Structural Alterations in Deep Brain Structures in Type 1 Diabetes
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
Grant support
P41 EB027061
NIBIB NIH HHS - United States
P41 EB015894
NIBIB NIH HHS - United States
UL1 TR002494
NCATS NIH HHS - United States
R01 DK099137
NIDDK NIH HHS - United States
P30 NS076408
NINDS NIH HHS - United States
KL2 TR002492
NCATS NIH HHS - United States
R56 DK099137
NIDDK NIH HHS - United States
T32 DK007203
NIDDK NIH HHS - United States
UL1 TR000114
NCATS NIH HHS - United States
KL2 TR000113
NCATS NIH HHS - United States
PubMed
32839347
PubMed Central
PMC7576566
DOI
10.2337/db19-1100
PII: db19-1100
Knihovny.cz E-resources
- MeSH
- Diabetes Mellitus, Type 1 pathology MeSH
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Brain pathology MeSH
- Retrospective Studies MeSH
- Case-Control Studies MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
Even though well known in type 2 diabetes, the existence of brain changes in type 1 diabetes (T1D) and both their neuroanatomical and clinical features are less well characterized. To fill the void in the current understanding of this disease, we sought to determine the possible neural correlate in long-duration T1D at several levels, including macrostructural, microstructural cerebral damage, and blood flow alterations. In this cross-sectional study, we compared a cohort of 61 patients with T1D with an average disease duration of 21 years with 54 well-matched control subjects without diabetes in a multimodal MRI protocol providing macrostructural metrics (cortical thickness and structural volumes), microstructural measures (T1-weighted/T2-weighted [T1w/T2w] ratio as a marker of myelin content, inflammation, and edema), and cerebral blood flow. Patients with T1D had higher T1w/T2w ratios in the right parahippocampal gyrus, the executive part of both putamina, both thalami, and the cerebellum. These alterations were reflected in lower putaminal and thalamic volume bilaterally. No cerebral blood flow differences between groups were found in any of these structures, suggesting nonvascular etiologies of these changes. Our findings implicate a marked nonvascular disruption in T1D of several essential neural nodes engaged in both cognitive and motor processing.
Center for Magnetic Resonance Research University of Minnesota Minneapolis MN
Department of Medicine University of Minnesota Minneapolis MN
Diagnostic Imaging Center Kuopio University Hospital Kuopio Finland
Division of Biostatistics School of Public Health University of Minnesota Minneapolis MN
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