Relationship between Executive Functioning and Glycemic Controls in Patients with Type 2 Diabetes

Type 2 diabetes (T2D) is a risk factor for Alzheimer’s disease. Executive dysfunction occurs in otherwise cognitively normal patients with T2D. To assess executive function, we investigated the relationship between executive function and glycemic controls using verbal fluency (VF) tests. The present study enrolled 130 patients with T2D (age, ≥60; including 11 patients with dementia) and excluded stroke survivors. Their HbA1c levels were recorded every ≤12 weeks for >5 years. All patients underwent VF tests. We analyzed the correlation between VF z-scores (standardized total scores) and glycemic control values (time-weighted average and maximum HbA1c levels for the past 5 years), or disease durations. As controls, we also investigated the relationships between stages of diabetic retinopathy (NDR/NPDR/PD) and past glycemic controls. The mean patient age was 74.7 years, the mean HbA1c at the baseline was 7.5%, median duration of education was 12 years, and mean disease duration was 18.3 years. Significant correlates for VF z-scores were age, years of education, and dementia in addition to glycemic control values. VF z-scores tended to correlate with average HbA1c levels, and significantly correlated with maximum HbA1c levels, for the past 5 years. The relationships between VF z-scores and maximum HbA1c levels remained significant after adjusting for age, years of education, and dementia. Generally, VF z-scores were strongly associated with maximum HbA1c levels for longer observation periods, i.e., VF z-scores correlated with maximum HbA1c levels for the past 5 years, best compared with maximum HbA1c levels for the past 4 years. As controls, diabetic retinopathy stages were also associated with average and maximum HbA1c levels. The diabetes duration was associated with diabetic retinopathy stages strongly, but not with VF z-scores. These results suggest that executive dysfunction may be caused by metabolic mechanisms other than diabetic retinopathy. Disclosure T. Minami: None. M. Yamada: None. Y. Ito: None. R. Furuta: None. S. Katsuragawa: None. S. Terui: None. T. Akiyama: None. F. Minagawa: None. Y. Terauchi: Research Support; Self; MSD K.K.. Speaker9s Bureau; Self; MSD K.K.. Advisory Panel; Self; MSD K.K.. Research Support; Self; Ono Pharmaceutical Co., Ltd.. Speaker9s Bureau; Self; Ono Pharmaceutical Co., Ltd.. Research Support; Self; Novartis Pharma K.K., Boehringer Ingelheim GmbH. Speaker9s Bureau; Self; Boehringer Ingelheim GmbH. Advisory Panel; Self; Boehringer Ingelheim GmbH. Research Support; Self; Mitsubishi Tanabe Pharma Corporation. Speaker9s Bureau; Self; Mitsubishi Tanabe Pharma Corporation. Advisory Panel; Self; Mitsubishi Tanabe Pharma Corporation. Research Support; Self; Daiichi Sankyo Company, Limited. Speaker9s Bureau; Self; Daiichi Sankyo Company, Limited. Advisory Panel; Self; Daiichi Sankyo Company, Limited. Research Support; Self; Sanwa Kagaku Kenkyusho Co., Ltd.. Speaker9s Bureau; Self; Sanwa Kagaku Kenkyusho Co., Ltd.. Research Support; Self; Novo Nordisk Inc.. Speaker9s Bureau; Self; Novo Nordisk Inc.. Advisory Panel; Self; Novo Nordisk Inc.. Research Support; Self; Eli Lilly and Company. Speaker9s Bureau; Self; Eli Lilly and Company. Advisory Panel; Self; Eli Lilly and Company. Research Support; Self; Sanofi. Speaker9s Bureau; Self; Sanofi. Advisory Panel; Self; Sanofi. Research Support; Self; Sumitomo Dainippon Pharma Co., Ltd.. Speaker9s Bureau; Self; Sumitomo Dainippon Pharma Co., Ltd.. Research Support; Self; Shionogi & Co., Ltd.. Speaker9s Bureau; Self; Shionogi & Co., Ltd., Bayer Yakuhin, Ltd., Astellas Pharma US, Inc., AstraZeneca. Advisory Panel; Self; AstraZeneca, Teijin Pharma Limited.