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Статті в журналах з теми "Cerebral ischemia, neuroscience, demyelination"

Автор: Grafiati

Опубліковано: 10 березня 2023

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1

Bernstein, Hans-Gert, Gerburg Keilhoff, Henrik Dobrowolny, Paul C. Guest, and Johann Steiner. "Perineuronal oligodendrocytes in health and disease: the journey so far." Reviews in the Neurosciences 31, no. 1 (December 18, 2019): 89–99. http://dx.doi.org/10.1515/revneuro-2019-0020.

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Abstract Perineuronal oligodendrocytes (pn-Ols) are located in the cerebral gray matter in close proximity to neuronal perikarya and less frequently near dendrites and neurites. Although their morphology is indistinguishable from that of other oligodendrocytes, it is not known if pn-Ols have a similar or different cell signature from that of typical myelinating oligodendroglial cells. In this review, we discussed the potential roles of these cells in myelination under normal and pathophysiologic conditions as functional and nutritional supporters of neurons, as restrainers of neuronal firing, and as possible players in glutamate-glutamine homeostasis. We also highlighted the occurrences in which perineuronal oligodendroglia are altered, such as in experimental demyelination, multiple sclerosis, cerebral ischemia, epilepsy, Alzheimer’s disease, schizophrenia, major depression, and bipolar disorder.

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2

Coppi, Elisabetta, Ilaria Dettori, Federica Cherchi, Irene Bulli, Martina Venturini, Daniele Lana, Maria Grazia Giovannini, Felicita Pedata, and Anna Maria Pugliese. "A2B Adenosine Receptors: When Outsiders May Become an Attractive Target to Treat Brain Ischemia or Demyelination." International Journal of Molecular Sciences 21, no. 24 (December 18, 2020): 9697. http://dx.doi.org/10.3390/ijms21249697.

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Adenosine is a signaling molecule, which, by activating its receptors, acts as an important player after cerebral ischemia. Here, we review data in the literature describing A2BR-mediated effects in models of cerebral ischemia obtained in vivo by the occlusion of the middle cerebral artery (MCAo) or in vitro by oxygen-glucose deprivation (OGD) in hippocampal slices. Adenosine plays an apparently contradictory role in this receptor subtype depending on whether it is activated on neuro-glial cells or peripheral blood vessels and/or inflammatory cells after ischemia. Indeed, A2BRs participate in the early glutamate-mediated excitotoxicity responsible for neuronal and synaptic loss in the CA1 hippocampus. On the contrary, later after ischemia, the same receptors have a protective role in tissue damage and functional impairments, reducing inflammatory cell infiltration and neuroinflammation by central and/or peripheral mechanisms. Of note, demyelination following brain ischemia, or autoimmune neuroinflammatory reactions, are also profoundly affected by A2BRs since they are expressed by oligodendroglia where their activation inhibits cell maturation and expression of myelin-related proteins. In conclusion, data in the literature indicate the A2BRs as putative therapeutic targets for the still unmet treatment of stroke or demyelinating diseases.

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3

Lin, HungWen, ReggieH C. Lee, MichelleH H. Lee, CelesteY C. Wu, Alexandre Couto e Silva, HarleeE Possoit, Tsung-Han Hsieh, and Alireza Minagar. "Cerebral ischemia and neuroregeneration." Neural Regeneration Research 13, no. 3 (2018): 373. http://dx.doi.org/10.4103/1673-5374.228711.

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4

Zhou, Yu‐Xi, Xin Wang, Dan Tang, Yan Li, Ying‐Fu Jiao, Yu Gan, Xiao‐Ming Hu, et al. "IL‐2mAb reduces demyelination after focal cerebral ischemia by suppressing CD8 + T cells." CNS Neuroscience & Therapeutics 25, no. 4 (November 15, 2018): 532–43. http://dx.doi.org/10.1111/cns.13084.

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5

Hayashi, Takeshi, Kentaro Deguchi, Shoko Nagotani, Hanzhe Zhang, Yoshihide Sehara, Atsushi Tsuchiya, and Koji Abe. "Cerebral Ischemia and Angiogenesis." Current Neurovascular Research 3, no. 2 (May 1, 2006): 119–29. http://dx.doi.org/10.2174/156720206776875902.

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6

Borlongan, Cesario V., Yasuo Tajima, John Q. Trojanowski, Virginia M. Y. Lee, and Paul R. Sanberg. "Cerebral ischemia and CNS transplantation." NeuroReport 9, no. 16 (November 1998): 3703–9. http://dx.doi.org/10.1097/00001756-199811160-00025.

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7

Krnjević, Krešimir. "Electrophysiology of cerebral ischemia." Neuropharmacology 55, no. 3 (September 2008): 319–33. http://dx.doi.org/10.1016/j.neuropharm.2008.01.002.

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8

Haun, Steven E. "Pharmacology of cerebral ischemia." Molecular and Chemical Neuropathology 16, no. 1-2 (February 1992): 203. http://dx.doi.org/10.1007/bf03159970.

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9

Hua, Y., G. Xi, G. M. de Courten-Myers, K. R. Wagner, and R. E. Myers. "FOCAL CEREBRAL ISCHEMIA." Journal of Neuropathology and Experimental Neurology 55, no. 5 (May 1996): 663. http://dx.doi.org/10.1097/00005072-199605000-00240.

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10

Zhao, Hanshu, Rachel Nepomuceno, Xin Gao, Lesley M. Foley, Shaoxia Wang, Gulnaz Begum, Wen Zhu, et al. "Deletion of the WNK3-SPAK kinase complex in mice improves radiographic and clinical outcomes in malignant cerebral edema after ischemic stroke." Journal of Cerebral Blood Flow & Metabolism 37, no. 2 (July 20, 2016): 550–63. http://dx.doi.org/10.1177/0271678x16631561.

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Анотація:

The WNK-SPAK kinase signaling pathway controls renal NaCl reabsorption and systemic blood pressure by regulating ion transporters and channels. A WNK3-SPAK complex is highly expressed in brain, but its function in this organ remains unclear. Here, we investigated the role of this kinase complex in brain edema and white matter injury after ischemic stroke. Wild-type, WNK3 knockout, and SPAK heterozygous or knockout mice underwent transient middle cerebral artery occlusion. One cohort of mice underwent magnetic resonance imaging. Ex-vivo brains three days post-ischemia were imaged by slice-selective spin-echo diffusion tensor imaging magnetic resonance imaging, after which the same brain tissues were subjected to immunofluorescence staining. A second cohort of mice underwent neurological deficit analysis up to 14 days post-transient middle cerebral artery occlusion. Relative to wild-type mice, WNK3 knockout, SPAK heterozygous, and SPAK knockout mice each exhibited a >50% reduction in infarct size and associated cerebral edema, significantly less demyelination, and improved neurological outcomes. We conclude that WNK3-SPAK signaling regulates brain swelling, gray matter injury, and demyelination after ischemic stroke, and that WNK3-SPAK inhibition has therapeutic potential for treating malignant cerebral edema in the setting of middle cerebral artery stroke.

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11

Adachi, Naoto. "Cerebral ischemia and brain histamine." Brain Research Reviews 50, no. 2 (December 2005): 275–86. http://dx.doi.org/10.1016/j.brainresrev.2005.08.002.

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12

Karma, A., T. A. Pirttila, M. K. Viljanen, Y. E. Lahde, and C. M. Raitta. "Secondary retinitis pigmentosa and cerebral demyelination in Lyme borreliosis." British Journal of Ophthalmology 77, no. 2 (February 1, 1993): 120–22. http://dx.doi.org/10.1136/bjo.77.2.120.

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13

Lim, Kai-Ying, Jia-Hui Chua, Jun-Rong Tan, Priyadharshni Swaminathan, Sugunavathi Sepramaniam, Arunmozhiarasi Armugam, Peter Tsun-Hon Wong, and Kandiah Jeyaseelan. "MicroRNAs in Cerebral Ischemia." Translational Stroke Research 1, no. 4 (July 31, 2010): 287–303. http://dx.doi.org/10.1007/s12975-010-0035-3.

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14

Hu, B. R., M. E. Martone, Y. Z. Jones, and C. L. Liu. "Protein Aggregation after Transient Cerebral Ischemia." Journal of Neuroscience 20, no. 9 (May 1, 2000): 3191–99. http://dx.doi.org/10.1523/jneurosci.20-09-03191.2000.

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15

Pelligrino, Dale A., Roberto Santizo, Verna L. Baughman, and Qiong Wang. "Cerebral vasodilating capacity during forebrain ischemia." NeuroReport 9, no. 14 (October 1998): 3285–91. http://dx.doi.org/10.1097/00001756-199810050-00026.

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16

WEI, D. "Triptolide for cerebral ischemia/reperfusion injury." Neural Regeneration Research 2, no. 3 (March 2007): 156–61. http://dx.doi.org/10.1016/s1673-5374(07)60035-8.

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17

Starosel’tseva, N. G. "Neurophysiological studies of chronic cerebral Ischemia." Neuroscience and Behavioral Physiology 39, no. 6 (June 11, 2009): 605–11. http://dx.doi.org/10.1007/s11055-009-9165-z.

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18

Chen, Tao, Yuanyuan Zhu, Jia Jia, Han Meng, Chao Xu, Panpan Xian, Zijie Li, Zhengang Tang, Yin Wu, and Yan Liu. "Mitochondrial Transplantation Promotes Remyelination and Long-Term Locomotion Recovery following Cerebral Ischemia." Mediators of Inflammation 2022 (September 15, 2022): 1–8. http://dx.doi.org/10.1155/2022/1346343.

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Анотація:

Cerebral ischemia usually leads to axonal degeneration and demyelination in the adjacent white matter. Promoting remyelination still remains a challenging issue in the field. Considering that ischemia deprives energy supply to neural cells and high metabolic activities are required by oligodendrocyte progenitor cells (OPCs) for myelin formation, we assessed the effects of transplanting exogenous healthy mitochondria on the degenerating process of oligodendrocytes following focal cerebral ischemia in the present study. Our results showed that exogenous mitochondria could efficiently restore the overall mitochondrial function and be effectively internalized by OPCs in the ischemic cortex. In comparison with control cortex, there were significantly less apoptotic and more proliferative OPCs in mitochondria-treated cortex. More importantly, higher levels of myelin basic protein (MBP) and more morphologically normal myelin-wrapped axons were observed in mitochondria-treated cortex at 21 days postinjury, as revealed by light and electron microscope. Behavior assay showed better locomotion recovery in mitochondria-treated mice. Further analysis showed that olig2 and lipid synthesis signaling were significantly increased in mitochondria-treated cortex. In together, our data illustrated an antidegenerating and myelination-promoting effect of exogenous mitochondria, indicating mitochondria transplantation as a potentially valuable treatment for ischemic stroke.

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19

Frenguelli, Bruno G. "Special issue on cerebral ischemia." Neuropharmacology 55, no. 3 (September 2008): 249. http://dx.doi.org/10.1016/j.neuropharm.2008.06.031.

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20

Bai, Hui-Yu, and Ai-Ping Li. "P2X7 receptors in cerebral ischemia." Neuroscience Bulletin 29, no. 3 (May 3, 2013): 390–98. http://dx.doi.org/10.1007/s12264-013-1338-7.

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21

Beck, Heike, and Karl H. Plate. "Angiogenesis after cerebral ischemia." Acta Neuropathologica 117, no. 5 (January 14, 2009): 481–96. http://dx.doi.org/10.1007/s00401-009-0483-6.

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22

Ahad, Mohamad Anuar, Kesevan Rajah Kumaran, Tiang Ning, Nur Izzati Mansor, Mohamad Azmeer Effendy, Thenmoly Damodaran, Kamilla Lingam, et al. "Insights into the neuropathology of cerebral ischemia and its mechanisms." Reviews in the Neurosciences 31, no. 5 (July 28, 2020): 521–38. http://dx.doi.org/10.1515/revneuro-2019-0099.

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Анотація:

AbstractCerebral ischemia is a result of insufficient blood flow to the brain. It leads to limited supply of oxygen and other nutrients to meet metabolic demands. These phenomena lead to brain damage. There are two types of cerebral ischemia: focal and global ischemia. This condition has significant impact on patient’s health and health care system requirements. Animal models such as transient occlusion of the middle cerebral artery and permanent occlusion of extracranial vessels have been established to mimic the conditions of the respective type of cerebral ischemia and to further understand pathophysiological mechanisms of these ischemic conditions. It is important to understand the pathophysiology of cerebral ischemia in order to identify therapeutic strategies for prevention and treatment. Here, we review the neuropathologies that are caused by cerebral ischemia and discuss the mechanisms that occur in cerebral ischemia such as reduction of cerebral blood flow, hippocampal damage, white matter lesions, neuronal cell death, cholinergic dysfunction, excitotoxicity, calcium overload, cytotoxic oedema, a decline in adenosine triphosphate (ATP), malfunctioning of Na+/K+-ATPase, and the blood-brain barrier breakdown. Altogether, the information provided can be used to guide therapeutic strategies for cerebral ischemia.

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23

Liebeskind, David S. "Collateral therapeutics for cerebral ischemia." Expert Review of Neurotherapeutics 4, no. 2 (March 2004): 255–65. http://dx.doi.org/10.1586/14737175.4.2.255.

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24

Croll, Susan D., and Stanley J. Wiegand. "Vascular Growth Factors in Cerebral Ischemia." Molecular Neurobiology 23, no. 2-3 (2001): 121–36. http://dx.doi.org/10.1385/mn:23:2-3:121.

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25

Savitz, Sean I., and Daniel M. Rosenbaum. "Review : Gene Expression after Cerebral Ischemia." Neuroscientist 5, no. 4 (July 1999): 238–53. http://dx.doi.org/10.1177/107385849900500413.

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26

Suzuki, M. "Ebselen in the acute cerebral ischemia." Neuroscience Research 38 (2000): S10. http://dx.doi.org/10.1016/s0168-0102(00)80907-4.

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27

Bussone, G., L. La Mantia, A. Boiardi, F. Frediani, E. A. Parati, and E. Lamperti. "Naloxone in cerebral ischemia: preliminary data." Italian Journal of Neurological Sciences 6, no. 1 (March 1985): 89–92. http://dx.doi.org/10.1007/bf02229224.

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28

Mueller, Rashmi N., Donald J. Deyo, David R. Brantley, John F. Disterhoft, and Mark H. Zornow. "Lubeluzole and conditioned learning after cerebral ischemia." Experimental Brain Research 152, no. 3 (October 1, 2003): 329–34. http://dx.doi.org/10.1007/s00221-003-1539-9.

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29

Li, Shasha, Jingjing Fan, Yi Li, Xinyu Fu, Lijuan Li, and Xiaoting Hao. "Nonhuman primate models of focal cerebral ischemia." Neural Regeneration Research 12, no. 2 (2017): 321. http://dx.doi.org/10.4103/1673-5374.200815.

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30

Paschen, W., R. Schmidt-Kastner, B. Djuricic, C. Meese, F. Linn, and K. A. Hossmann. "Polyamine Changes in Reversible Cerebral Ischemia." Journal of Neurochemistry 49, no. 1 (July 1987): 35–37. http://dx.doi.org/10.1111/j.1471-4159.1987.tb03390.x.

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31

Anan’ina, Tatiana, Alena Kisel, Marina Kudabaeva, Galina Chernysheva, Vera Smolyakova, Konstantin Usov, Elena Krutenkova, Mark Plotnikov, and Marina Khodanovich. "Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat." International Journal of Molecular Sciences 21, no. 17 (August 28, 2020): 6246. http://dx.doi.org/10.3390/ijms21176246.

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Анотація:

(1) Background: Although myelin disruption is an integral part of ischemic brain injury, it is rarely the subject of research, particularly in animal models. This study assessed for the first time, myelin and oligodendrocyte loss in a three-vessel model of global cerebral ischemia (GCI), which causes hippocampal damage. In addition, we investigated the relationships between demyelination and changes in microglia and astrocytes, as well as oligodendrogenesis in the hippocampus; (2) Methods: Adult male Wistar rats (n = 15) underwent complete interruption of cerebral blood flow for 7 min by ligation of the major arteries supplying the brain or sham-operation. At 10 and 30 days after the surgery, brain slices were stained for neurodegeneration with Fluoro-Jade C and immunohistochemically to assess myelin content (MBP+ percentage of total area), oligodendrocyte (CNP+ cells) and neuronal (NeuN+ cells) loss, neuroinflammation (Iba1+ cells), astrogliosis (GFAP+ cells) and oligodendrogenesis (NG2+ cells); (3) Results: 10 days after GCI significant myelin and oligodendrocyte loss was found only in the stratum oriens and stratum pyramidale. By the 30th day, demyelination in these hippocampal layers intensified and affected the substratum radiatum. In addition to myelin damage, activation and an increase in the number of microglia and astrocytes in the corresponding layers, a loss of the CA1 pyramidal neurons, and neurodegeneration in the neocortex and thalamus was observed. At a 10-day time point, we observed rod-shaped microglia in the substratum radiatum. Parallel with ongoing myelin loss on the 30th day after ischemia, we found significant oligodendrogenesis in demyelinated hippocampal layers; (4) Conclusions: Our study showed that GCI-simulating cardiac arrest in humans—causes not only the loss of pyramidal neurons in the CA1 field, but also the myelin loss of adjacent layers of the hippocampus.

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32

Liang, Shengxiang, Jiayong Zhang, Qingqing Zhang, Le Li, Yuhao Zhang, Tingting Jin, Bingxue Zhang, et al. "Longitudinal tracing of white matter integrity on diffusion tensor imaging in the chronic cerebral ischemia and acute cerebral ischemia." Brain Research Bulletin 154 (January 2020): 135–41. http://dx.doi.org/10.1016/j.brainresbull.2019.10.015.

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33

ATAİZİ, Zeki Serdar. "Cerebral ischemia models in rats." Journal of Cellular Neuroscience and Oxidative Stress 10, no. 3 (August 18, 2018): 787. http://dx.doi.org/10.37212/jcnos.610115.

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34

Wong, Ma-Li, Sara A. Loddick, Peter B. Bongiorno, Philip W. Gold, Nancy J. Rothwell, and Julio Licinio. "Focal cerebral ischemia induces CRH mRNA in rat cerebral cortex and amygdala." NeuroReport 6, no. 13 (September 1995): 1785–88. http://dx.doi.org/10.1097/00001756-199509000-00019.

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35

Xin, Qing, Bingyuan Ji, Baohua Cheng, Chunmei Wang, Haiqing Liu, Xiaoyu Chen, Jing Chen, and Bo Bai. "Endoplasmic reticulum stress in cerebral ischemia." Neurochemistry International 68 (March 2014): 18–27. http://dx.doi.org/10.1016/j.neuint.2014.02.001.

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36

Nagafuji, Toshiaki, Masakazu Sugiyama, Toru Matsui, Atsushi Muto, and Shigetaka Naito. "Nitric oxide synthase in cerebral ischemia." Molecular and Chemical Neuropathology 26, no. 2 (October 1995): 107–57. http://dx.doi.org/10.1007/bf02815009.

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37

Gao, Qiang, Ling-Yi Liao, BensonWui-Man Lau, and DalindaIsabel Sánchez-Vidaña. "Exogenous neural stem cell transplantation for cerebral ischemia." Neural Regeneration Research 14, no. 7 (2019): 1129. http://dx.doi.org/10.4103/1673-5374.251188.

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38

Engelhorn, Tobias, Sabine Heiland, Wolf-Ruediger Schabitz, Stefan Schwab, Elmar Busch, Michael Forsting, and Arnd Doerfler. "Decompressive craniectomy in acute cerebral ischemia in rats." Neuroscience Letters 370, no. 2-3 (November 2004): 85–90. http://dx.doi.org/10.1016/j.neulet.2004.07.092.

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39

Liu, C. L., P. Ge, F. Zhang, and B. R. Hu. "Co-translational protein aggregation after transient cerebral ischemia." Neuroscience 134, no. 4 (January 2005): 1273–84. http://dx.doi.org/10.1016/j.neuroscience.2005.05.015.

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40

Sugawara, Taku, Hiroyuki Kinouchi, Masaya Oda, Hidehiko Shoji, Tomoya Omae, and Kazuo Mizoi. "Candesartan reduces superoxide production after global cerebral ischemia." NeuroReport 16, no. 4 (March 2005): 325–28. http://dx.doi.org/10.1097/00001756-200503150-00004.

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41

McIver, S. R., M. Muccigrosso, E. R. Gonzales, J. M. Lee, M. S. Roberts, M. S. Sands, and M. P. Goldberg. "Oligodendrocyte degeneration and recovery after focal cerebral ischemia." Neuroscience 169, no. 3 (September 2010): 1364–75. http://dx.doi.org/10.1016/j.neuroscience.2010.04.070.

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42

Siegel, C. S., and L. D. McCullough. "NAD+ and Nicotinamide: Sex Differences in Cerebral Ischemia." Neuroscience 237 (May 2013): 223–31. http://dx.doi.org/10.1016/j.neuroscience.2013.01.068.

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43

Yu, Juan, Li-nan Yang, Yan-yun Wu, Bao-hua Li, Sheng-mei Weng, Chun-lan Hu, and Yong-ling Han. "13-Methyltetradecanoic acid mitigates cerebral ischemia/reperfusion injury." Neural Regeneration Research 11, no. 9 (2016): 1431. http://dx.doi.org/10.4103/1673-5374.191216.

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44

Lee, Younghyurk, Minji Choi, Sang Ryong Kim, and Seok-Geun Lee. "AEG-1 regulates brain damage in cerebral ischemia." IBRO Reports 6 (September 2019): S253. http://dx.doi.org/10.1016/j.ibror.2019.07.788.

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45

Karhunen, Heli, Jukka Jolkkonen, Juhani Sivenius, and Asla Pitkänen. "Epileptogenesis after Experimental Focal Cerebral Ischemia." Neurochemical Research 30, no. 12 (December 2005): 1529–42. http://dx.doi.org/10.1007/s11064-005-8831-y.

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46

Nozaki, Kazuhiko, Masaki Nishimura, and Nobuo Hashimoto. "Mitogen-Activated Protein Kinases and Cerebral Ischemia." Molecular Neurobiology 23, no. 1 (2001): 01–20. http://dx.doi.org/10.1385/mn:23:1:01.

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47

Kokaia, Zaal, and Olle Lindvall. "43 Regulation of neurotrophins in cerebral ischemia." International Journal of Developmental Neuroscience 14 (July 1996): 61. http://dx.doi.org/10.1016/0736-5748(96)80238-3.

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48

Ma, Yihui, Yan Qu, and Zhou Fei. "Vascular endothelial growth factor in cerebral ischemia." Journal of Neuroscience Research 89, no. 7 (April 5, 2011): 969–78. http://dx.doi.org/10.1002/jnr.22628.

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49

Gutierrez, J. A., K.-F. Liu, J. H. Garcia, M. Fisher, and Y. Hasegawa. "HYPOGLYCEMIA AND GLOBAL CEREBRAL ISCHEMIA." Journal of Neuropathology and Experimental Neurology 54, no. 3 (May 1995): 461. http://dx.doi.org/10.1097/00005072-199505000-00216.

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Steinberg, Gary K., Eng H. Lo, David M. Kunis, Gerald A. Grant, Alex Poljak, and Robert DeLaPaz. "Dextromethorphan alters cerebral blood flow and protects against cerebral injury following focal ischemia." Neuroscience Letters 133, no. 2 (December 1991): 225–28. http://dx.doi.org/10.1016/0304-3940(91)90575-e.

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