The blood-brain barrier (BBB) regulates differing needs of the various brain regions by controlling transport of blood-borne components from the neurovascular circulation into the brain parenchyma. The mechanisms underlying region-specific transport across the BBB are not completely understood. Previous work showed that pericytes are key regulators of BBB function. Here we investigated whether pericytes influence BBB permeability in a region-specific manner by analysing the regional permeability of the BBB in the pdgf-b mouse model of pericyte depletion. We show that BBB permeability is heterogeneous in pdgf-b mice, being significantly higher in the cortex, striatum and hippocampus compared to the interbrain and midbrain. However, we show that this regional heterogeneity in BBB permeability is not explained by local differences in pericyte coverage. Region-specific differences in permeability were not associated with disruption of tight junctions but may result from changes in transcytosis across brain endothelial cells. Our data show that certain brain regions are able to maintain low BBB permeability despite substantial pericyte loss and suggest that additional, locally-acting mechanisms may contribute to control of transport.
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http://dx.doi.org/10.1177/0271678X17697340 | DOI Listing |
J Tradit Complement Med
November 2024
Department of Pharmacology, SRM College of Pharmacy, SRM Institute of Science and Technology, Kattankulathur, 603 203, Chengalpattu, Tamil Nadu, India.
Background: Luteolin, a natural flavonoid, exhibits antioxidant and anti-inflammatory properties and has been investigated for potential health benefits. Its focus on migraine management arises from its ability to mitigate neuroinflammation, a key factor in migraine attacks.
Methods: pkCSM and Swiss ADME were employed to assess luteolin's pharmacokinetic properties, revealing challenges such as low water solubility and limited skin permeability.
Tissue Cell
January 2025
Department of Neurology, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong 510282, PR China. Electronic address:
Background: Parkinson's Disease (PD) often presents with a compromised blood-brain barrier (BBB), which hyperglycemia may exacerbate. Pericytes, a key cell for BBB integrity, are potential therapeutic targets for neurodegenerative disorders. Few studies have developed 3D PD cell models incorporating neurovascular units (NVU) through the co-culture of human endothelial, pericytes, astrocytes, and SH-SY5Y cells to evaluate BBB impairment and the role of pericytes under hyperglycemic condition.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
January 2025
Translational Neuroimaging Group, Center for Image Sciences, University Medical Center Utrecht and Utrecht University, Utrecht, The Netherlands.
Futile recanalization hampers prognoses for ischemic stroke patients despite successful recanalization therapy. Allegedly, hypertension and reperfusion deficits contribute, but a better understanding is needed of how they interact and mediate disease outcome. We reassessed data from spontaneously hypertensive and normotensive Wistar-Kyoto rats (male, n = 6-7/group) that were subjected to two-hour embolic middle cerebral artery occlusion and thrombolysis in preclinical trials.
View Article and Find Full Text PDFParasitol Res
January 2025
Department of Parasitology, Chung Shan Medical University, Taichung, 402, Taiwan.
Prostaglandin E2 (PGE-2) is synthesised by cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase 1 (mPGES-1). PGE-2 exhibits pro-inflammatory properties in inflammatory conditions. However, there remains limited understanding of the COX-2/mPGES-1/PGE-2 pathway in Angiostrongylus cantonensis-induced meningoencephalitis.
View Article and Find Full Text PDFZh Nevrol Psikhiatr Im S S Korsakova
January 2025
Pirogov Russian National Research Medical University (Pirogov University), Moscow, Russia.
Hemorrhagic transformation (HT) is a serious complication that worsens outcomes and increases mortality in patients with ischemic stroke (IS). HT can occur both spontaneously and after reperfusion therapy. Severe ischemic injury in IS is not sufficient in itself to cause HT; one of the key elements in its development is reperfusion.
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