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A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
Published on: February 28, 2013
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Cognitive functioning and structural brain abnormalities in people with Type 2 diabetes mellitus.
B Mankovsky1, N Zherdova1, E van den Berg2
1Department of Diabetology, National Medical Academy for Postgraduate Education, Kiev, Ukraine.
Diabetic Medicine : a Journal of the British Diabetic Association
|September 20, 2018
Summary
Type 2 diabetes is linked to cognitive decline. Increased white matter hyperintensities in the brain correlate with slower processing speed in individuals with long-standing diabetes.
Area of Science:
- Neurology
- Endocrinology
- Radiology
Background:
- Type 2 diabetes mellitus (T2DM) is increasingly recognized for its association with cognitive dysfunction.
- The precise structural brain changes underlying cognitive impairment in T2DM remain incompletely understood.
Purpose of the Study:
- To investigate the relationship between cognitive functioning and structural brain abnormalities in individuals with long-standing T2DM.
- To identify specific brain correlates of cognitive deficits in this population.
Main Methods:
- Ninety-three participants with T2DM underwent cognitive assessments focusing on memory, processing speed, and executive functioning.
- Brain MRI was utilized to quantify brain tissue volumes and white matter hyperintensities (WMH).
- Linear regression analyses, adjusted for age, sex, and education, were performed to assess associations.
Main Results:
- A significant association was found between increased white matter hyperintensity volume and decreased processing speed (P=0.009).
- No significant relationships were observed between WMH volume and memory or executive function.
- Brain tissue volumes did not show significant correlations with cognitive performance.
Conclusions:
- In individuals with long-standing, less controlled T2DM, elevated white matter hyperintensities are linked to reduced processing speed.
- Cerebral small vessel disease, indicated by WMH, is suggested as a potential mechanism for cognitive dysfunction in T2DM.
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