ArticleThe Journal of pharmacology and experimental therapeutics2016
Blood-Brain Barrier Disruption and Neurovascular Unit Dysfunction in Diabetic Mice: Protection with the Mitochondrial Carbonic Anhydrase Inhibitor Topiramate.
Article in The Journal of pharmacology and experimental therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
54 citing papers in PubMed, 99 citations in OpenAlex.
- Huntington's disease vasculopathy is barrier-type-selective and arteriolar-dominant with spatially-coupled astrogliosis and reversible by S1pr1 stimulation.Nature communications · 2026Article
- A Systemically Administered Humanized Anti-Nav1.7 Antibody with Long-Lasting Analgesic Activity and Preserved Physiological Nociception.Pharmaceutics · 2026Article
- Strategies for blood-brain barrier rejuvenation and repair.Nature reviews. Drug discovery · 2026Review
- Neuroendocrine-immune perturbations in metabolic disease: pathophysiological mechanisms underlying cognitive impairment.Frontiers in human neuroscience · 2026Review
- NG2-Glia Cause Diabetic Blood-Brain Barrier Disruption by Secreting MMP-9.Diabetes & metabolism journal · 2026Article
- Article
- Role of Necroptosis and Neuroinflammation in CSVD-Associated Cognitive Decline in db/db Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Blood-Brain Barrier Integrity and Transport of Major Hormones are Unchanged in Mice With Euglycemic Hyperinsulinemia.Endocrinology · 2025Article
- Novel Insights into the Mechanism and Treatment of Diabetes-Related Brain Complications: Focusing on the Blood-Brain Barrier Impairment.Aging and disease · 2025Review
- Review
- Carbonic anhydrase, its inhibitors and vascular function.Frontiers in molecular biosciences · 2024Review
- Methylglyoxal, a highly reactive dicarbonyl compound, as a threat for blood brain barrier integrity.Fluids and barriers of the CNS · 2023Review
- Cellular senescence and the blood-brain barrier: Implications for aging and age-related diseases.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Overview and New Insights into the Metabolic Syndrome: Risk Factors and Emerging Variables in the Development of Type 2 Diabetes and Cerebrocardiovascular Disease.Medicina (Kaunas, Lithuania) · 2023Review
- The causal effect of HbA1c on white matter brain aging by two-sample Mendelian randomization analysis.Frontiers in neuroscience · 2023Article
- Article
- Insulin Resistance in Peripheral Tissues and the Brain: A Tale of Two Sites.Biomedicines · 2022Review
- Transcellular routes of blood-brain barrier disruption.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- The Mighty Mitochondria Are Unifying Organelles and Metabolic Hubs in Multiple Organs of Obesity, Insulin Resistance, Metabolic Syndrome, and Type 2 Diabetes: An Observational Ultrastructure Study.International journal of molecular sciences · 2022Review
- Glial and Vascular Cell Regulation of the Blood-Brain Barrier in Diabetes.Diabetes & metabolism journal · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
All forms of diabetes mellitus are characterized by chronic hyperglycemia, resulting in the development of a number of microvascular and macrovascular pathologies. Diabetes is also associated with changes in brain microvasculature, leading to dysfunction and ultimately disruption of the blood-brain barrier (BBB). These changes are correlated with a decline in cognitive function. In diabetes, BBB damage is associated with increased oxidative stress and reactive oxygen species. This occurs because of the increased oxidative metabolism of glucose caused by hyperglycemia. Decreasing the production of bicarbonate with the use of a mitochondrial carbonic anhydrase inhibitor (mCAi) limits oxidative metabolism and the production of reactive oxygen species. In this study, we have demonstrated that 1) streptozotocin-induced diabetes resulted in BBB disruption, 2) ultrastructural studies showed a breakdown of the BBB and changes to the neurovascular unit (NVU), including a loss of brain pericytes and retraction of astrocytes, the two cell types that maintain the BBB, and 3) treatment with topiramate, a mCAi, attenuated the effects of diabetes on BBB disruption and ultrastructural changes in the neurovascular unit.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.