Abstract
Diabetes mellitus type 1 and 2 is associated with cognitive impairment. Previous studies have reported a relationship between changes in cerebral metabolite levels and the variability of glycemia. However, the specific risk factors that affect the metabolic changes associated with type 1 and type 2 diabetes in cognitive dysfunction remain uncertain. The aim of the study was to evaluate the specificity of hippocampal spectroscopy in type 1 and type 2 diabetes and cognitive dysfunction. Materials and methods: 65 patients with type 1 diabetes with cognitive deficits and 20 patients without, 75 patients with type 2 diabetes with cognitive deficits and 20 patients without have participated in the study. The general clinical analysis and evaluation of risk factors of cognitive impairment were carried out. Neuropsychological testing included the Montreal Scale of Cognitive Dysfunction Assessment (MoCA test). Magnetic resonance spectroscopy (MRS) was performed in the hippocampal area, with the assessment of N-acetylaspartate (NAA), choline (Cho), creatine (Cr), and phosphocreatine (PCr) levels. Statistical processing was performed using the commercially available IBM SPSS software. Results: Changes in the content of NAA, choline Cho, phosphocreatine Cr2 and their ratios were observed in type 1 diabetes. More pronounced changes in hippocampal metabolism were observed in type 2 diabetes for all of the studied metabolites. Primary risk factors of neurometabolic changes in patients with type 1 diabetes were episodes of severe hypoglycemia in the history of the disease, diabetic ketoacidosis (DKA), chronic hyperglycemia, and increased body mass index (BMI). In type 2 diabetes, arterial hypertension (AH), BMI, and patient’s age are of greater importance, while the level of glycated hemoglobin (HbA1c), duration of the disease, level of education and insulin therapy are of lesser importance. Conclusion: Patients with diabetes have altered hippocampal metabolism, which may serve as an early predictive marker. The main modifiable factors have been identified, correction of which may slow down the progression of cognitive dysfunction.
Highlights
With a change in the modern lifestyle, the incidence of diabetes increases from year to year [12]
The prevalence of cognitive dysfunction caused by diabetes is 10.8–65.0%, and its occurrence is associated with hippocampal atrophy [13,14,15]
The literature suggests lower values of NAA of the hippocampus on both sides in patients with diabetic retinopathy, which is in accordance with our results, as in our study, patients with cognitive impairment had a decrease in this metabolite [16]
Summary
Clinical studies indicate that type 1 and type 2 diabetes are risk factors for cognitive decline, while structural and functional deficits are associated with synaptic plasticity processes. Experimental data derived from rodent model of diabetes demonstrate the decline in learning and memory of varying extent, owing to the hippocampus dysfunction. These changes are associated with an increase in oxidative stress, levels of pro-inflammatory cytokines, β-amyloid, as well as dysfunction of the hypothalamic-pituitary-adrenal axis [1]. Hypothesis: patients with type 1 and type 2 diabetes have risk factors for impaired neurometabolism in the hippocampus, which is clinically manifested by cognitive impairment
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