Journal articles: 'Blood Brain Barriers'

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Dunn, Jeff F., and Albert M. Isaacs. "The impact of hypoxia on blood-brain, blood-CSF, and CSF-brain barriers." Journal of Applied Physiology 131, no. 3 (September 1, 2021): 977–85. http://dx.doi.org/10.1152/japplphysiol.00108.2020.

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The blood-brain barrier (BBB), blood-cerebrospinal fluid (CSF) barrier (BCSFB), and CSF-brain barriers (CSFBB) are highly regulated barriers in the central nervous system comprising complex multicellular structures that separate nerves and glia from blood and CSF, respectively. Barrier damage has been implicated in the pathophysiology of diverse hypoxia-related neurological conditions, including stroke, multiple sclerosis, hydrocephalus, and high-altitude cerebral edema. Much is known about the damage to the BBB in response to hypoxia, but much less is known about the BCSFB and CSFBB. Yet, it is known that these other barriers are implicated in damage after hypoxia or inflammation. In the 1950s, it was shown that the rate of radionucleated human serum albumin passage from plasma to CSF was five times higher during hypoxic than normoxic conditions in dogs, due to BCSFB disruption. Severe hypoxia due to administration of the bacterial toxin lipopolysaccharide is associated with disruption of the CSFBB. This review discusses the anatomy of the BBB, BCSFB, and CSFBB and the impact of hypoxia and associated inflammation on the regulation of those barriers.

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Wood, Heather. "Crossing blood–brain barriers." Nature Reviews Neuroscience 2, no. 1 (January 2001): 8. http://dx.doi.org/10.1038/35049039.

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Hendricks, Benjamin K., Aaron A. Cohen-Gadol, and James C. Miller. "Novel delivery methods bypassing the blood-brain and blood-tumor barriers." Neurosurgical Focus 38, no. 3 (March 2015): E10. http://dx.doi.org/10.3171/2015.1.focus14767.

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Glioblastoma (GBM) is the most common primary brain tumor and carries a grave prognosis. Despite years of research investigating potentially new therapies for GBM, the median survival rate of individuals with this disease has remained fairly stagnant. Delivery of drugs to the tumor site is hampered by various barriers posed by the GBM pathological process and by the complex physiology of the blood-brain and blood–cerebrospinal fluid barriers. These anatomical and physiological barriers serve as a natural protection for the brain and preserve brain homeostasis, but they also have significantly limited the reach of intraparenchymal treatments in patients with GBM. In this article, the authors review the functional capabilities of the physical and physiological barriers that impede chemotherapy for GBM, with a specific focus on the pathological alterations of the blood-brain barrier (BBB) in this disease. They also provide an overview of current and future methods for circumventing these barriers in therapeutic interventions. Although ongoing research has yielded some potential options for future GBM therapies, delivery of chemotherapy medications across the BBB remains elusive and has limited the efficacy of these medications.

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Rhea, Elizabeth M., Therese S. Salameh, Aric F. Logsdon, Angela J. Hanson, Michelle A. Erickson, and William A. Banks. "Blood-Brain Barriers in Obesity." AAPS Journal 19, no. 4 (April 10, 2017): 921–30. http://dx.doi.org/10.1208/s12248-017-0079-3.

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Koziara, J. M., P. R. Lockman, D. D. Allen, and R. J. Mumper. "The Blood-Brain Barrier and Brain Drug Delivery." Journal of Nanoscience and Nanotechnology 6, no. 9 (September 1, 2006): 2712–35. http://dx.doi.org/10.1166/jnn.2006.441.

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The present report encompasses a thorough review of drug delivery to the brain with a particular focus on using drug carriers such as liposomes and nanoparticles. Challenges in brain drug delivery arise from the presence of one of the strictest barriers in vivo—the blood-brain barrier (BBB). This barrier exists at the level of endothelial cells of brain vasculature and its role is to maintain brain homeostasis. To better understand the principles of brain drug delivery, relevant knowledge of the blood-brain barrier anatomy and physiology is briefly reviewed. Several approaches to overcome the BBB have been reviewed including the use of carrier systems. In addition, strategies to enhance brain drug delivery by specific brain targeting are discussed.

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Herold, Schroten, and Schwerk. "Virulence Factors of Meningitis-Causing Bacteria: Enabling Brain Entry across the Blood–Brain Barrier." International Journal of Molecular Sciences 20, no. 21 (October 29, 2019): 5393. http://dx.doi.org/10.3390/ijms20215393.

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Infections of the central nervous system (CNS) are still a major cause of morbidity and mortality worldwide. Traversal of the barriers protecting the brain by pathogens is a prerequisite for the development of meningitis. Bacteria have developed a variety of different strategies to cross these barriers and reach the CNS. To this end, they use a variety of different virulence factors that enable them to attach to and traverse these barriers. These virulence factors mediate adhesion to and invasion into host cells, intracellular survival, induction of host cell signaling and inflammatory response, and affect barrier function. While some of these mechanisms differ, others are shared by multiple pathogens. Further understanding of these processes, with special emphasis on the difference between the blood–brain barrier and the blood–cerebrospinal fluid barrier, as well as virulence factors used by the pathogens, is still needed.

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McCabe, Shannon Morgan, and Ningning Zhao. "The Potential Roles of Blood–Brain Barrier and Blood–Cerebrospinal Fluid Barrier in Maintaining Brain Manganese Homeostasis." Nutrients 13, no. 6 (May 27, 2021): 1833. http://dx.doi.org/10.3390/nu13061833.

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Manganese (Mn) is a trace nutrient necessary for life but becomes neurotoxic at high concentrations in the brain. The brain is a “privileged” organ that is separated from systemic blood circulation mainly by two barriers. Endothelial cells within the brain form tight junctions and act as the blood–brain barrier (BBB), which physically separates circulating blood from the brain parenchyma. Between the blood and the cerebrospinal fluid (CSF) is the choroid plexus (CP), which is a tissue that acts as the blood–CSF barrier (BCB). Pharmaceuticals, proteins, and metals in the systemic circulation are unable to reach the brain and spinal cord unless transported through either of the two brain barriers. The BBB and the BCB consist of tightly connected cells that fulfill the critical role of neuroprotection and control the exchange of materials between the brain environment and blood circulation. Many recent publications provide insights into Mn transport in vivo or in cell models. In this review, we will focus on the current research regarding Mn metabolism in the brain and discuss the potential roles of the BBB and BCB in maintaining brain Mn homeostasis.

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Mo, Francesca, Alessia Pellerino, Riccardo Soffietti, and Roberta Rudà. "Blood–Brain Barrier in Brain Tumors: Biology and Clinical Relevance." International Journal of Molecular Sciences 22, no. 23 (November 23, 2021): 12654. http://dx.doi.org/10.3390/ijms222312654.

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The presence of barriers, such as the blood–brain barrier (BBB) and brain–tumor barrier (BTB), limits the penetration of antineoplastic drugs into the brain, resulting in poor response to treatments. Many techniques have been developed to overcome the presence of these barriers, including direct injections of substances by intranasal or intrathecal routes, chemical modification of drugs or constituents of BBB, inhibition of efflux pumps, physical disruption of BBB by radiofrequency electromagnetic radiation (EMP), laser-induced thermal therapy (LITT), focused ultrasounds (FUS) combined with microbubbles and convection enhanced delivery (CED). However, most of these strategies have been tested only in preclinical models or in phase 1–2 trials, and none of them have been approved for treatment of brain tumors yet. Concerning the treatment of brain metastases, many molecules have been developed in the last years with a better penetration across BBB (new generation tyrosine kinase inhibitors like osimertinib for non-small-cell lung carcinoma and neratinib/tucatinib for breast cancer), resulting in better progression-free survival and overall survival compared to older molecules. Promising studies concerning neural stem cells, CAR-T (chimeric antigen receptors) strategies and immunotherapy with checkpoint inhibitors are ongoing.

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LANE, NANCY J. "Morphology of Glial Blood-Brain Barriers." Annals of the New York Academy of Sciences 633, no. 1 Glial-Neurona (December 1991): 348–62. http://dx.doi.org/10.1111/j.1749-6632.1991.tb15626.x.

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Castro Dias, Mariana, Josephine A. Mapunda, Mykhailo Vladymyrov, and Britta Engelhardt. "Structure and Junctional Complexes of Endothelial, Epithelial and Glial Brain Barriers." International Journal of Molecular Sciences 20, no. 21 (October 29, 2019): 5372. http://dx.doi.org/10.3390/ijms20215372.

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The homeostasis of the central nervous system (CNS) is ensured by the endothelial, epithelial, mesothelial and glial brain barriers, which strictly control the passage of molecules, solutes and immune cells. While the endothelial blood-brain barrier (BBB) and the epithelial blood-cerebrospinal fluid barrier (BCSFB) have been extensively investigated, less is known about the epithelial and mesothelial arachnoid barrier and the glia limitans. Here, we summarize current knowledge of the cellular composition of the brain barriers with a specific focus on describing the molecular constituents of their junctional complexes. We propose that the brain barriers maintain CNS immune privilege by dividing the CNS into compartments that differ with regard to their role in immune surveillance of the CNS. We close by providing a brief overview on experimental tools allowing for reliable in vivo visualization of the brain barriers and their junctional complexes and thus the respective CNS compartments.

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Veryser, Lieselotte, Evelien Wynendaele, Lien Taevernier, Frederick Verbeke, Tanmayee Joshib, Pratima Tatke, and Bart De Spiegeleer. "N-alkylamides: from plant to brain." Functional Foods in Health and Disease 4, no. 6 (July 25, 2014): 264. http://dx.doi.org/10.31989/ffhd.v4i6.6.

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Background: Plant N-alkylamides (NAAs) are bio-active compounds with a broad functional spectrum. In order to reach their pharmacodynamic targets, they have to overcome several barriers of the body in the absorption phase. The permeability kinetics of spilanthol (a diene NAA) and pellitorine (a triene NAA) across these barriers (i.e. skin, oral/gut mucosa, blood-brain barrier) were investigated.Methods: The skin and oral mucosa permeability were investigated using human skin and pig mucosa in an ex vivo in vitro Franz diffusion cell set-up. The gut absorption characteristics were examined using the in vitro Caco-2 cell monolayer test system. The initial blood-brain barrier transport kinetics were investigated in an in vivo mice model using multiple time regression and efflux experiments. Quantification of both NAAs was conducted using HPLC-UV and bio-analytical UPLC-MS methods.Results: We demonstrated that spilanthol and pellitorine are able to penetrate the skin after topical administration. It is likely that spilanthol and pellitorine can pass the endothelial gut as they easily pass the Caco-2 cells in the monolayer model. It has been shown that spilanthol also crosses the oral mucosa as well as the blood-brain barrier. Conclusion: It was demonstrated that NAAs pass various physiological barriers i.e. the skin, oral and gut mucosa, and after having reached the systemic circulation, also the blood-brain barrier. As such, NAAs are cosmenutriceuticals which can be active in the brain.Key words: Plant N-alkylamides, pharmacokinetics, mucosa/skin, blood-brain barrier (BBB), cosmenutriceuticals

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Cattelotte, Julie, Pascal André, Mélissa Ouellet, Fanchon Bourasset, Jean-Michel Scherrmann, and Salvatore Cisternino. "In Situ Mouse Carotid Perfusion Model: Glucose and Cholesterol Transport in the Eye and Brain." Journal of Cerebral Blood Flow & Metabolism 28, no. 8 (April 30, 2008): 1449–59. http://dx.doi.org/10.1038/jcbfm.2008.34.

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The in situ mouse brain perfusion method for measuring blood—brain barrier permeability was adapted to assess transport of solutes at the blood—brain and blood—eye barriers. The procedure was checked with radiolabeled markers in oxygenated bicarbonate-buffered fluid infused for 30 to 120 secs via a carotid artery. Vascular flow estimated with diazepam was 2.2-fold lower in the eye than in the brain. The vascular volume and the integrity markers sucrose and inulin indicated that a perfusion flow rate of 2.5 mL/min preserved the physical integrity of these organs. However, the brain vasculature integrity was more sensitive to acute perfusion pressure than the eye vasculature. The functional capacities of blood barriers were assessed with d-glucose; its transport followed Michaelis—Menten kinetics with an apparent Km of 7.6 mmol/L and a Vmax of 23 μmol/sec per g in the brain, and a Km of 22.9 mmol/L and a Vmax of 40 μmol/sec per g in the eye. The transport of cholesterol to the brain and eye was significantly enhanced by adding the Abca1 inhibitor probucol, suggesting an Abca1-mediated efflux at the mouse brain and eye blood barriers. Thus in situ carotid perfusion is suitable for elucidating transport processes at the blood—brain and blood-eye barriers.

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Fanea, Laura, Leontin I. David, Andrei Lebovici, Francesca Carbone, and Silviu A. Sfrangeu. "Theoretical Compartment Modeling of DCE-MRI Data Based on the Transport across Physiological Barriers in the Brain." Computational and Mathematical Methods in Medicine 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/482565.

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Neurological disorders represent major causes of lost years of healthy life and mortality worldwide. Development of their quantitative interdisciplinaryin vivoevaluation is required. Compartment modeling (CM) of brain data acquiredin vivousing magnetic resonance imaging techniques with clinically available contrast agents can be performed to quantitatively assess brain perfusion. Transport of1H spins in water molecules across physiological compartmental brain barriers in three different pools was mathematically modeled and theoretically evaluated in this paper and the corresponding theoretical compartment modeling of dynamic contrast enhanced magnetic resonance imaging (DCE-MRI) data was analyzed. The pools considered were blood, tissue, and cerebrospinal fluid (CSF). The blood and CSF data were mathematically modeled assuming continuous flow of the1H spins in these pools. Tissue data was modeled using three CMs. Results in this paper show that transport across physiological brain barriers such as the blood to brain barrier, the extracellular space to the intracellular space barrier, or the blood to CSF barrier can be evaluated quantitatively. Statistical evaluations of this quantitative information may be performed to assess tissue perfusion, barriers' integrity, and CSF flowin vivoin the normal or disease-affected brain or to assess response to therapy.

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Kakaroubas, Nicholas, Samuel Brennan, Matthew Keon, and Nitin K. Saksena. "Pathomechanisms of Blood-Brain Barrier Disruption in ALS." Neuroscience Journal 2019 (July 10, 2019): 1–16. http://dx.doi.org/10.1155/2019/2537698.

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The blood-brain barrier (BBB) and the blood-spinal cord barrier (BSCB) are responsible for controlling the microenvironment within neural tissues in humans. These barriers are fundamental to all neurological processes as they provide the extreme nutritional demands of neural tissue, remove wastes, and maintain immune privileged status. Being a semipermeable membrane, both the BBB and BSCB allow the diffusion of certain molecules, whilst restricting others. In amyotrophic lateral sclerosis (ALS) and other neurodegenerative diseases, these barriers become hyperpermeable, allowing a wider variety of molecules to pass through leading to more severe and more rapidly progressing disease. The intention of this review is to discuss evidence that BBB hyperpermeability is potentially a disease driving feature in ALS and other neurodegenerative diseases. The various biochemical, physiological, and genomic factors that can influence BBB permeability in ALS and other neurodegenerative diseases are also discussed, in addition to novel therapeutic strategies centred upon the BBB.

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Tietz, Silvia, and Britta Engelhardt. "Brain barriers: Crosstalk between complex tight junctions and adherens junctions." Journal of Cell Biology 209, no. 4 (May 25, 2015): 493–506. http://dx.doi.org/10.1083/jcb.201412147.

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Unique intercellular junctional complexes between the central nervous system (CNS) microvascular endothelial cells and the choroid plexus epithelial cells form the endothelial blood–brain barrier (BBB) and the epithelial blood–cerebrospinal fluid barrier (BCSFB), respectively. These barriers inhibit paracellular diffusion, thereby protecting the CNS from fluctuations in the blood. Studies of brain barrier integrity during development, normal physiology, and disease have focused on BBB and BCSFB tight junctions but not the corresponding endothelial and epithelial adherens junctions. The crosstalk between adherens junctions and tight junctions in maintaining barrier integrity is an understudied area that may represent a promising target for influencing brain barrier function.

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Novack, Gary D., and Irving H. Leopold. "The Blood-Aqueous and Blood-Brain Barriers to Permeability." American Journal of Ophthalmology 105, no. 4 (April 1988): 412–16. http://dx.doi.org/10.1016/0002-9394(88)90308-x.

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Cartwright, Tara A., Christopher R. Campos, Ronald E. Cannon, and David S. Miller. "Mrp1 is Essential for Sphingolipid Signaling to P-Glycoprotein in Mouse Blood–Brain and Blood–Spinal Cord Barriers." Journal of Cerebral Blood Flow & Metabolism 33, no. 3 (November 21, 2012): 381–88. http://dx.doi.org/10.1038/jcbfm.2012.174.

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At the blood–brain and blood–spinal cord barriers, P-glycoprotein, an ATP-driven drug efflux pump, is a major obstacle to central nervous system (CNS) pharmacotherapy. Recently, we showed that signaling through tumor necrosis factor-α (TNF-α), sphingolipids, and sphingosine-1-phosphate receptor 1 (S1PR1) rapidly and reversibly reduced basal P-glycoprotein transport activity in the rat blood–brain barrier. The present study extends those findings to the mouse blood–brain and blood–spinal cord barriers and, importantly, identifies multidrug resistance-associated protein 1 (Mrp1, Abcc1) as the transporter that mediates S1P efflux from brain and spinal cord endothelial cells. In brain and spinal cord capillaries isolated from wild-type mice, TNF-α, sphingosine, S1P, the S1PR agonist fingolimod (FTY720), and its active, phosphorylated metabolite, FTY720P, reduced P-glycoprotein transport activity; these effects were abolished by a specific S1PR1 antagonist. In brain and spinal cord capillaries isolated from Mrp1-null mice, neither TNF-α nor sphingosine nor FTY720 reduced P-glycoprotein transport activity. However, S1P and FTY720P had the same S1PR1-dependent effects on transport activity as in capillaries from wild-type mice. Thus, deletion of Mrp1 alone terminated endogenous signaling to S1PR1. These results identify Mrp1 as the transporter essential for S1P efflux from the endothelial cells and thus for inside-out S1P signaling to P-glycoprotein at the blood–brain and blood–spinal cord barriers.

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Erickson, Michelle, and William Banks. "Age-Associated Changes in the Immune System and Blood–Brain Barrier Functions." International Journal of Molecular Sciences 20, no. 7 (April 2, 2019): 1632. http://dx.doi.org/10.3390/ijms20071632.

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Age is associated with altered immune functions that may affect the brain. Brain barriers, including the blood–brain barrier (BBB) and blood–CSF barrier (BCSFB), are important interfaces for neuroimmune communication, and are affected by aging. In this review, we explore novel mechanisms by which the aging immune system alters central nervous system functions and neuroimmune responses, with a focus on brain barriers. Specific emphasis will be on recent works that have identified novel mechanisms by which BBB/BCSFB functions change with age, interactions of the BBB with age-associated immune factors, and contributions of the BBB to age-associated neurological disorders. Understanding how age alters BBB functions and responses to pathological insults could provide important insight on the role of the BBB in the progression of cognitive decline and neurodegenerative disease.

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Nishijima, Daniel K. "Leaky blood-brain barriers and memory loss." Science Translational Medicine 7, no. 273 (February 4, 2015): 273ec22. http://dx.doi.org/10.1126/scitranslmed.aaa5560.

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Shih, Alan H., and Ross L. Levine. "IDH1 Mutations Disrupt Blood, Brain, and Barriers." Cancer Cell 22, no. 3 (September 2012): 285–87. http://dx.doi.org/10.1016/j.ccr.2012.08.022.

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Christensen, Brian, Andrea E. Toth, Simone S. E. Nielsen, Carsten Scavenius, Steen V. Petersen, Jan J. Enghild, Jan T. Rasmussen, Morten S. Nielsen, and Esben S. Sørensen. "Transport of a Peptide from Bovine αs1-Casein across Models of the Intestinal and Blood–Brain Barriers." Nutrients 12, no. 10 (October 16, 2020): 3157. http://dx.doi.org/10.3390/nu12103157.

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The effect of food components on brain growth and development has attracted increasing attention. Milk has been shown to contain peptides that deliver important signals to the brains of neonates and infants. In order to reach the brain, milk peptides have to resist proteolytic degradation in the gastrointestinal tract, cross the gastrointestinal barrier and later cross the highly selective blood–brain barrier (BBB). To investigate this, we purified and characterized endogenous peptides from bovine milk and investigated their apical to basal transport by using human intestinal Caco-2 cells and primary porcine brain endothelial cell monolayer models. Among 192 characterized milk peptides, only the αS1-casein peptide 185PIGSENSEKTTMPLW199, and especially fragments of this peptide processed during the transport, could cross both the intestinal barrier and the BBB cell monolayer models. This peptide was also shown to resist simulated gastrointestinal digestion. This study demonstrates that a milk derived peptide can cross the major biological barriers in vitro and potentially reach the brain, where it may deliver physiological signals.

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Landers, Kelly, and Kerry Richard. "Traversing barriers – How thyroid hormones pass placental, blood-brain and blood-cerebrospinal fluid barriers." Molecular and Cellular Endocrinology 458 (December 2017): 22–28. http://dx.doi.org/10.1016/j.mce.2017.01.041.

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Hajal, Cynthia, Baptiste Le Roi, Roger D. Kamm, and Ben M. Maoz. "Biology and Models of the Blood–Brain Barrier." Annual Review of Biomedical Engineering 23, no. 1 (July 13, 2021): 359–84. http://dx.doi.org/10.1146/annurev-bioeng-082120-042814.

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The blood–brain barrier (BBB) is one of the most selective endothelial barriers. An understanding of its cellular, morphological, and biological properties in health and disease is necessary to develop therapeutics that can be transported from blood to brain. In vivo models have provided some insight into these features and transport mechanisms adopted at the brain, yet they have failed as a robust platform for the translation of results into clinical outcomes. In this article, we provide a general overview of major BBB features and describe various models that have been designed to replicate this barrier and neurological pathologies linked with the BBB. We propose several key parameters and design characteristics that can be employed to engineer physiologically relevant models of the blood–brain interface and highlight the need for a consensus in the measurement of fundamental properties of this barrier.

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Poduslo, J. F., G. L. Curran, and C. T. Berg. "Macromolecular permeability across the blood-nerve and blood-brain barriers." Proceedings of the National Academy of Sciences 91, no. 12 (June 7, 1994): 5705–9. http://dx.doi.org/10.1073/pnas.91.12.5705.

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McLay, R. "Granulocyte-macrophage colony-stimulating factor crosses the blood-- brain and blood--spinal cord barriers." Brain 120, no. 11 (November 1, 1997): 2083–91. http://dx.doi.org/10.1093/brain/120.11.2083.

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Muldoon, Leslie L., Jorge I. Alvarez, David J. Begley, Ruben J. Boado, Gregory J. del Zoppo, Nancy D. Doolittle, Britta Engelhardt, et al. "Immunologic Privilege in the Central Nervous System and the Blood–Brain Barrier." Journal of Cerebral Blood Flow & Metabolism 33, no. 1 (October 17, 2012): 13–21. http://dx.doi.org/10.1038/jcbfm.2012.153.

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The brain is in many ways an immunologically and pharmacologically privileged site. The blood–brain barrier (BBB) of the cerebrovascular endothelium and its participation in the complex structure of the neurovascular unit (NVU) restrict access of immune cells and immune mediators to the central nervous system (CNS). In pathologic conditions, very well-organized immunologic responses can develop within the CNS, raising important questions about the real nature and the intrinsic and extrinsic regulation of this immune privilege. We assess the interactions of immune cells and immune mediators with the BBB and NVU in neurologic disease, cerebrovascular disease, and intracerebral tumors. The goals of this review are to outline key scientific advances and the status of the science central to both the neuroinflammation and CNS barriers fields, and highlight the opportunities and priorities in advancing brain barriers research in the context of the larger immunology and neuroscience disciplines. This review article was developed from reports presented at the 2011 Annual Blood-Brain Barrier Consortium Meeting.

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Saint-Pol, Julien, Fabien Gosselet, Sophie Duban-Deweer, Gwënaël Pottiez, and Yannis Karamanos. "Targeting and Crossing the Blood-Brain Barrier with Extracellular Vesicles." Cells 9, no. 4 (April 1, 2020): 851. http://dx.doi.org/10.3390/cells9040851.

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The blood–brain barrier (BBB) is one of the most complex and selective barriers in the human organism. Its role is to protect the brain and preserve the homeostasis of the central nervous system (CNS). The central elements of this physical and physiological barrier are the endothelial cells that form a monolayer of tightly joined cells covering the brain capillaries. However, as endothelial cells regulate nutrient delivery and waste product elimination, they are very sensitive to signals sent by surrounding cells and their environment. Indeed, the neuro-vascular unit (NVU) that corresponds to the assembly of extracellular matrix, pericytes, astrocytes, oligodendrocytes, microglia and neurons have the ability to influence BBB physiology. Extracellular vesicles (EVs) play a central role in terms of communication between cells. The NVU is no exception, as each cell can produce EVs that could help in the communication between cells in short or long distances. Studies have shown that EVs are able to cross the BBB from the brain to the bloodstream as well as from the blood to the CNS. Furthermore, peripheral EVs can interact with the BBB leading to changes in the barrier’s properties. This review focuses on current knowledge and potential applications regarding EVs associated with the BBB.

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Tiani, Kendra A., Patrick J. Stover, and Martha S. Field. "The Role of Brain Barriers in Maintaining Brain Vitamin Levels." Annual Review of Nutrition 39, no. 1 (August 21, 2019): 147–73. http://dx.doi.org/10.1146/annurev-nutr-082018-124235.

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It is increasingly recognized that tissue-specific nutrient deficiencies can exist in the absence of whole-body deficiency and that these deficiencies may result from disease or disease-related physiological processes. Brain and central nervous system tissues require adequate nutrient levels to function. Many nutrients are concentrated in the cerebrospinal fluid relative to the serum in healthy individuals, and other nutrients resist depletion in the presence of whole-body nutrient depletion. The endothelial, epithelial, and arachnoid brain barriers work in concert to selectively transport, concentrate, and maintain levels of the specific nutrients required by the brain while also blocking the passage of blood-borne toxins and pathogens to brain and central nervous system tissues. These barriers preserve nutrient levels within the brain and actively concentrate nutrients within the cerebrospinal fluid and brain. The roles of physical and energetic barriers, including the blood–brain and blood–nerve barriers, in maintaining brain nutrient levels in health and disease are discussed.

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Rao, Shilpa C., and Arinola O. Sanyaolu. "Breaking Barriers: Modeling the Blood–Brain Barrier in Parkinson's Disease Using a Human‐Brain‐Chip." Movement Disorders 37, no. 4 (February 28, 2022): 699. http://dx.doi.org/10.1002/mds.28968.

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AYDİN, Mehmet, Mustafa Can GÜLER, Canan ATALAY, and Osman Nuri KELEŞ. "Toward to Explain of Working Principles of Blood-Brain Barriers Like X-Ray Devices: A Neurophysical Hypothesis." Journal of Contemporary Medicine 13, no. 1 (January 31, 2023): 42–46. http://dx.doi.org/10.16899/jcm.1203348.

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Objective: The blood-brain barrier is an electromagnetic mechanism on a neurophysical basis. In this study, we compared the X-Ray device, which is similar to the blood-brain barrier in many ways. Material and Methods: We collected brain samples from deep temporal cortex sections of ten rats, stained them via the glial fibrillary acidic protein (GFAP) technique, visualized the architectural structures of the blood-brain barriers, and compared them with X-ray devices. Results: With the arterioles forming the tube blood-brain barrier in the X-ray device, the anode-cathode that provides the electric current and determines the direction of the current flow corresponds to the astrocytes surrounding the anode-cathode vessel, the cooling system to the cerebrospinal fluid circulating the vessel, and the electrons emitted from the cathode to the particles flowing in the vessel. Conclusion: With the architecture presented by the blood-brain barrier, we envision it functioning as an X-Ray and optical reader that display objects in passenger baggage and direct them according to barcode numbers.

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O'Brown, Natasha M., Sarah J. Pfau, and Chenghua Gu. "Bridging barriers: a comparative look at the blood–brain barrier across organisms." Genes & Development 32, no. 7-8 (April 1, 2018): 466–78. http://dx.doi.org/10.1101/gad.309823.117.

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ABBOTT, N. JOAN. "Permeability and Transport of Glial Blood-Brain Barriers." Annals of the New York Academy of Sciences 633, no. 1 Glial-Neurona (December 1991): 378–94. http://dx.doi.org/10.1111/j.1749-6632.1991.tb15628.x.

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Zhao, Yinan, Yanguo Xin, Zhiyi He, and Wenyu Hu. "Function of Connexins in the Interaction between Glial and Vascular Cells in the Central Nervous System and Related Neurological Diseases." Neural Plasticity 2018 (June 10, 2018): 1–13. http://dx.doi.org/10.1155/2018/6323901.

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Neuronal signaling together with synapse activity in the central nervous system requires a precisely regulated microenvironment. Recently, the blood-brain barrier is considered as a “neuro-glia-vascular unit,” a structural and functional compound composed of capillary endothelial cells, glial cells, pericytes, and neurons, which plays a pivotal role in maintaining the balance of the microenvironment in and out of the brain. Tight junctions and adherens junctions, which function as barriers of the blood-brain barrier, are two well-known kinds in the endothelial cell junctions. In this review, we focus on the less-concerned contribution of gap junction proteins, connexins in blood-brain barrier integrity under physio-/pathology conditions. In the neuro-glia-vascular unit, connexins are expressed in the capillary endothelial cells and prominent in astrocyte endfeet around and associated with maturation and function of the blood-brain barrier through a unique signaling pathway and an interaction with tight junction proteins. Connexin hemichannels and connexin gap junction channels contribute to the physiological or pathological progress of the blood-brain barrier; in addition, the interaction with other cell-cell-adhesive proteins is also associated with the maintenance of the blood-brain barrier. Lastly, we explore the connexins and connexin channels involved in the blood-brain barrier in neurological diseases and any programme for drug discovery or delivery to target or avoid the blood-brain barrier.

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Alarcan, Hugo, Yara Al Ojaimi, Debora Lanznaster, Jean-Michel Escoffre, Philippe Corcia, Patrick Vourc’h, Christian R. Andres, Charlotte Veyrat-Durebex, and Hélène Blasco. "Taking Advantages of Blood–Brain or Spinal Cord Barrier Alterations or Restoring Them to Optimize Therapy in ALS?" Journal of Personalized Medicine 12, no. 7 (June 29, 2022): 1071. http://dx.doi.org/10.3390/jpm12071071.

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Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder that still lacks an efficient therapy. The barriers between the central nervous system (CNS) and the blood represent a major limiting factor to the development of drugs for CNS diseases, including ALS. Alterations of the blood–brain barrier (BBB) or blood–spinal cord barrier (BSCB) have been reported in this disease but still require further investigations. Interestingly, these alterations might be involved in the complex etiology and pathogenesis of ALS. Moreover, they can have potential consequences on the diffusion of candidate drugs across the brain. The development of techniques to bypass these barriers is continuously evolving and might open the door for personalized medical approaches. Therefore, identifying robust and non-invasive markers of BBB and BSCB alterations can help distinguish different subgroups of patients, such as those in whom barrier disruption can negatively affect the delivery of drugs to their CNS targets. The restoration of CNS barriers using innovative therapies could consequently present the advantage of both alleviating the disease progression and optimizing the safety and efficiency of ALS-specific therapies.

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Garg, Yogesh, Deepak N. Kapoor, Abhishek K. Sharma, and Amit Bhatia. "Drug Delivery Systems and Strategies to Overcome the Barriers of Brain." Current Pharmaceutical Design 28, no. 8 (March 2022): 619–41. http://dx.doi.org/10.2174/1381612828666211222163025.

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Abstract: The transport of drugs to the central nervous system is the most challenging task for conventional drug delivery systems. The reduced permeability of drugs through the blood-brain barrier is a major hurdle in delivering drugs to the brain. Hence, various strategies for improving drug delivery through the blood-brain barrier are being explored. Novel drug delivery systems (NDDS) offer several advantages, including high chemical and biological stability, suitability for both hydrophobic and hydrophilic drugs, and can be administered through different routes. Furthermore, the conjugation of suitable ligands with these carriers tends to potentiate targeting to the endothelium of the brain and could facilitate the internalization of drugs through endocytosis. Further, the intranasal route has also shown potential, as a promising alternate route, for the delivery of drugs to the brain. This can deliver the drugs directly to the brain through the olfactory pathway. In recent years, several advancements have been made to target and overcome the barriers of the brain. This article deals with a detailed overview of the diverse strategies and delivery systems to overcome the barriers of the brain for effective delivery of drugs.

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Borkowski, Julia, Horst Schroten, and Christian Schwerk. "Interactions and Signal Transduction Pathways Involved during Central Nervous System Entry by Neisseria meningitidis across the Blood–Brain Barriers." International Journal of Molecular Sciences 21, no. 22 (November 20, 2020): 8788. http://dx.doi.org/10.3390/ijms21228788.

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The Gram-negative diplococcus Neisseria meningitidis, also called meningococcus, exclusively infects humans and can cause meningitis, a severe disease that can lead to the death of the afflicted individuals. To cause meningitis, the bacteria have to enter the central nervous system (CNS) by crossing one of the barriers protecting the CNS from entry by pathogens. These barriers are represented by the blood–brain barrier separating the blood from the brain parenchyma and the blood–cerebrospinal fluid (CSF) barriers at the choroid plexus and the meninges. During the course of meningococcal disease resulting in meningitis, the bacteria undergo several interactions with host cells, including the pharyngeal epithelium and the cells constituting the barriers between the blood and the CSF. These interactions are required to initiate signal transduction pathways that are involved during the crossing of the meningococci into the blood stream and CNS entry, as well as in the host cell response to infection. In this review we summarize the interactions and pathways involved in these processes, whose understanding could help to better understand the pathogenesis of meningococcal meningitis.

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Logsdon, Aric F., Michelle A. Erickson, Elizabeth M. Rhea, Therese S. Salameh, and William A. Banks. "Gut reactions: How the blood–brain barrier connects the microbiome and the brain." Experimental Biology and Medicine 243, no. 2 (November 23, 2017): 159–65. http://dx.doi.org/10.1177/1535370217743766.

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A growing body of evidence indicates that the microbiome interacts with the central nervous system (CNS) and can regulate many of its functions. One mechanism for this interaction is at the level of the blood–brain barriers (BBBs). In this minireview, we examine the several ways the microbiome is known to interact with the CNS barriers. Bacteria can directly release factors into the systemic circulation or can translocate into blood. Once in the blood, the microbiome and its factors can alter peripheral immune cells to promote interactions with the BBB and ultimately with other elements of the neurovascular unit. Bacteria and their factors or cytokines and other immune-active substances released from peripheral sites under the influence of the microbiome can cross the BBB, alter BBB integrity, change BBB transport rates, or induce release of neuroimmune substances from the barrier cells. Metabolic products produced by the microbiome, such as short-chain fatty acids, can cross the BBB to affect brain function. Through these and other mechanisms, microbiome–BBB interactions can influence the course of diseases as illustrated by multiple sclerosis. Impact statement The connection between the gut microbiome and central nervous system (CNS) disease is not fully understood. Host immune systems are influenced by changes to the microbiota and offers new treatment strategies for CNS disease. Preclinical studies provide evidence of changes to the blood–brain barrier when animals are subject to experimental gut infection or when the animals lack a normal gut microbiome. The intestine also contains a barrier, and bacterial factors can translocate to the blood and interact with host immune cells. These metastatic bacterial factors can signal T-cells to become more CNS penetrant, thus providing a novel intervention for treating CNS disease. Studies in humans show the therapeutic effects of T-cell engineering for the treatment of leukemia, so perhaps a similar approach for CNS disease could prove effective. Future research should begin to define the bacterial species that can cause immune cells to differentiate and how these interactions vary amongst CNS disease models.

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Gomez-Zepeda, David, Méryam Taghi, Jean-Michel Scherrmann, Xavier Decleves, and Marie-Claude Menet. "ABC Transporters at the Blood–Brain Interfaces, Their Study Models, and Drug Delivery Implications in Gliomas." Pharmaceutics 12, no. 1 (December 23, 2019): 20. http://dx.doi.org/10.3390/pharmaceutics12010020.

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Drug delivery into the brain is regulated by the blood–brain interfaces. The blood–brain barrier (BBB), the blood–cerebrospinal fluid barrier (BCSFB), and the blood–arachnoid barrier (BAB) regulate the exchange of substances between the blood and brain parenchyma. These selective barriers present a high impermeability to most substances, with the selective transport of nutrients and transporters preventing the entry and accumulation of possibly toxic molecules, comprising many therapeutic drugs. Transporters of the ATP-binding cassette (ABC) superfamily have an important role in drug delivery, because they extrude a broad molecular diversity of xenobiotics, including several anticancer drugs, preventing their entry into the brain. Gliomas are the most common primary tumors diagnosed in adults, which are often characterized by a poor prognosis, notably in the case of high-grade gliomas. Therapeutic treatments frequently fail due to the difficulty of delivering drugs through the brain barriers, adding to diverse mechanisms developed by the cancer, including the overexpression or expression de novo of ABC transporters in tumoral cells and/or in the endothelial cells forming the blood–brain tumor barrier (BBTB). Many models have been developed to study the phenotype, molecular characteristics, and function of the blood–brain interfaces as well as to evaluate drug permeability into the brain. These include in vitro, in vivo, and in silico models, which together can help us to better understand their implication in drug resistance and to develop new therapeutics or delivery strategies to improve the treatment of pathologies of the central nervous system (CNS). In this review, we present the principal characteristics of the blood–brain interfaces; then, we focus on the ABC transporters present on them and their implication in drug delivery; next, we present some of the most important models used for the study of drug transport; finally, we summarize the implication of ABC transporters in glioma and the BBTB in drug resistance and the strategies to improve the delivery of CNS anticancer drugs.

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Yokel, Robert A. "Nanoparticle brain delivery: a guide to verification methods." Nanomedicine 15, no. 4 (February 2020): 409–32. http://dx.doi.org/10.2217/nnm-2019-0169.

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Many reports conclude nanoparticle (NP) brain entry based on bulk brain analysis. Bulk brain includes blood, cerebrospinal fluid and blood vessels within the brain contributing to the blood–brain and blood–cerebrospinal fluid barriers. Considering the brain as neurons, glia and their extracellular space (brain parenchyma), most studies did not show brain parenchymal NP entry. Blood–brain and blood–cerebrospinal fluid barriers anatomy and function are reviewed. Methods demonstrating brain parenchymal NP entry are presented. Results demonstrating bulk brain versus brain parenchymal entry are classified. Studies are reviewed, critiqued and classified to illustrate results demonstrating bulk brain versus parenchymal entry. Brain, blood and peripheral organ NP timecourses are compared and related to brain parenchymal entry evidence suggesting brain NP timecourse informs about brain parenchymal entry.

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MØLLGÅRD, K., and N. R. SAUNDERS. "THE DEVELOPMENT OF THE HUMAN BLOOD-BRAIN AND BLOOD-CSF BARRIERS." Neuropathology and Applied Neurobiology 12, no. 4 (July 1986): 337–58. http://dx.doi.org/10.1111/j.1365-2990.1986.tb00146.x.

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Xiang, Jianming, Steven R. Ennis, Galaleldin E. Abdelkarim, Mutsuo Fujisawa, Nobuyuki Kawai, and Richard F. Keep. "Glutamine transport at the blood–brain and blood–cerebrospinal fluid barriers." Neurochemistry International 43, no. 4-5 (September 2003): 279–88. http://dx.doi.org/10.1016/s0197-0186(03)00013-5.

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Taggi, Valerio, Mario Riera Romo, Micheline Piquette-Miller, Henriette E. Meyer zu Schwabedissen, and Sibylle Neuhoff. "Transporter Regulation in Critical Protective Barriers: Focus on Brain and Placenta." Pharmaceutics 14, no. 7 (June 29, 2022): 1376. http://dx.doi.org/10.3390/pharmaceutics14071376.

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Drug transporters play an important role in the maintenance of chemical balance and homeostasis in different tissues. In addition to their physiological functions, they are crucial for the absorption, distribution, and elimination of many clinically important drugs, thereby impacting therapeutic efficacy and toxicity. Increasing evidence has demonstrated that infectious, metabolic, inflammatory, and neurodegenerative diseases alter the expression and function of drug transporters. However, the current knowledge on transporter regulation in critical protective barriers, such as the brain and placenta, is still limited and requires more research. For instance, while many studies have examined P-glycoprotein, it is evident that research on the regulation of highly expressed transporters in the blood–brain barrier and blood–placental barrier are lacking. The aim of this review is to summarize the currently available literature in order to better understand transporter regulation in these critical barriers.

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Dymova, Maya A., Elena V. Kuligina, and Vladimir A. Richter. "Molecular Mechanisms of Drug Resistance in Glioblastoma." International Journal of Molecular Sciences 22, no. 12 (June 15, 2021): 6385. http://dx.doi.org/10.3390/ijms22126385.

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Glioblastoma multiforme (GBM) is the most common and fatal primary brain tumor, is highly resistant to conventional radiation and chemotherapy, and is not amenable to effective surgical resection. The present review summarizes recent advances in our understanding of the molecular mechanisms of therapeutic resistance of GBM to already known drugs, the molecular characteristics of glioblastoma cells, and the barriers in the brain that underlie drug resistance. We also discuss the progress that has been made in the development of new targeted drugs for glioblastoma, as well as advances in drug delivery across the blood–brain barrier (BBB) and blood–brain tumor barrier (BBTB).

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Allen, Barrett D., and Charles L. Limoli. "Breaking barriers: Neurodegenerative repercussions of radiotherapy induced damage on the blood-brain and blood-tumor barrier." Free Radical Biology and Medicine 178 (January 2022): 189–201. http://dx.doi.org/10.1016/j.freeradbiomed.2021.12.002.

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Sangha, Vishal, Md Tozammel Hoque, Jeffrey Henderson, and Reina Bendayan. "Localization of the Folate Transport Systems in the Murine Central Nervous System." Current Developments in Nutrition 5, Supplement_2 (June 2021): 922. http://dx.doi.org/10.1093/cdn/nzab049_035.

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Abstract Objectives Folates are critical for normal neurodevelopment, and folate transport in the brain is primarily mediated by folate receptor alpha (FRα) at the blood-cerebrospinal fluid barrier (BCSFB). However, studies have reported folate transporter/receptor expression in other brain compartments, which may significantly contribute to overall brain folate uptake. The objective of this study is to characterize the localization of the folate transport systems i.e., reduced folate carrier (RFC), proton-coupled folate transporter (PCFT), and FRα in the mouse central nervous system, which will provide insight on novel routes of brain folate transport. In particular, folate transporter/receptor localization is examined at brain barriers [blood-brain barrier (BBB), BCSFB, arachnoid barrier (AB)] and in brain parenchyma (astrocytes, microglia, neurons). Methods The localization of RFC, PCFT and FRα was observed in the brains of C57BL6/N wildtype mice by applying immunohistochemistry (IHC). Mouse brains were isolated, and IHC was performed on frozen coronal sections. Transporter/receptor localization was examined at brain barriers (BBB, BCSFB, AB) and in brain parenchyma (astrocytes, neurons, microglia) using specific antibodies. Standard IHC markers were utilized to identify various brain compartments, with confocal microscopy used for imaging. Results At the mouse BBB and BCSFB, localization of RFC, PCFT and FRα was observed, which is consistent with previous reported data and our own work. At the AB, in astrocytes and neurons localization of RFC and PCFT (but not FRα) was observed. In microglia, no expression of the folate transporters or receptor was detected. Conclusions RFC and PCFT localization at the AB may represent a novel route of folate transport into the CSF, with transporter expression in neurons and astrocytes facilitating folate uptake into brain parenchyma cellular targets. Modulating folate transport at these brain compartments may provide a novel strategy in increasing brain folate uptake in disorders associated with defective FRα and impaired brain folate transport at the BCSFB. Funding Sources This work is supported by the Natural Sciences and Engineering Research Council of Canada (RB). VS is a recipient of several graduate scholarships.

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Rahner-Welsch, Sylvia, Johannes Vogel, and Wolfgang Kuschinsky. "Regional Congruence and Divergence of Glucose Transporters (GLUT1) and Capillaries in Rat Brains." Journal of Cerebral Blood Flow & Metabolism 15, no. 4 (July 1995): 681–86. http://dx.doi.org/10.1038/jcbfm.1995.84.

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The association of glucose transporters (GLUT1) and brain capillaries was tested in different brain structures of rats by a direct comparison of the topologies of capillaries and GLUT1 in identical brain sections. Antibody staining of capillaries (fibronectin) and GLUT1 were made visible by fluorescence microscopy. The results showed differences between brain structures containing a tight and a leaky blood–brain barrier. All capillaries of brain structures with a tight blood–brain barrier showed congruent staining of GLUT1 and capillary morphology. The circumventricular organs that are known to have leaky barrier capillaries were stained by fibronectin antibodies but not by GLUT1 antibodies. Ependymal cells showed moderate staining by GLUT1 antibodies both in areas with tight and leaky barriers. The subcommissural organ appeared to be unique showing neither capillary nor GLUT1 stain. It is concluded that glucose transporters (GLUT1) exist in all brain capillaries of blood–brain barrier structures, whereas they are absent in leaky barrier structures. Moderate amounts of glucose transporter (GLUT1) can also be detected in ependymal cells.

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Felker, James, and Sameer Agnihotri. "Not all mouse blood-brain barriers are created equal." Neuro-Oncology 23, no. 5 (March 13, 2021): 705–6. http://dx.doi.org/10.1093/neuonc/noab056.

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Kinglsey, Charles P. "The blood-brain barriers to advances in cardiac anesthesia." Current Opinion in Anaesthesiology 8, no. 1 (February 1995): 33–35. http://dx.doi.org/10.1097/00001503-199502000-00006.

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Marques, Fernanda, João Sousa, Nuno Sousa, and Joana Palha. "Blood–brain-barriers in aging and in Alzheimer’s disease." Molecular Neurodegeneration 8, no. 1 (2013): 38. http://dx.doi.org/10.1186/1750-1326-8-38.

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Kohli, Neha, Donevan R. Westerveld, Alexandra C. Ayache, Amrisha Verma, Pollob Shil, Tuhina Prasad, Ping Zhu, Sic L. Chan, Qiuhong Li, and Henry Daniell. "Oral Delivery of Bioencapsulated Proteins Across Blood–Brain and Blood–Retinal Barriers." Molecular Therapy 22, no. 3 (March 2014): 535–46. http://dx.doi.org/10.1038/mt.2013.273.

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Journal articles on the topic 'Blood Brain Barriers'

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