RETRACTED: Application of Hydrogen Proton Magnetic Resonance Technology Combined with Brain Neurometabolite Analysis in the Treatment of Cognitive Impairment Caused by Type 2 Diabetes Mellitus

Abstract

This study used hydrogen proton magnetic resonance imaging to detect the changes of white matter and the medial cortex in the prefrontal cortex of patients with type 2 diabetes, analyzed its relationship with cognitive function and blood glucose level, and discussed the recognition of patients with type 2 diabetes from the perspective of brain metabolism. We discuss the neural mechanisms affected by the disorder. The experiment recruited 65 volunteers, including 32 control subjects and 33 patients with type 2 diabetes. All volunteers underwent clinical cognitive function and psychological evaluation, including a simple intelligent mental state examination scale, digital breadth test, Raven intelligence test, Flanker paradigm experiment, connection test, auditory word learning test, depression self-evaluation scale, and anxiety self-rating scale. All subjects underwent multivoxel proton magnetic resonance scanning, and the spectral data were processed and metabolite concentration analysis was completed by Functool software. The detected regions of interest included the bilateral prefrontal white matter and bilateral prefrontal cortex. This study found that the N-acetylaspartate (NAA) and NAA/myo-inositol (MI) of the right prefrontal cortex were reduced, the right prefrontal white matter choline-containing compounds increased, and the MI of the bilateral prefrontal cortex increased in the type 2diabetes group compared with the control group. The NAA value of the right prefrontal cortex in the type 2 diabetes group was negatively correlated with the glycated hemoglobin concentration. The study found that the right prefrontal cortex NAA value of patients with type 2 diabetes was negatively correlated with the glycated hemoglobin concentration, reflecting that recent blood glucose levels can affect the changes of brain metabolites, and reasonable control of blood glucose can effectively delay brain neurons caused by diabetes.