Abstract
BackgroundThis is an exploratory study using a novel imaging modality, quantitative ultrashort time-to-echo, contrast enhanced (QUTE-CE) magnetic resonance imaging to evaluate the permeability of the blood–brain barrier in a rat model of type 2 diabetes with the presumption that small vessel disease is a contributing factor to neuropathology in diabetes.MethodsThe BBZDR/Wor rat, a model of type 2 diabetes, and age-matched controls were studied for changes in blood–brain barrier permeability. QUTE-CE, a quantitative vascular biomarker, generated angiographic images with over 500,000 voxels that were registered to a 3D MRI rat brain atlas providing site-specific information on blood–brain barrier permeability in 173 different brain areas.ResultsIn this model of diabetes, without the support of insulin treatment, there was global capillary pathology with over 84% of the brain showing a significant increase in blood–brain barrier permeability over wild-type controls. Areas of the cerebellum and midbrain dopaminergic system were not significantly affected.ConclusionSmall vessel disease as assessed by permeability in the blood–brain barrier in type 2 diabetes is pervasive and includes much of the brain. The increase in blood–brain barrier permeability is a likely contributing factor to diabetic encephalopathy and dementia.
Highlights
This is an exploratory study using a novel imaging modality, quantitative ultrashort time-to-echo, contrast enhanced (QUTE-CE) magnetic resonance imaging to evaluate the permeability of the blood–brain barrier in a rat model of type 2 diabetes with the presumption that small vessel disease is a contributing factor to neuropathology in diabetes
Vascular dementia is a serious consequence of diabetes [1]
Failure in the blood brain barrier lies at the foundation of cerebral small vessel disease and contributes to the pathogenesis of diabetic encephalopathy
Summary
This is an exploratory study using a novel imaging modality, quantitative ultrashort time-to-echo, contrast enhanced (QUTE-CE) magnetic resonance imaging to evaluate the permeability of the blood–brain barrier in a rat model of type 2 diabetes with the presumption that small vessel disease is a contributing factor to neuropathology in diabetes. Failure in the blood brain barrier lies at the foundation of cerebral small vessel disease and contributes to the pathogenesis of diabetic encephalopathy [3] Methods for in vivo quantification and localization of changes in blood–brain barrier permeability are needed to understand and diagnose the early onset of vascular dementia with type 2 diabetes. It is difficult to model the effects of contrast agent on both T2* and T1 given the short acquisition time, and strong dependence on microstructural properties such as vessel size, tortuosity and orientation. These and other methodological issues with the use of DCE-MRI for blood–brain barrier permeability have resulted in significant differences in the reported rates of leakage [5]
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