Type 2 diabetes damages the brain and alters its microstructure

A recent study published in the journal scientific reportresearchers are looking at microstructural changes in brain tissue. type 2 diabetic (T2D) Using a whole-brain diffusion tensor imaging (DTI)-based mean diffusion rate (MD) procedure to distinguish between acute and chronic phases of tissue changes. In this study, we hypothesized that T2D patients have altered MD values ​​in mood and cognitive regulatory domains compared to healthy individuals.

study: Microstructural alterations in brain tissue contribute to cognitive and mood disturbances in adults with type 2 diabetes. Image credit: Elif Bayraktar / Shutterstock.com

Background

T2D, a chronic metabolic disorder, has been shown to alter cognition and mood and as a result is often considered an early risk factor for Alzheimer’s disease (AD) and vascular dementia. In fact, epidemiological studies have shown that T2D increases the risk of infections.

Cognitive and mood disorders are 1.5 and 2 times higher, respectively.

Structural magnetic resonance imaging (MRI) fails to detect subtle abnormalities in brain tissue due to insufficient sensitivity to tissue changes. However, DTI, a non-invasive procedure, shows changes in the microstructural organization of the brain in gray and white matter. DTI also enables the measurement of MD, which reflects the movement of water molecules, by which he reveals the nature and extent of brain tissue damage in T2D patients.

To date, researchers have not examined direct correlations between tissue changes in brain regions that mediate cognition and mood based on MD. Similarly, symptom scores for mood and cognition in T2D patients have not been reported.

About research

In this study, researchers recruited 68 T2D patients on medication from the Gonda Diabetes Center at the University of California, Los Angeles (UCLA) in addition to 101 healthy nondiabetic controls. The age of the individual in both study cohorts he ranged from 40 to 65 years.

The Diabetic Complications Severity Index (DCSI) was determined from each patient’s clinical records. Anxiety and depression symptoms were assessed by the Beck Anxiety Inventory (BAI) and Beck Depression Inventory (BDI-II), respectively. A BDI-II value or BAI value greater than 9 indicates depression or anxiety, respectively. The Montreal Cognitive Assessment (MoCA) was also performed and a score of 26 or higher indicated no cognitive impairment.

DTI data were collected using generalized autocalibration partial parallel acquisition (GRAPPA), a single-shot echo-planar imaging technique with an acceleration factor of 2. Visual assessments of her T1, T2, and her PD-weighted images of all subjects were then performed for various pathologies, including cystic lesions, infarcts, or tumors.

MD maps obtained from all DTI series were quantified, readjusted and averaged to remove variability from head motion-related variability and other image artifacts. Non-diffusion weighted images were also readjusted and averaged.

Statistical parametric maps showing brain regions with significant MD differences between groups were overlaid on mean anatomical images for identification by MRIcroN software. This allowed us to obtain region of interest (ROI) values ​​in brain regions with significant associations with mood and cognitive values ​​between T2D and controls. Whole-brain MD maps were also correlated voxel-by-voxel with mood and cognitive scores (including BAI, BDI-II, and MoCA subscores) using partial correlations.

Changes in brain structure in diabetic patients

Extensive microstructural disruption was observed in brain regions controlling cognitive and mood functions in T2D patients compared with controls. Most of these changes were in the chronic phase and only a few sites in the acute phase. Patients with T2D also exhibited impairments in the visuospatial, language, and attentional cognitive subdomains, as well as higher depression and anxiety scores, compared with healthy controls.

Cognitive and mood regulatory networks span large regions of the human brain. Extensive ultrastructural tissue alterations in these regions therefore play a unique role in cognitive and mood disorders in patients with T2D.

These findings provide important insights into not only these alterations, but also the fine structural neuropathological alterations that may contribute to mood and cognitive dysfunction in patients with T2D. Of note, all disruptions in the microstructural integrity of brain tissue occurred predominantly in the temporal, parietal, temporal cortex, and subcortical regions.

Similar to previous studies, regions that showed chronic histological changes with increasing MD values ​​in patients with T2D included the frontal, precentral, and superior parietal gyri, from the cerebellum to the parasite, and the anterior crural gyrus. It contained brain fibers leading from the to the cortex.

Conclusion

Findings show how MD can facilitate early detection of microstructural alterations in brain tissue in cognitive and mood-regulatory areas that contribute to mood changes and cognitive impairment in patients with T2D.