was not associated with any greater cognitive decline compared to participants with normal fasting glucose.
Baseline diabetes and incident glucose disorders were associated with a 2.5 and 2.2 fold greater decline in total brain volume, respectively. Stable IFG did not impact cognition or brain volumetry.
Conclusions: Diabetes and incident glucose disorders predict decline in cognition and brain volumes in non-demented elderly at 2 years. Diabetes care in the elderly demands recognition of cognitive decline which may potentially compromise diabetes self-care.