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Articoli di riviste sul tema "Blood-brain barrier Pathophysiology"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 7 febbraio 2022

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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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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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Abstract (sommario):

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

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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 arteriog

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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 ar

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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 bloo

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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 t

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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

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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 transp

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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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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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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

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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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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

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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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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.

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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 subsequ

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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

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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

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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, transcellul

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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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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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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 experi

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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

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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

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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 caus

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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

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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 BB

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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 cyt

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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-th

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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), he

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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 sur

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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 tis

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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-Dawle

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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 o

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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 pa

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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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Abstract (sommario):

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 n

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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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Abstract (sommario):

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

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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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Abstract (sommario):

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

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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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Abstract (sommario):

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 barrie

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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 prote

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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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Abstract (sommario):

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 (bra

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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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Abstract (sommario):

: 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 inflam

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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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Abstract (sommario):

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,

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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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Abstract (sommario):

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 an

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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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Abstract (sommario):

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

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