Research Paper Volume 14, Issue 12 pp 4976—4989
Differential impact of glycemic control and comorbid conditions on the neurophysiology underlying task switching in older adults with type 2 diabetes
- 1 Institute for Human Neuroscience, Boys Town National Research Hospital, Boys Town, NE 68010, USA
- 2 Department of Psychology, University of Nebraska Omaha, Omaha, NE 68182, USA
- 3 Department of Internal Medicine, Division of Diabetes, Endocrinology and Metabolism, University of Nebraska Medical Center, Omaha, NE 68198, USA
Received: April 11, 2022 Accepted: June 4, 2022 Published: June 17, 2022https://doi.org/10.18632/aging.204129
How to Cite
Copyright: © 2022 Embury et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Type 2 diabetes is known to negatively affect higher order cognition and the brain, but the underlying mechanisms are not fully understood. In particular, glycemic control and common comorbidities are both thought to contribute to alterations in cortical neurophysiology in type 2 diabetes, but their specific impact remains unknown. The current study probed the dynamics underlying cognitive control in older participants with type 2 diabetes, with and without additional comorbid conditions (i.e., cardiovascular disease, nephropathy, peripheral neuropathy, retinopathy), using a task switching paradigm and a dynamic functional brain mapping method based on magnetoencephalography (MEG). We hypothesized that neural dynamics would be differentially impacted by the level of glycemic control (i.e., diabetes itself) and the burden of additional comorbid conditions. Supporting this hypothesis, our findings indicated separable, but widespread alterations across frontal, parietal, temporal and cerebellum regions in neural task-switch costs in type 2 diabetes that were differentially attributable to glycemic control and the presence of comorbid conditions. These effects were spatially non-overlapping and the effects were not statistically related to one another. Further, several of the effects that were related to the presence of comorbidities were associated with behavioral performance, indicating progressive deficits in brain function with extended disease. These findings provide insight on the underlying neuropathology and may inform future treatment plans to curtail the neural impact of type 2 diabetes.
ACR: Albumin Creatinine Ratio; ALT: Alanine aminotransferase; AST: Aspartate Transaminase; BESA: Brain Electrical Source Analysis; GABA: Gamma-Amino Butyric Acid; MEG: Magneto Encephalo Graphy; UNMC: University of Nebraska Medical Center.