Blood–retina-barrier disruption accompanying blood–brain-barrier dysfunction in posterior reversible encephalopathy syndrome

Özkan, Esra Eroğlu; Göçmen, Rahşan; Topçuoğlu, Mehmet Akif; Arsava, Ethem Murat

doi:10.1016/j.jns.2014.08.035

Cited by 15 publications

(5 citation statements)

References 9 publications

(11 reference statements)

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“…The BBB and BRB provide a structural and functional barrier, which impedes and regulates the influx of compounds from the blood into the brain or retina, respectively. There is growing evidence suggesting that the disruption of the BRB and BBB is an early hallmark of the subsequent retinal edema and central nervous system (CNS) dysfunction [4,5]. However, the mechanisms by which diet or metabolic syndrome induces dysfunction of the BBB and BRB are not completely understood.…”

Section: Introductionmentioning

confidence: 99%

Disruption of the hippocampal and hypothalamic blood–brain barrier in a diet-induced obese model of type II diabetes: prevention and treatment by the mitochondrial carbonic anhydrase inhibitor, topiramate

Salameh

Mortell

Logsdon

et al. 2019

Fluids Barriers CNS

104

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Background: Type II diabetes is a vascular risk factor for cognitive impairment and increased risk of dementia. Disruption of the blood-retinal barrier (BRB) and blood-brain barrier (BBB) are hallmarks of subsequent retinal edema and central nervous system dysfunction. However, the mechanisms by which diet or metabolic syndrome induces dysfunction are not understood. A proposed mechanism is an increase in reactive oxygen species (ROS) and oxidative stress. Inhibition of mitochondrial carbonic anhydrase (mCA) decreases ROS and oxidative stress. In this study, topiramate, a mCA inhibitor, was examined for its ability to protect the BRB and BBB in diet-induced obese type II diabetic mice. Methods: BBB and BRB permeability were assessed using 14 C-sucrose and 99m Tc-albumin in CD-1 mice fed a lowfat (control) or a high-fat diet. Topiramate administration was compared to saline controls in both preventative and efficacy arms examining BRB and BBB disruption. Body weight and blood glucose were measured weekly and body composition was assessed using EchoMRI. Metabolic activity was measured using a comprehensive laboratory animal monitoring system. Brain tissues collected from the mice were assessed for changes in oxidative stress and tight junction proteins. Results: High-fat feeding caused increased entry of 14 C-sucrose and 99m Tc-albumin into the brains of diet-induced obese type II diabetic mice. Increased permeability to 14 C-sucrose was observed in the hypothalamus and hippocampus, and attenuated by topiramate treatment, while increased permeability to 99m Tc-albumin occurred in the whole brain and was also attenuated by topiramate. Treatment with topiramate decreased measures of oxidative stress and increased expression of the tight junction proteins ZO-1 and claudin-12. In the retina, we observed increased entry of 99m Tc-albumin simultaneously with increased entry into the whole brain during the preventative arm. This occurred prior to increased entry to the retina for 14 C-sucrose which occurred during the efficacy arm. Treatment with topiramate had no effect on the retina.

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Section: Introductionmentioning

confidence: 99%

Disruption of the hippocampal and hypothalamic blood–brain barrier in a diet-induced obese model of type II diabetes: prevention and treatment by the mitochondrial carbonic anhydrase inhibitor, topiramate

Salameh

Mortell

Logsdon

et al. 2019

Fluids Barriers CNS

104

View full text Add to dashboard Cite

show abstract

“…Supporting these findings, previous studies reported cases of PRES also complicated by renal artery stenosis in which RAS is inappropriately activated [8], and of which symptoms became worse despite well-controlled blood pressure by non-RAS inhibitors [9]. Therefore, inappropriate activation of the RAS may contribute to the pathophysiology of PRES, and its inhibition is effective for treating PRES.…”

Section: Dear Sirsmentioning

confidence: 54%

Posterior reversible encephalopathy syndrome treated with renin–angiotensin system blockade

Mishima

Hashimoto

Akiyama

et al. 2015

Journal of the Neurological Sciences

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“…The preferential formation of edema in the posterior regions is due to the elevated BBB permeability. BBB permeability to EB varies regionally in response to autoregulatory breakthrough, such that increase in BBB permeability was significantly greater in the posterior regions than in the anterior regions (27, 28). The blue-stained area in the cerebrum, cerebellum, and other regions with EB observed staining in the experimental group were concordant with the distribution of cerebral edema on ADC maps.…”

Section: Discussionmentioning

confidence: 99%

Blood–Brain Barrier Disruption as a Potential Target for Therapy in Posterior Reversible Encephalopathy Syndrome: Evidence From Multimodal MRI in Rats

Quan-lai¹,

Huang

Shen

et al. 2019

Front. Neurol.

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Background: To explore blood–brain barrier disruption in hypertensive posterior reversible encephalopathy syndrome.Methods: The hypertension rat models were successfully established and scanned on 7T micro-MRI. MRI parameter maps including apparent diffusion coefficient, T1 value, and perfusion metrics such as cerebral blood volume, cerebral blood flow, mean transit time and time to peak maps, were calculated.Results: The ADC values of the experimental group were higher than those of the control group both in cortical (P < 0.01) and subcortical (P < 0.05) regions. Voxel-wise analysis of ADC maps localized vasogenic edema primarily to the posterior portion of the brain. The increase in cerebral blood volume and cerebral blood flow values were found in the cortical and subcortical regions of rats with acute hypertension. No correlation was found between perfusion metrics and mean arterial pressure. The Evans blue dye content was higher in the posterior brain region than the anterior one (P < 0.05).Conclusions: Cerebral vasogenic edema resulting from acute hypertension supports the hypothesis of posterior reversible encephalopathy syndrome as the result of blood–brain barrier disruption, which maybe the potential therapeutic target for intervention.

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Blood–retina-barrier disruption accompanying blood–brain-barrier dysfunction in posterior reversible encephalopathy syndrome

Cited by 15 publications

References 9 publications

Disruption of the hippocampal and hypothalamic blood–brain barrier in a diet-induced obese model of type II diabetes: prevention and treatment by the mitochondrial carbonic anhydrase inhibitor, topiramate

Disruption of the hippocampal and hypothalamic blood–brain barrier in a diet-induced obese model of type II diabetes: prevention and treatment by the mitochondrial carbonic anhydrase inhibitor, topiramate

Posterior reversible encephalopathy syndrome treated with renin–angiotensin system blockade

Blood–Brain Barrier Disruption as a Potential Target for Therapy in Posterior Reversible Encephalopathy Syndrome: Evidence From Multimodal MRI in Rats

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