Impaired Glucose Tolerance as a Risk Factor for Cognitive Dysfunction

Growing evidence suggests that impaired glucose tolerance may contribute to the development of cognitive dysfunction in otherwise healthy individuals. Thus, older individuals who are at the high end of normal on the measure of insulin resistance likely represent a large population at additional risk for cognitive dysfunction. The goal of this study was to further clarify the relationship between preclinical insulin resistance, as measured by fasting blood glucose levels, and cognitive functioning in otherwise healthy older adults. It was hypothesized that glucose levels at the higher end of the normal range represent a risk factor for cognitive dysfunction, particularly seen in the early cognitive processing stages like attention and memory. To assess cognition, participants completed the Brief Cognitive Rating Scale (BCRS; Reisberg, 1988), Global Deterioration Scale (GDS; Reisberg, 1982), Mattis Dementia Rating Scale (MDRS; Mattis, 1988), Repeatable Battery for the Assessment of Neuropsychological Status (RBANS; Randolph, 1988), Letter Number Sequencing Test (LNS; Wechsler, 1997), Cognitive Change Index (CCI; Rattanabannakit, 2016), Symbol Digit Modalities Test (SDMT; Forn, 2013), and the Delis-Kaplan Executive Function System (D-KEFS; Delis, 2001). A series of correlations between fasting glucose levels and performance on each of these cognitive tests were computed. Higher fasting glucose levels were positively associated with BCRS (p ≤ 0.001) and GDS scores (p ≤ 0.001) and negatively correlated with performance on the RBANS domain of delayed memory (p ≤ 0.035). However, fasting blood glucose levels were not significantly associated with performance on other measures. In addition, participants were divided into a high fasting blood glucose group (fasting blood glucose level ≥ to 100 mg/dL; clinically categorized as prediabetes) and a low fasting blood glucose group (fasting blood glucose level \u3c 100 mg/dL). A t-test was performed to assess whether participants in the high fasting blood glucose group would show significant group differences in cognitive performance from the low fasting blood glucose group. However, the present findings did not show a significant relationship. One limitation of this study was its small sample size (n=19). Thus, future studies are needed to further clarify the relationship between impaired glucose tolerance and pre-clinical cognitive dysfunction in an at-risk population of elderly individuals. This may help to inform future developments of strategies to help in the prevention and treatment of cognitive dysfunction in this population