Статті в журналах: "Blood-brain barrier Pathophysiology"

1

Selmaj, Krzysztof. "Pathophysiology of the blood-brain barrier." Springer Seminars in Immunopathology 18, no. 1 (1996): 57–73. http://dx.doi.org/10.1007/bf00792609.

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2

Chodobski, Adam, Brian J. Zink, and Joanna Szmydynger-Chodobska. "Blood–Brain Barrier Pathophysiology in Traumatic Brain Injury." Translational Stroke Research 2, no. 4 (November 11, 2011): 492–516. http://dx.doi.org/10.1007/s12975-011-0125-x.

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3

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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4

McCaffrey, Gwen, and Thomas P. Davis. "Physiology and Pathophysiology of the Blood-Brain Barrier." Journal of Investigative Medicine 60, no. 8 (December 1, 2012): 1131–40. http://dx.doi.org/10.2310/jim.0b013e318276de79.

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5

Edvinsson, L., and P. Tfelt-Hansen. "The Blood-Brain Barrier in Migraine Treatment." Cephalalgia 28, no. 12 (December 2008): 1245–58. http://dx.doi.org/10.1111/j.1468-2982.2008.01675.x.

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Salient aspects of the anatomy and function of the blood-barrier barrier (BBB) are reviewed in relation to migraine pathophysiology and treatment. The main function of the BBB is to limit the access of circulating substances to the neuropile. Smaller lipophilic substances have some access to the central nervous system by diffusion, whereas other substances can cross the BBB by carrier-mediated influx transport, receptor-mediated transcytosis and absorptive-mediated transcytosis. Studies of drugs relevant to migraine pathophysiology and treatment have been examined with the pressurized arteriography method. The drugs, given both luminally and abluminally, provide important notions regarding antimigraine site of action, probably abluminal to the BBB. The problems with the BBB in animal models designed to study the pathophysiology, acute treatment models and preventive treatments are discussed with special emphasize on the triptans and calcitonin gene-related peptide (CGRP). The human experimental headache model, especially the use of glycerol trinitrate (the nitric oxide model), and experiences with CGRP administrations utilize the systemic administration of the agonists with effects on other vascular beds also. We discuss how this can be related to genuine migraine attacks. Our view is that there exists no clear proof of breakdown or leakage of the BBB during migraine attacks, and that antimigraine drugs need to pass the BBB for efficacy.

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6

Vinters, Harry V., and William M. Pardridge. "The Blood-Brain Barrier in Alzheimer's Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 13, S4 (November 1986): 446–48. http://dx.doi.org/10.1017/s0317167100037094.

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Abstract:The current evidence for and against abnormalities of the blood-brain barrier in “normal” aging and Alzheimer's disease is reviewed. Recent studies of cerebral amyloid angiopathy, a microangiopathy commonly observed in Alzheimer's disease and one suggested to result from blood-brain barrier derangement, are discussed with particular attention to the biochemical nature of the vascular amyloid material, and features it shares with the amyloid found in senile plaque cores and with neurofibrillary tangles. Modern techniques that will probably clarify blood-brain barrier pathophysiology are reviewed.

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7

Khan, Naveed Ahmed. "Acanthamoeba and the blood–brain barrier: the breakthrough." Journal of Medical Microbiology 57, no. 9 (September 1, 2008): 1051–57. http://dx.doi.org/10.1099/jmm.0.2008/000976-0.

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Acanthamoeba granulomatous encephalitis is a rare disease that almost always proves fatal. Death occurs mainly due to neurological complications; however, the pathogenesis and pathophysiology associated with this disease remain incompletely understood. Haematogenous spread is a key step in the development of Acanthamoeba encephalitis, but it is not clear how circulating amoebae breakthrough the blood–brain barrier to gain entry into the central nervous system to produce the disease. This review of the literature describes the parasite factors and immune-mediated mechanisms involved in the blood–brain barrier dysfunction leading to neuropathogenesis.

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8

Tunkel, A. R., B. Wispelwey, V. J. Quagliarello, S. W. Rosser, A. J. Lesse, E. J. Hansen, and W. M. Scheld. "Pathophysiology of Blood-Brain Barrier Alterations during Experimental Haemophilus influenzae Meningitis." Journal of Infectious Diseases 165, Supplement 1 (June 1, 1992): S119—S120. http://dx.doi.org/10.1093/infdis/165-supplement_1-s119.

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9

Barichello, Tatiana, Glauco D. Fagundes, Jaqueline S. Generoso, Samuel Galvão Elias, Lutiana R. Simões, and Antonio Lucio Teixeira. "Pathophysiology of neonatal acute bacterial meningitis." Journal of Medical Microbiology 62, no. 12 (December 1, 2013): 1781–89. http://dx.doi.org/10.1099/jmm.0.059840-0.

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Neonatal meningitis is a severe acute infectious disease of the central nervous system and an important cause of morbidity and mortality worldwide. The inflammatory reaction involves the meninges, the subarachnoid space and the brain parenchymal vessels and contributes to neuronal injury. Neonatal meningitis leads to deafness, blindness, cerebral palsy, seizures, hydrocephalus or cognitive impairment in approximately 25–50 % of survivors. Bacterial pathogens can reach the blood–brain barrier and be recognized by antigen-presenting cells through the binding of Toll-like receptors. They induce the activation of NFκB or mitogen-activated protein kinase pathways and subsequently upregulate leukocyte populations and express numerous proteins involved in inflammation and the immune response. Many brain cells can produce cytokines, chemokines and other pro-inflammatory molecules in response to bacterial stimuli, and polymorphonuclear leukocytes are attracted, activated and released in large amounts of superoxide anion and nitric oxide, leading to peroxynitrite formation and generating oxidative stress. This cascade leads to lipid peroxidation, mitochondrial damage and breakdown of the blood–brain barrier, thus contributing to cell injury during neonatal meningitis. This review summarizes information on the pathophysiology and adjuvant treatment of acute bacterial meningitis in neonates.

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10

Khadka, Bikram, Jae-Young Lee, Ki-Taek Kim, and Jong-Sup Bae. "Recent progress in therapeutic drug delivery systems for treatment of traumatic CNS injuries." Future Medicinal Chemistry 12, no. 19 (October 2020): 1759–78. http://dx.doi.org/10.4155/fmc-2020-0178.

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Most therapeutics for the treatment of traumatic central nervous system injuries, such as traumatic brain injury and spinal cord injury, encounter various obstacles in reaching the target tissue and exerting pharmacological effects, including physiological barriers like the blood–brain barrier and blood–spinal cord barrier, instability rapid elimination from the injured tissue or cerebrospinal fluid and off-target toxicity. For central nervous system delivery, nano- and microdrug delivery systems are regarded as the most suitable and promising carriers. In this review, the pathophysiology and biomarkers of traumatic central nervous system injuries (traumatic brain injury and spinal cord injury) are introduced. Furthermore, various drug delivery systems, novel combinatorial therapies and advanced therapies for the treatment of traumatic brain injury and spinal cord injury are emphasized.

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11

Helms, Hans C., N. Joan Abbott, Malgorzata Burek, Romeo Cecchelli, Pierre-Olivier Couraud, Maria A. Deli, Carola Förster, et al. "In vitro models of the blood–brain barrier: An overview of commonly used brain endothelial cell culture models and guidelines for their use." Journal of Cerebral Blood Flow & Metabolism 36, no. 5 (February 11, 2016): 862–90. http://dx.doi.org/10.1177/0271678x16630991.

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The endothelial cells lining the brain capillaries separate the blood from the brain parenchyma. The endothelial monolayer of the brain capillaries serves both as a crucial interface for exchange of nutrients, gases, and metabolites between blood and brain, and as a barrier for neurotoxic components of plasma and xenobiotics. This “blood-brain barrier” function is a major hindrance for drug uptake into the brain parenchyma. Cell culture models, based on either primary cells or immortalized brain endothelial cell lines, have been developed, in order to facilitate in vitro studies of drug transport to the brain and studies of endothelial cell biology and pathophysiology. In this review, we aim to give an overview of established in vitro blood–brain barrier models with a focus on their validation regarding a set of well-established blood–brain barrier characteristics. As an ideal cell culture model of the blood–brain barrier is yet to be developed, we also aim to give an overview of the advantages and drawbacks of the different models described.

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12

H. Greig, N. "Pathophysiology of the Blood-Brain Barrier: Long Term Consequences of Barrier Dysfunction for the Brain (Fernstrom Foundation Series)." Neurology 42, no. 1 (January 1, 1992): 267. http://dx.doi.org/10.1212/wnl.42.1.267-b.

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13

Huber, Jason D., Richard D. Egleton, and Thomas P. Davis. "Molecular physiology and pathophysiology of tight junctions in the blood–brain barrier." Trends in Neurosciences 24, no. 12 (December 2001): 719–25. http://dx.doi.org/10.1016/s0166-2236(00)02004-x.

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14

Montagne, Axel, Zhen Zhao, and Berislav V. Zlokovic. "Alzheimer’s disease: A matter of blood–brain barrier dysfunction?" Journal of Experimental Medicine 214, no. 11 (October 23, 2017): 3151–69. http://dx.doi.org/10.1084/jem.20171406.

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The blood–brain barrier (BBB) keeps neurotoxic plasma-derived components, cells, and pathogens out of the brain. An early BBB breakdown and/or dysfunction have been shown in Alzheimer’s disease (AD) before dementia, neurodegeneration and/or brain atrophy occur. However, the role of BBB breakdown in neurodegenerative disorders is still not fully understood. Here, we examine BBB breakdown in animal models frequently used to study the pathophysiology of AD, including transgenic mice expressing human amyloid-β precursor protein, presenilin 1, and tau mutations, and apolipoprotein E, the strongest genetic risk factor for AD. We discuss the role of BBB breakdown and dysfunction in neurodegenerative process, pitfalls in BBB measurements, and how targeting the BBB can influence the course of neurological disorder. Finally, we comment on future approaches and models to better define, at the cellular and molecular level, the underlying mechanisms between BBB breakdown and neurodegeneration as a basis for developing new therapies for BBB repair to control neurodegeneration.

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15

Sulhan, Suraj, Kristopher A. Lyon, Lee A. Shapiro, and Jason H. Huang. "Neuroinflammation and blood-brain barrier disruption following traumatic brain injury: Pathophysiology and potential therapeutic targets." Journal of Neuroscience Research 98, no. 1 (September 27, 2018): 19–28. http://dx.doi.org/10.1002/jnr.24331.

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16

Berezowski, Vincent, Andrew M. Fukuda, Roméo Cecchelli, and Jérôme Badaut. "Endothelial Cells and Astrocytes: AConcerto en Duoin Ischemic Pathophysiology." International Journal of Cell Biology 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/176287.

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The neurovascular/gliovascular unit has recently gained increased attention in cerebral ischemic research, especially regarding the cellular and molecular changes that occur in astrocytes and endothelial cells. In this paper we summarize the recent knowledge of these changes in association with edema formation, interactions with the basal lamina, and blood-brain barrier dysfunctions. We also review the involvement of astrocytes and endothelial cells with recombinant tissue plasminogen activator, which is the only FDA-approved thrombolytic drug after stroke. However, it has a narrow therapeutic time window and serious clinical side effects. Lastly, we provide alternative therapeutic targets for future ischemia drug developments such as peroxisome proliferator- activated receptors and inhibitors of the c-Jun N-terminal kinase pathway. Targeting the neurovascular unit to protect the blood-brain barrier instead of a classical neuron-centric approach in the development of neuroprotective drugs may result in improved clinical outcomes after stroke.

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17

Shah, Kaushik, and Thomas Abbruscato. "The Role of Blood-Brain Barrier Transporters in Pathophysiology and Pharmacotherapy of Stroke." Current Pharmaceutical Design 20, no. 10 (March 31, 2014): 1510–22. http://dx.doi.org/10.2174/13816128113199990465.

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18

Ahn, Song Ih, and YongTae Kim. "Human Blood–Brain Barrier on a Chip: Featuring Unique Multicellular Cooperation in Pathophysiology." Trends in Biotechnology 39, no. 8 (August 2021): 749–52. http://dx.doi.org/10.1016/j.tibtech.2021.01.010.

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19

Wong, Ka, Muhammad Riaz, Yuning Xie, Xue Zhang, Qiang Liu, Huoji Chen, Zhaoxiang Bian, Xiaoyu Chen, Aiping Lu, and Zhijun Yang. "Review of Current Strategies for Delivering Alzheimer’s Disease Drugs across the Blood-Brain Barrier." International Journal of Molecular Sciences 20, no. 2 (January 17, 2019): 381. http://dx.doi.org/10.3390/ijms20020381.

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Effective therapy for Alzheimer’s disease is a major challenge in the pharmaceutical sciences. There are six FDA approved drugs (e.g., donepezil, memantine) that show some effectiveness; however, they only relieve symptoms. Two factors hamper research. First, the cause of Alzheimer’s disease is not fully understood. Second, the blood-brain barrier restricts drug efficacy. This review summarized current knowledge relevant to both of these factors. First, we reviewed the pathophysiology of Alzheimer’s disease. Next, we reviewed the structural and biological properties of the blood-brain barrier. We then described the most promising drug delivery systems that have been developed in recent years; these include polymeric nanoparticles, liposomes, metallic nanoparticles and cyclodextrins. Overall, we aim to provide ideas and clues to design effective drug delivery systems for penetrating the blood-brain barrier to treat Alzheimer’s disease.

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20

Barichello, Tatiana, Jaqueline S. Generoso, Allan Collodel, Ana Paula Moreira, and Sérgio Monteiro de Almeida. "Pathophysiology of acute meningitis caused by Streptococcus pneumoniae and adjunctive therapy approaches." Arquivos de Neuro-Psiquiatria 70, no. 5 (May 2012): 366–72. http://dx.doi.org/10.1590/s0004-282x2012000500011.

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Pneumococcal meningitis is a life-threatening disease characterized by an acute purulent infection affecting piamater, arachnoid and the subarachnoid space. The intense inflammatory host's response is potentially fatal and contributes to the neurological sequelae. Streptococcus pneumoniae colonizes the nasopharynx, followed by bacteremia, microbial invasion and blood-brain barrier traversal. S. pneumoniae is recognized by antigen-presenting cells through the binding of Toll-like receptors inducing the activation of factor nuclear kappa B or mitogen-activated protein kinase pathways and subsequent up-regulation of lymphocyte populations and expression of numerous proteins involved in inflammation and immune response. Many brain cells can produce cytokines, chemokines and others pro-inflammatory molecules in response to bacteria stimuli, as consequence, polymorphonuclear are attracted, activated and released in large amounts of superoxide anion and nitric oxide, leading to the peroxynitrite formation, generating oxidative stress. This cascade leads to lipid peroxidation, mitochondrial damage, blood-brain barrier breakdown contributing to cell injury during pneumococcal meningitis.

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21

Werf, Y. D. Van Der, M. J. L. De Jongste, and G. J. Ter Horst. "The immune system mediates blood-brain barrier damage; possible implications for pathophysiology of neuropsychiatric illnesses." Acta Neuropsychiatrica 7, no. 4 (December 1995): 114–21. http://dx.doi.org/10.1017/s0924270800037315.

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SummaryIn this investigation the effects of immune activation on the brain are characterized. In order to study this, we used a model for chronic immune activation, the myocardial infarction, and intravenous injections with the pro-inflammatory cytokine Tumour Necrosis Factor alpha (TNF-α). The incentive for this study is the observation that myocardial infarction is accompanied by behavioural and neuronal abnormalities. The effects of myocardial infarction on the brain and its functioning are widespread. In order to examine the mechanism through which this interaction occurs, a group of rats underwent an experimentally induced myocardial infarction whereafter immunohistochemistry was performed on slices of the brain. This experiment revealed regional serum protein extravasation, pointing to leakage of the blood-brain barrier. This process occurred in certain cortical, subcortical and hindbrain areas in discrete patches. The leakage was co-localized with the expression of the immune activation marker ICAM-1. A second group of rats was therefore injected with TNF-α, a major pro-inflammatory cytokine, to assess the involvement of the immune system in the effects shown. This procedure rendered the same results. It is concluded that myocardial infarction may interfere with the integrity of the blood-brain barrier and possibly with brain functioning through activation of the immune system. The relevance for pathophysiological processes is discussed.

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22

Ali, Shan, Zuzanna Górska, Renata Duchnowska, and Jacek Jassem. "Molecular Profiles of Brain Metastases: A Focus on Heterogeneity." Cancers 13, no. 11 (May 28, 2021): 2645. http://dx.doi.org/10.3390/cancers13112645.

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Brain metastasis is a common and devastating clinical entity. Intratumor heterogeneity in brain metastases poses a crucial challenge to precision medicine. However, advances in next-generation sequencing, new insight into the pathophysiology of driver mutations, and the creation of novel tumor models have allowed us to gain better insight into the genetic landscapes of brain metastases, their temporal evolution, and their response to various treatments. A plethora of genomic studies have identified the heterogeneous clonal landscape of tumors and, at the same time, introduced potential targets for precision medicine. As an example, we present phenotypic alterations in brain metastases originating from three malignancies with the highest brain metastasis frequency: lung cancer, breast cancer, and melanoma. We discuss the barriers to precision medicine, tumor heterogeneity, the significance of blood-based biomarkers in tracking clonal evolution, the phylogenetic relationship between primary and metastatic tumors, blood–brain barrier heterogeneity, and limitations to ongoing research.

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23

Pong, Sovannarath, Rakesh Karmacharya, Marianna Sofman, Jeffrey R. Bishop, and Paulo Lizano. "The Role of Brain Microvascular Endothelial Cell and Blood-Brain Barrier Dysfunction in Schizophrenia." Complex Psychiatry 6, no. 1-2 (2020): 30–46. http://dx.doi.org/10.1159/000511552.

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Background: Despite decades of research, little clarity exists regarding pathogenic mechanisms related to schizophrenia. Investigations on the disease biology of schizophrenia have primarily focused on neuronal alterations. However, there is substantial evidence pointing to a significant role for the brain’s microvasculature in mediating neuroinflammation in schizophrenia. Summary: Brain microvascular endothelial cells (BMEC) are a central element of the microvasculature that forms the blood-brain barrier (BBB) and shields the brain against toxins and immune cells via paracellular, transcellular, transporter, and extracellular matrix proteins. While evidence for BBB dysfunction exists in brain disorders, including schizophrenia, it is not known if BMEC themselves are functionally compromised and lead to BBB dysfunction. Key Messages: Genome-wide association studies, postmortem investigations, and gene expression analyses have provided some insights into the role of the BBB in schizophrenia pathophysiology. However, there is a significant gap in our understanding of the role that BMEC play in BBB dysfunction. Recent advances differentiating human BMEC from induced pluripotent stem cells (iPSC) provide new avenues to examine the role of BMEC in BBB dysfunction in schizophrenia.

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24

Drouin-Ouellet, Janelle, Stephen J. Sawiak, Giulia Cisbani, Marie Lagacé, Wei-Li Kuan, Martine Saint-Pierre, Richard J. Dury, et al. "Cerebrovascular and blood-brain barrier impairments in Huntington's disease: Potential implications for its pathophysiology." Annals of Neurology 78, no. 2 (April 9, 2015): 160–77. http://dx.doi.org/10.1002/ana.24406.

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25

Lee, Mi Ji, Jihoon Cha, Hyun Ah Choi, Sook-Young Woo, Seonwoo Kim, Shuu-Jiun Wang, and Chin-Sang Chung. "Blood-brain barrier breakdown in reversible cerebral vasoconstriction syndrome: Implications for pathophysiology and diagnosis." Annals of Neurology 81, no. 3 (March 2017): 454–66. http://dx.doi.org/10.1002/ana.24891.

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26

Lécuyer, Marc-André, Olivia Saint-Laurent, Lyne Bourbonnière, Sandra Larouche, Catherine Larochelle, Laure Michel, Marc Charabati, et al. "Dual role of ALCAM in neuroinflammation and blood–brain barrier homeostasis." Proceedings of the National Academy of Sciences 114, no. 4 (January 9, 2017): E524—E533. http://dx.doi.org/10.1073/pnas.1614336114.

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Activated leukocyte cell adhesion molecule (ALCAM) is a cell adhesion molecule found on blood–brain barrier endothelial cells (BBB-ECs) that was previously shown to be involved in leukocyte transmigration across the endothelium. In the present study, we found that ALCAM knockout (KO) mice developed a more severe myelin oligodendrocyte glycoprotein (MOG)35–55–induced experimental autoimmune encephalomyelitis (EAE). The exacerbated disease was associated with a significant increase in the number of CNS-infiltrating proinflammatory leukocytes compared with WT controls. Passive EAE transfer experiments suggested that the pathophysiology observed in active EAE was linked to the absence of ALCAM on BBB-ECs. In addition, phenotypic characterization of unimmunized ALCAM KO mice revealed a reduced expression of BBB junctional proteins. Further in vivo, in vitro, and molecular analysis confirmed that ALCAM is associated with tight junction molecule assembly at the BBB, explaining the increased permeability of CNS blood vessels in ALCAM KO animals. Collectively, our data point to a biologically important function of ALCAM in maintaining BBB integrity.

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27

Cho, Soohyun, Yu-Hsiang Ling, Mi Ji Lee, Shih-Pin Chen, Jong-Ling Fuh, Jiing-Feng Lirng, Jihoon Cha, Yen-Feng Wang, Shuu-Jiun Wang, and Chin-Sang Chung. "Temporal Profile of Blood-Brain Barrier Breakdown in Reversible Cerebral Vasoconstriction Syndrome." Stroke 51, no. 5 (May 2020): 1451–57. http://dx.doi.org/10.1161/strokeaha.119.028656.

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Background and Purpose— Reversible cerebral vasoconstriction syndrome (RCVS) has a unique temporal course of vasoconstriction. Blood-brain barrier (BBB) breakdown is part of the pathophysiology of RCVS, but its temporal course is unknown. We aimed to investigate the temporal profile of BBB breakdown and relevant clinical profiles in a large sample size. Methods— In this prospective observatory bicenter study, patients who underwent contrast-enhanced fluid-attenuated inversion recovery magnetic resonance imaging within 2 months from onset were included. The presence and extent of BBB breakdown were evaluated using contrast-enhanced fluid-attenuated inversion recovery magnetic resonance imaging. Contrast-enhanced fluid-attenuated inversion recovery magnetic resonance imaging data were analyzed using a semiautomated segmentation technique to quantitatively measure the area of Gadolinium leakage into cerebrospinal fluid space. The univariable and multivariable linear regressions were performed to investigate the independent effect of time from onset with adjustment for other covariates. Results— In the 186 patients with angiogram-proven RCVS included in this analysis, BBB breakdown was observed in 52.6%, 56.8%, 30.3%, 40.0%, and 23.8% in the first, second, third, fourth, and ≥fifth week after onset. The extent of BBB breakdown peaked at first and second week, whereas the peak of vasoconstriction was observed at the third week after onset. Multivariable analysis showed the second week from onset (β, 3.35 [95% CI, 0.07–6.64]; P =0.046) and blood pressure surge (β, 3.84 [95% CI, 1.75–5.92]; P <0.001) were independently associated with a greater extent of BBB breakdown. A synergistic effect of time from onset and blood pressure surge was found ( P for interaction=0.006). Conclusions— Frequency and extent of BBB breakdown are more prominent during the early stage in patients with RCVS, with an earlier peak than that of vasoconstriction. The temporal course of BBB breakdown may provide a pathophysiologic background of the temporal course of neurological complications of RCVS.

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28

Simińska, Donata, Klaudyna Kojder, Dariusz Jeżewski, Ireneusz Kojder, Marta Skórka, Izabela Gutowska, Dariusz Chlubek, and Irena Baranowska-Bosiacka. "The Pathophysiology of Post-Traumatic Glioma." International Journal of Molecular Sciences 19, no. 8 (August 19, 2018): 2445. http://dx.doi.org/10.3390/ijms19082445.

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Malignant glioma is a brain tumor with a very high mortality rate resulting from the specific morphology of its infiltrative growth and poor early detection rates. The causes of one of its very specific types, i.e., post-traumatic glioma, have been discussed for many years, with some studies providing evidence for mechanisms where the reaction to an injury may in some cases lead to the onset of carcinogenesis in the brain. In this review of the available literature, we discuss the consequences of breaking the blood–brain barrier and consequences of the influx of immune-system cells to the site of injury. We also analyze the influence of inflammatory mediators on the expression of genes controlling the process of apoptosis and the effect of chemical mutagenic factors on glial cells in the brain. We present the results of experimental studies indicating a relationship between injury and glioma development. However, epidemiological studies on post-traumatic glioma, of which only a few confirm the conclusions of experimental research, indicate that any potential relationship between injury and glioma, if any, is indirect.

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29

Chang, Olivia Hui-Chiun, Alexandra Stanculescu, Chi Dola, and William Benjamin Rothwell. "Recurrent Posterior Reversible Encephalopathy Syndrome Potentially Related to AIDS and End-Stage Renal Disease: A Case Report and Review of the Literature." Case Reports in Medicine 2012 (2012): 1–3. http://dx.doi.org/10.1155/2012/914035.

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Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological syndrome that is characterized by clinical features including headache, altered mental status, cortical blindness, seizures, and other focal neurological signs as well as subcortical edema without infarction on neuroimaging. Under the umbrella of hypertensive encephalopathy, PRES is defined by reversible cerebral edema due to dysfunction of the cerebrovascular blood-brain barrier unit. The pathophysiology of PRES is thought to result from abnormalities in the transmembrane flow of intravascular fluid and proteins caused by two phenomena: one, cerebral autoregulatory failure and two, loss of integrity of the blood-brain barrier. PRES is not a common disease in patients with human immunodeficiency virus (HIV) and AIDS with only three previously reported cases. Both the HIV and end-stage renal disease appear to further compromise the blood brain barrier. Although uncommon, PRES recurrence has been described. To the best of our knowledge, this is the first report demonstrating recurrent PRES in a HIV patient on hemodialysis for end-stage renal disease.

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30

Pantoni, Leonardo, and Michela Simoni. "Pathophysiology of Cerebral Small Vessels in Vascular Cognitive Impairment." International Psychogeriatrics 15, S1 (July 2003): 59–65. http://dx.doi.org/10.1017/s1041610203008974.

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Cerebral small-vessel alterations play a central role in determining lesions of subcortical structures and eventually may lead to cognitive impairment. Small-vessel diseases are classified according to the pathological viewpoint. The most important ones are the changes in small arteries and arterioles caused by prolonged hypertension. These small-vessel changes may result in ischemic damage to the brain parenchyma and blood-barrier alterations. Both mechanisms are thought to contribute to the occurrence of white-matter changes and lacunar infarcts. Modern magnetic resonance techniques such as diffusion, perfusion, and spectroscopy may allow the in vivo study of the pathophysiology of small-vessel diseases and the consequences on the brain parenchyma.

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31

Mora, Pierre, Pierre-Louis Hollier, Sarah Guimbal, Alice Abelanet, Aïssata Diop, Lauriane Cornuault, Thierry Couffinhal, et al. "Blood–brain barrier genetic disruption leads to protective barrier formation at the Glia Limitans." PLOS Biology 18, no. 11 (November 30, 2020): e3000946. http://dx.doi.org/10.1371/journal.pbio.3000946.

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Inflammation of the central nervous system (CNS) induces endothelial blood–brain barrier (BBB) opening as well as the formation of a tight junction barrier between reactive astrocytes at the Glia Limitans. We hypothesized that the CNS parenchyma may acquire protection from the reactive astrocytic Glia Limitans not only during neuroinflammation but also when BBB integrity is compromised in the resting state. Previous studies found that astrocyte-derived Sonic hedgehog (SHH) stabilizes the BBB during CNS inflammatory disease, while endothelial-derived desert hedgehog (DHH) is expressed at the BBB under resting conditions. Here, we investigated the effects of endothelial Dhh on the integrity of the BBB and Glia Limitans. We first characterized DHH expression within endothelial cells at the BBB, then demonstrated that DHH is down-regulated during experimental autoimmune encephalomyelitis (EAE). Using a mouse model in which endothelial Dhh is inducibly deleted, we found that endothelial Dhh both opens the BBB via the modulation of forkhead box O1 (FoxO1) transcriptional activity and induces a tight junctional barrier at the Glia Limitans. We confirmed the relevance of this glial barrier system in human multiple sclerosis active lesions. These results provide evidence for the novel concept of “chronic neuroinflammatory tolerance” in which BBB opening in the resting state is sufficient to stimulate a protective barrier at the Glia Limitans that limits the severity of subsequent neuroinflammatory disease. In summary, genetic disruption of the BBB generates endothelial signals that drive the formation under resting conditions of a secondary barrier at the Glia Limitans with protective effects against subsequent CNS inflammation. The concept of a reciprocally regulated CNS double barrier system has implications for treatment strategies in both the acute and chronic phases of multiple sclerosis pathophysiology.

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van der Mast, Rose C. "Pathophysiology of Delirium." Journal of Geriatric Psychiatry and Neurology 11, no. 3 (October 1998): 138–45. http://dx.doi.org/10.1177/089198879801100304.

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Hypotheses about the pathophysiology of delirium are speculative and largely based on animal research. According to the neurotransmitter hypothesis, decreased oxidative metabolism in the brain causes cerebral dysfunction due to abnormalities of various neurotransmitter systems. Reduced cholinergic function, excess release of dopamine, norepinephrine, and glutamate, and both decreased and increased serotonergic and γ-aminobutyric acid activity may underlie the different symptoms and clinical presentations of delirium. According to the inflammatory hypothesis, increased cerebral secretion of cytokines due to a wide range of physically stressful events plays an important role in the occurrence of delirium. Since cytokines can influence the activity of various neurotransmitter systems, these mechanisms may interact. Also, more fundamental processes like intraneuronal signal transduction, second messenger systems that at the same time use neurotransmitters as first messengers and play an important role in their synthesis and release, may be disturbed. Furthermore, severe illness and physiologic stress may give rise to modification of blood-brain barrier permeability, the sick euthyroid syndrome with abnormalities of thyroid hormone concentrations, and increased activity of the hypothalamic-pituitary-adrenal axis. These circumstances possibly also contribute to changes in neurotransmitter synthesis and release of cytokines in the brain, and consequently to the occurrence of delirium. Elderly patients are more at risk for developing delirium, very likely due to age-related cerebral changes in stress-regulating neurotransmitter and intracellular signal transduction systems. This paper will expand upon these current theories and discuss their applicability to research and clinical work with elderly patients suffering from delirium.

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Lippmann, Kristina, Lyn Kamintsky, Soo Young Kim, Svetlana Lublinsky, Ofer Prager, Julia Friederike Nichtweiss, Seda Salar, Daniela Kaufer, Uwe Heinemann, and Alon Friedman. "Epileptiform activity and spreading depolarization in the blood–brain barrier-disrupted peri-infarct hippocampus are associated with impaired GABAergic inhibition and synaptic plasticity." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (July 20, 2016): 1803–19. http://dx.doi.org/10.1177/0271678x16652631.

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Peri-infarct opening of the blood–brain barrier may be associated with spreading depolarizations, seizures, and epileptogenesis as well as cognitive dysfunction. We aimed to investigate the mechanisms underlying neural network pathophysiology in the blood–brain barrier-dysfunctional hippocampus. Photothrombotic stroke within the rat neocortex was associated with increased intracranial pressure, vasogenic edema, and peri-ischemic blood–brain barrier dysfunction that included the ipsilateral hippocampus. Intrahippocampal recordings revealed electrographic seizures within the first week in two-thirds of animals, accompanied by a reduction in gamma and increase in theta frequency bands. Synaptic interactions were studied in parasagittal hippocampal slices at 24 h and seven days post-stroke. Field potential recordings in CA1 and CA3 uncovered multiple population spikes, epileptiform episodes, and spreading depolarizations at 24 h. Input–output analysis revealed that fEPSP-spike coupling was significantly enhanced at seven days. In addition, CA1 feedback and feedforward inhibition were diminished. Slices generating epileptiform activity at seven days revealed impaired bidirectional long-term plasticity following high and low-frequency stimulation protocols. Microarray and PCR data confirmed changes in expression of astrocyte-related genes and suggested downregulation in expression of GABAA-receptor subunits. We conclude that blood-brain barrier dysfunction in the peri-infarct hippocampus is associated with early disinhibition, hyperexcitability, and abnormal synaptic plasticity.

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Shanker Sharma, Hari, Dafin F. Muresanu, José V. Lafuente, Ala Nozari, Ranjana Patnaik, Stephen D. Skaper, and Aruna Sharma. "Pathophysiology of Blood-Brain Barrier in Brain Injury in Cold and Hot Environments: Novel Drug Targets for Neuroprotection." CNS & Neurological Disorders - Drug Targets 15, no. 9 (October 7, 2016): 1045–71. http://dx.doi.org/10.2174/1871527315666160902145145.

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Patel, Jay P., and Benicio N. Frey. "Disruption in the Blood-Brain Barrier: The Missing Link between Brain and Body Inflammation in Bipolar Disorder?" Neural Plasticity 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/708306.

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The blood-brain barrier (BBB) regulates the transport of micro- and macromolecules between the peripheral blood and the central nervous system (CNS) in order to maintain optimal levels of essential nutrients and neurotransmitters in the brain. In addition, the BBB plays a critical role protecting the CNS against neurotoxins. There has been growing evidence that BBB disruption is associated with brain inflammatory conditions such as Alzheimer’s disease and multiple sclerosis. Considering the increasing role of inflammation and oxidative stress in the pathophysiology of bipolar disorder (BD), here we propose a novel model wherein transient or persistent disruption of BBB integrity is associated with decreased CNS protection and increased permeability of proinflammatory (e.g., cytokines, reactive oxygen species) substances from the peripheral blood into the brain. These events would trigger the activation of microglial cells and promote localized damage to oligodendrocytes and the myelin sheath, ultimately compromising myelination and the integrity of neural circuits. The potential implications for research in this area and directions for future studies are discussed.

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Li, Wen, Jianhua Qiu, Xiang-Ling Li, Sezin Aday, Jingdong Zhang, Grace Conley, Jun Xu, et al. "BBB pathophysiology–independent delivery of siRNA in traumatic brain injury." Science Advances 7, no. 1 (January 2021): eabd6889. http://dx.doi.org/10.1126/sciadv.abd6889.

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Small interfering RNA (siRNA)–based therapeutics can mitigate the long-term sequelae of traumatic brain injury (TBI) but suffer from poor permeability across the blood-brain barrier (BBB). One approach to overcoming this challenge involves treatment administration while BBB is transiently breached after injury. However, it offers a limited window for therapeutic intervention and is applicable to only a subset of injuries with substantially breached BBB. We report a nanoparticle platform for BBB pathophysiology–independent delivery of siRNA in TBI. We achieved this by combined modulation of surface chemistry and coating density on nanoparticles, which maximized their active transport across BBB. Engineered nanoparticles injected within or outside the window of breached BBB in TBI mice showed threefold higher brain accumulation compared to nonengineered PEGylated nanoparticles and 50% gene silencing. Together, our data suggest that this nanoparticle platform is a promising next-generation drug delivery approach for the treatment of TBI.

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Nishibori, Masahiro, Dengli Wang, Daiki Ousaka, and Hidenori Wake. "High Mobility Group Box-1 and Blood–Brain Barrier Disruption." Cells 9, no. 12 (December 10, 2020): 2650. http://dx.doi.org/10.3390/cells9122650.

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Increasing evidence suggests that inflammatory responses are involved in the progression of brain injuries induced by a diverse range of insults, including ischemia, hemorrhage, trauma, epilepsy, and degenerative diseases. During the processes of inflammation, disruption of the blood–brain barrier (BBB) may play a critical role in the enhancement of inflammatory responses and may initiate brain damage because the BBB constitutes an interface between the brain parenchyma and the bloodstream containing blood cells and plasma. The BBB has a distinct structure compared with those in peripheral tissues: it is composed of vascular endothelial cells with tight junctions, numerous pericytes surrounding endothelial cells, astrocytic endfeet, and a basement membrane structure. Under physiological conditions, the BBB should function as an important element in the neurovascular unit (NVU). High mobility group box-1 (HMGB1), a nonhistone nuclear protein, is ubiquitously expressed in almost all kinds of cells. HMGB1 plays important roles in the maintenance of chromatin structure, the regulation of transcription activity, and DNA repair in nuclei. On the other hand, HMGB1 is considered to be a representative damage-associated molecular pattern (DAMP) because it is translocated and released extracellularly from different types of brain cells, including neurons and glia, contributing to the pathophysiology of many diseases in the central nervous system (CNS). The regulation of HMGB1 release or the neutralization of extracellular HMGB1 produces beneficial effects on brain injuries induced by ischemia, hemorrhage, trauma, epilepsy, and Alzheimer’s amyloidpathy in animal models and is associated with improvement of the neurological symptoms. In the present review, we focus on the dynamics of HMGB1 translocation in different disease conditions in the CNS and discuss the functional roles of extracellular HMGB1 in BBB disruption and brain inflammation. There might be common as well as distinct inflammatory processes for each CNS disease. This review will provide novel insights toward an improved understanding of a common pathophysiological process of CNS diseases, namely, BBB disruption mediated by HMGB1. It is proposed that HMGB1 might be an excellent target for the treatment of CNS diseases with BBB disruption.

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Mansour, Ahmed, Sherif Rashad, Kuniyasu Niizuma, Miki Fujimura, and Teiji Tominaga. "A novel model of cerebral hyperperfusion with blood-brain barrier breakdown, white matter injury, and cognitive dysfunction." Journal of Neurosurgery 133, no. 5 (November 2020): 1460–72. http://dx.doi.org/10.3171/2019.7.jns19212.

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OBJECTIVECerebral hyperperfusion (CHP) is associated with considerable morbidity. Its pathophysiology involves disruption of the blood-brain barrier (BBB) with subsequent events such as vasogenic brain edema and ischemic and/or hemorrhagic complications. Researchers are trying to mimic the condition of CHP; however, a proper animal model is still lacking. In this paper the authors report a novel surgically induced CHP model that mimics the reported pathophysiology of clinical CHP including BBB breakdown, white matter (WM) injury, inflammation, and cognitive impairment.METHODSMale Sprague-Dawley rats were subjected to unilateral common carotid artery (CCA) occlusion and contralateral CCA stenosis. Three days after the initial surgery, the stenosis of CCA was released to induce CHP. Cortical regional cerebral blood flow was measured using laser speckle flowmetry. BBB breakdown was assessed by Evans blue dye extravasation and matrix metalloproteinase–9 levels. WM injury was investigated with Luxol fast blue staining. Cognitive function was assessed using the Barnes circular maze. Other changes pertaining to inflammation were also assessed. Sham-operated animals were prepared and used as controls.RESULTSCerebral blood flow was significantly raised in the cerebral cortex after CHP induction. CHP induced BBB breakdown evident by Evans blue dye extravasation, and matrix metalloproteinase–9 was identified as a possible culprit. WM degeneration was evident in the corpus callosum and corpus striatum. Immunohistochemistry revealed macrophage activation and glial cell upregulation as an inflammatory response to CHP in the striatum and cerebral cortex. CHP also caused significant impairments in spatial learning and memory compared with the sham-operated animals.CONCLUSIONSThe authors report a novel CHP model in rats that represents the pathophysiology of CHP observed in various clinical scenarios. This model was produced without the use of pharmacological agents; therefore, it is ideal to study the pathology of CHP as well as to perform preclinical drug trials.

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Bykov, Yu V., and V. A. Baturin. "Pathophysiological Mechanisms of Cerebral Edema in Diabetic Ketoacidosis in Pediatric Practice." Medicina 9, no. 1 (2021): 116–27. http://dx.doi.org/10.29234/2308-9113-2021-9-1-116-127.

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Diabetic ketoacidosis is a frequent complication of type 1 diabetes mellitus in children and adolescents. One of the leading causes of death in this pathology is cerebral edema. This complication is often asymptomatic, which makes it difficult to diagnose. The main risk factors for cerebral edema in children include the true factors (low partial pressure of carbon dioxide, high blood urea nitrogen, concomitant psychiatric pathology, etc.) and iatrogenic factors (large volume of infusion therapy, rapid decrease in blood glucose levels, administration of bicarbonate, etc.). The pathophysiology of this complication is not yet fully understood. The main pathophysiological elements of cerebral edema in children with DKA include the disruption of blood-brain barrier permeability, edema of brain cells, and dysfunction of cell membranes. Important roles are also played by hypercapnia and reduction of osmotic pressure. Based on the character of pathophysiologic changes, cerebral edema in children and adolescents with DKA is subdivided into vasogenic and cytotoxic. Gaining a better understanding of the pathophysiological mechanisms of this complication will increase the quality of care provided in pediatric practice.

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Bieber, Michael, Michael K. Schuhmann, Julia Volz, Gangasani Jagadeesh Kumar, Jayathirtha Rao Vaidya, Bernhard Nieswandt, Mirko Pham, Guido Stoll, Christoph Kleinschnitz, and Peter Kraft. "Description of a Novel Phosphodiesterase (PDE)-3 Inhibitor Protecting Mice From Ischemic Stroke Independent From Platelet Function." Stroke 50, no. 2 (February 2019): 478–86. http://dx.doi.org/10.1161/strokeaha.118.023664.

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Background and Purpose— Acetylsalicylic acid and clopidogrel are the 2 main antithrombotic drugs for secondary prevention in patients with ischemic stroke (IS) without indication for anticoagulation. Because of their limited efficacy and potential side effects, novel antiplatelet agents are urgently needed. Cilostazol, a specific phosphodiesterase (PDE)-3 inhibitor, protected from IS in clinical studies comprising mainly Asian populations. Nevertheless, the detailed mechanistic role of PDE-3 inhibitors in IS pathophysiology is hardly understood. In this project, we analyzed the efficacy and pathophysiologic mechanisms of a novel and only recently described PDE-3 inhibitor (substance V) in a mouse model of focal cerebral ischemia. Methods— Focal cerebral ischemia was induced by transient middle cerebral artery occlusion in 6- to 8-week-old male C57Bl/6 wild-type mice receiving substance V or vehicle 1 hour after ischemia induction. Infarct volumes and functional outcomes were assessed between day 1 and day 7, and findings were validated by magnetic resonance imaging. Blood-brain barrier damage, as well as the extent of local inflammatory response and cell death, was determined. Results— Inhibition of PDE-3 by pharmacological blockade with substance V significantly reduced infarct volumes and improved neurological outcome on day 1 and 7 after experimental cerebral ischemia. Reduced blood-brain barrier damage, attenuated brain tissue inflammation, and decreased local cell death could be identified as potential mechanisms. PDE-3 inhibitor treatment did neither increase the number of intracerebral hemorrhages nor affect platelet function. Conclusions— The novel PDE-3 inhibitor substance V protected mice from IS independent from platelet function. Pharmaceutical inactivation of PDE-3 might become a promising therapeutic approach to combat IS via inhibition of thromboinflammatory mechanisms and stabilization of the blood-brain barrier.

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T. de Barros, Cecilia, Alessandra C. Rios, Thaís F. R. Alves, Fernando Batain, Kessi M. M. Crescencio, Laura J. Lopes, Aleksandra Zielińska, et al. "Cachexia: Pathophysiology and Ghrelin Liposomes for Nose-to-Brain Delivery." International Journal of Molecular Sciences 21, no. 17 (August 19, 2020): 5974. http://dx.doi.org/10.3390/ijms21175974.

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Cachexia, a severe multifactorial condition that is underestimated and unrecognized in patients, is characterized by continuous muscle mass loss that leads to progressive functional impairment, while nutritional support cannot completely reverse this clinical condition. There is a strong need for more effective and targeted therapies for cachexia patients. There is a need for drugs that act on cachexia as a distinct and treatable condition to prevent or reverse excess catabolism and inflammation. Due to ghrelin properties, it has been studied in the cachexia and other treatments in a growing number of works. However, in the body, exogenous ghrelin is subject to very rapid degradation. In this context, the intranasal release of ghrelin-loaded liposomes to cross the blood-brain barrier and the release of the drug into the central nervous system may be a promising alternative to improve its bioavailability. The administration of nose-to-brain liposomes for the management of cachexia was addressed only in a limited number of published works. This review focuses on the discussion of the pathophysiology of cachexia, synthesis and physiological effects of ghrelin and the potential treatment of the diseased using ghrelin-loaded liposomes through the nose-to-brain route.

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Mohanty, Sureswar, Srikant Kumar Swain, and Chinmay Biswal. "Brain Edema: Newer Concept of Treatment." Annals of the National Academy of Medical Sciences (India) 55, no. 04 (October 2019): 189–92. http://dx.doi.org/10.1055/s-0040-1701154.

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AbstractBrain edema is excess accumulation of water in intracellular or extracellular spaces of the brain. It may be due to traumatic brain injury, neoplasm, infection, or following surgery. Advent of electron microscope and molecular pathophysiology of fluid transport through blood–brain barrier has elucidated the mechanism of edema formation, that is, ion channels and transport of fluid into extracellular space. Currently approved treatments, such as decompressive craniectomy and osmotherapy, controlled hyperventilation, and administration of diuretics, were developed prior to any knowledge of modern cerebral edema pathophysiology. These therapies attempt to manage downstream end-stage events without directly attenuating the underlying molecular mechanisms of cerebral edema. Next few years will yield new knowledge of how particular proteins drive edema influx, paving the way for rationally designed therapeutics that directly target key steps in cerebral edema formation, thereby achieving what currently approved therapies do not. Pharmacological agents which can block edema formation are being tried experimentally and clinically. Development in imaging, that is, computed tomography and diffusion tensor magnetic resonance imaging, has helped in antemortem assessment of evolution and resolution of brain edema as a dynamic pathophysiology. Animal studies shows release of vasoactive substances, that is, histamine, serotonin, adrenaline, nitric oxide, substance P, prostaglandins, tumor necrosis factor-α, and cytokines, in the injured brain results in activation of inflammatory cascade, which is the important cause of brain edema.

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Stanimirovic, Danica B., and Alon Friedman. "Pathophysiology of the Neurovascular Unit: Disease Cause or Consequence?" Journal of Cerebral Blood Flow & Metabolism 32, no. 7 (March 7, 2012): 1207–21. http://dx.doi.org/10.1038/jcbfm.2012.25.

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Pathophysiology of the neurovascular unit (NVU) is commonly seen in neurological diseases. The typical features of NVU pathophysiology include tissue hypoxia, inflammatory and angiogenic activation, as well as initiation of complex molecular interactions between cellular (brain endothelial cells, astroctyes, pericytes, inflammatory cells, and neurons) and acellular (basal lamina) components of the NVU, jointly resulting in increased blood–brain barrier permeability, brain edema, neurovascular uncoupling, and neuronal dysfunction and damage. The evidence of important role of the brain vascular compartment in disease pathogenesis has elicited the debate whether the primary vascular events may be a cause of the neurological disease, as opposed to a mere participant recruited by a primary neuronal origin of pathology? Whereas some hereditary and acquired cerebral angiopathies could be considered a primary cause of neurological symptoms of the disease, the epidemiological studies showing a high degree of comorbidity among vascular disease and dementias, including Alzheimer's disease, as well as migraine and epilepsy, suggested that primary vascular pathology may be etiological factor causing neuronal dysfunction or degeneration in these diseases. This review focuses on recent hypotheses and evidence, suggesting that pathophysiology of the NVU may be initiating trigger for neuronal pathology and subsequent neurological manifestations of the disease.

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Krueger, Martin, Wolfgang Härtig, Clara Frydrychowicz, Wolf C. Mueller, Andreas Reichenbach, Ingo Bechmann, and Dominik Michalski. "Stroke-induced blood–brain barrier breakdown along the vascular tree – No preferential affection of arteries in different animal models and in humans." Journal of Cerebral Blood Flow & Metabolism 37, no. 7 (October 1, 2016): 2539–54. http://dx.doi.org/10.1177/0271678x16670922.

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Stroke-induced blood–brain barrier breakdown promotes complications like cerebral edema and hemorrhagic transformation, especially in association with therapeutical recanalization of occluded vessels. As arteries, capillaries and veins display distinct functional and morphological characteristics, we here investigated patterns of blood–brain barrier breakdown for each segment of the vascular tree in rodent models of embolic, permanent, and transient middle cerebral artery occlusion, added by analyses of human stroke tissue. Twenty-four hours after ischemia induction, loss of blood–brain barrier function towards FITC-albumin was equally observed for arteries, capillaries, and veins in rodent brains. Noteworthy, veins showed highest ratios of leaky vessels, whereas capillaries exhibited the most and arteries the least widespread perivascular tracer extravasation. In contrast, human autoptic stroke tissue exhibited pronounced extravasations of albumin around arteries and veins, while the pericapillary immunoreactivity appeared only faint. Although electron microscopy revealed comparable alterations of the arterial and capillary endothelium throughout the applied animal models, structural loss of arterial smooth muscle cells was only observed in the translationally relevant model of embolic middle cerebral artery occlusion. In light of the so far available concepts of stroke treatment, the consideration of a differential vascular pathophysiology along the cerebral vasculature is likely to allow development of novel effective treatment strategies.

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Reiber, Hansotto. "Cerebrospinal fluid - physiology, analysis and interpretation of protein patterns for diagnosis of neurological diseases." Multiple Sclerosis Journal 4, no. 3 (June 1998): 99–107. http://dx.doi.org/10.1177/135245859800400302.

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The state of the art in routine CSF analysis is reviewed with particular reference to multiple sclerosis regarding: (1) The physiology and pathophysiology of blood-CSF barrier function and dysfunction with the CSF flow rate as main modulator of blood- and brain-derived protein concentrations in CSF; (2) The neuroimmunological aspects regarding (a) patterns of disease-related immunoglobulin class response (IgG, lgA, IgM) in actual Reiber graphs with reference to specific parameters and optional tests, and (b) the oligoclonal, polyspecific antibody synthesis in brain; (3) Particular marker proteins in CSF and blood for differential diagnosis of neurological diseases; (4) Mathematical base for evaluations of CSF data with an example of a multiple sclerosis patient for calculation of intrathecal immunoglobulin and antibody synthesis as well as Antibody Index.

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Salmina, Alla B., Ekaterina V. Kharitonova, Yana V. Gorina, Elena A. Teplyashina, Natalia A. Malinovskaya, Elena D. Khilazheva, Angelina I. Mosyagina, et al. "Blood–Brain Barrier and Neurovascular Unit In Vitro Models for Studying Mitochondria-Driven Molecular Mechanisms of Neurodegeneration." International Journal of Molecular Sciences 22, no. 9 (April 28, 2021): 4661. http://dx.doi.org/10.3390/ijms22094661.

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Pathophysiology of chronic neurodegeneration is mainly based on complex mechanisms related to aberrant signal transduction, excitation/inhibition imbalance, excitotoxicity, synaptic dysfunction, oxidative stress, proteotoxicity and protein misfolding, local insulin resistance and metabolic dysfunction, excessive cell death, development of glia-supported neuroinflammation, and failure of neurogenesis. These mechanisms tightly associate with dramatic alterations in the structure and activity of the neurovascular unit (NVU) and the blood–brain barrier (BBB). NVU is an ensemble of brain cells (brain microvessel endothelial cells (BMECs), astrocytes, pericytes, neurons, and microglia) serving for the adjustment of cell-to-cell interactions, metabolic coupling, local microcirculation, and neuronal excitability to the actual needs of the brain. The part of the NVU known as a BBB controls selective access of endogenous and exogenous molecules to the brain tissue and efflux of metabolites to the blood, thereby providing maintenance of brain chemical homeostasis critical for efficient signal transduction and brain plasticity. In Alzheimer’s disease, mitochondria are the target organelles for amyloid-induced neurodegeneration and alterations in NVU metabolic coupling or BBB breakdown. In this review we discuss understandings on mitochondria-driven NVU and BBB dysfunction, and how it might be studied in current and prospective NVU/BBB in vitro models for finding new approaches for the efficient pharmacotherapy of Alzheimer’s disease.

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Huang, Qin, Fang Yu, Di Liao, and Jian Xia. "Microbiota-Immune System Interactions in Human Neurological Disorders." CNS & Neurological Disorders - Drug Targets 19, no. 7 (November 26, 2020): 509–26. http://dx.doi.org/10.2174/1871527319666200726222138.

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: Recent studies implicate microbiota-brain communication as an essential factor for physiology and pathophysiology in brain function and neurodevelopment. One of the pivotal mechanisms about gut to brain communication is through the regulation and interaction of gut microbiota on the host immune system. In this review, we will discuss the role of microbiota-immune systeminteractions in human neurological disorders. The characteristic features in the development of neurological diseases include gut dysbiosis, the disturbed intestinal/Blood-Brain Barrier (BBB) permeability, the activated inflammatory response, and the changed microbial metabolites. Neurological disorders contribute to gut dysbiosis and some relevant metabolites in a top-down way. In turn, the activated immune system induced by the change of gut microbiota may deteriorate the development of neurological diseases through the disturbed gut/BBB barrier in a down-top way. Understanding the characterization and identification of microbiome-immune- brain signaling pathways will help us to yield novel therapeutic strategies by targeting the gut microbiome in neurological disease.

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Sharma, Rishabh, Wai Lam Leung, Akram Zamani, Terence J. O’Brien, Pablo M. Casillas Espinosa, and Bridgette D. Semple. "Neuroinflammation in Post-Traumatic Epilepsy: Pathophysiology and Tractable Therapeutic Targets." Brain Sciences 9, no. 11 (November 9, 2019): 318. http://dx.doi.org/10.3390/brainsci9110318.

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Epilepsy is a common chronic consequence of traumatic brain injury (TBI), contributing to increased morbidity and mortality for survivors. As post-traumatic epilepsy (PTE) is drug-resistant in at least one-third of patients, there is a clear need for novel therapeutic strategies to prevent epilepsy from developing after TBI, or to mitigate its severity. It has long been recognized that seizure activity is associated with a local immune response, characterized by the activation of microglia and astrocytes and the release of a plethora of pro-inflammatory cytokines and chemokines. More recently, increasing evidence also supports a causal role for neuroinflammation in seizure induction and propagation, acting both directly and indirectly on neurons to promote regional hyperexcitability. In this narrative review, we focus on key aspects of the neuroinflammatory response that have been implicated in epilepsy, with a particular focus on PTE. The contributions of glial cells, blood-derived leukocytes, and the blood–brain barrier will be explored, as well as pro- and anti-inflammatory mediators. While the neuroinflammatory response to TBI appears to be largely pro-epileptogenic, further research is needed to clearly demonstrate causal relationships. This research has the potential to unveil new drug targets for PTE, and identify immune-based biomarkers for improved epilepsy prediction.

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Crupi, Rosalia, Marika Cordaro, Salvatore Cuzzocrea, and Daniela Impellizzeri. "Management of Traumatic Brain Injury: From Present to Future." Antioxidants 9, no. 4 (April 2, 2020): 297. http://dx.doi.org/10.3390/antiox9040297.

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TBI (traumatic brain injury) is a major cause of death among youth in industrialized societies. Brain damage following traumatic injury is a result of direct and indirect mechanisms; indirect or secondary injury involves the initiation of an acute inflammatory response, including the breakdown of the blood–brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors. TBI can cause changes in molecular signaling and cellular functions and structures, in addition to tissue damage, such as hemorrhage, diffuse axonal damages, and contusions. TBI typically disturbs brain functions such as executive actions, cognitive grade, attention, memory data processing, and language abilities. Animal models have been developed to reproduce the different features of human TBI, better understand its pathophysiology, and discover potential new treatments. For many years, the first approach to manage TBI has been treatment of the injured tissue with interventions designed to reduce the complex secondary-injury cascade. Several studies in the literature have stressed the importance of more closely examining injuries, including endothelial, microglia, astroglia, oligodendroglia, and precursor cells. Significant effort has been invested in developing neuroprotective agents. The aim of this work is to review TBI pathophysiology and existing and potential new therapeutic strategies in the management of inflammatory events and behavioral deficits associated with TBI.

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Wang, Gaiqing, Anatol Manaenko, Anwen Shao, Yibo Ou, Peng Yang, Enkhjargal Budbazar, Derek Nowrangi, John H. Zhang, and Jiping Tang. "Low-density lipoprotein receptor-related protein-1 facilitates heme scavenging after intracerebral hemorrhage in mice." Journal of Cerebral Blood Flow & Metabolism 37, no. 4 (July 20, 2016): 1299–310. http://dx.doi.org/10.1177/0271678x16654494.

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Heme-degradation after erythrocyte lysis plays an important role in the pathophysiology of intracerebral hemorrhage. Low-density lipoprotein receptor-related protein-1 is a receptor expressed predominately at the neurovascular interface, which facilitates the clearance of the hemopexin and heme complex. In the present study, we investigated the role of low-density lipoprotein receptor-related protein-1 in heme removal and neuroprotection in a mouse model of intracerebral hemorrhage. Endogenous low-density lipoprotein receptor-related protein-1 and hemopexin were increased in ipsilateral brain after intracerebral hemorrhage, accompanied by increased hemoglobin levels, brain water content, blood–brain barrier permeability and neurological deficits. Exogenous human recombinant low-density lipoprotein receptor-related protein-1 protein reduced hematoma volume, brain water content surrounding hematoma, blood–brain barrier permeability and improved neurological function three days after intracerebral hemorrhage. The expression of malondialdehyde, fluoro-Jade C positive cells and cleaved caspase 3 was increased three days after intracerebral hemorrhage in the ipsilateral brain tissues and decreased with recombinant low-density lipoprotein receptor-related protein-1. Intracerebral hemorrhage decreased and recombinant low-density lipoprotein receptor-related protein-1 increased the levels of superoxide dismutase 1. Low-density lipoprotein receptor-related protein-1 siRNA reduced the effect of human recombinant low-density lipoprotein receptor-related protein-1 on all outcomes measured. Collectively, our findings suggest that low-density lipoprotein receptor-related protein-1 contributed to heme clearance and blood–brain barrier protection after intracerebral hemorrhage. The use of low-density lipoprotein receptor-related protein-1 as supplement provides a novel approach to ameliorating intracerebral hemorrhage brain injury via its pleiotropic neuroprotective effects.

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