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Journal articles on the topic 'NEUROPROTECTANTS'

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Author: Grafiati
Published: 11 September 2023

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1

Palmer, Katharine J., and Joanne Dalton. "Neuroprotectants in Stroke." Drugs in R & D 1, no. 1 (January 1999): 9–13. http://dx.doi.org/10.2165/00126839-199901010-00002.

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2

Schreihofer, D. A. "Phytoestrogens as neuroprotectants." Drugs of Today 45, no. 8 (2009): 609. http://dx.doi.org/10.1358/dot.2009.45.8.1395520.

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3

Shi, Ligen, Marcelo Rocha, Rehana K. Leak, Jingyan Zhao, Tarun N. Bhatia, Hongfeng Mu, Zhishuo Wei, et al. "A new era for stroke therapy: Integrating neurovascular protection with optimal reperfusion." Journal of Cerebral Blood Flow & Metabolism 38, no. 12 (September 7, 2018): 2073–91. http://dx.doi.org/10.1177/0271678x18798162.

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Recent advances in stroke reperfusion therapies have led to remarkable improvement in clinical outcomes, but many patients remain severely disabled, due in part to the lack of effective neuroprotective strategies. In this review, we show that 95% of published preclinical studies on “neuroprotectants” (1990–2018) reported positive outcomes in animal models of ischemic stroke, while none translated to successful Phase III trials. There are many complex reasons for this failure in translational research, including that the majority of clinical trials did not test early delivery of neuroprotectants in combination with successful reperfusion. In contrast to the clinical trials, >80% of recent preclinical studies examined the neuroprotectant in animal models of transient ischemia with complete reperfusion. Furthermore, only a small fraction of preclinical studies included long-term functional assessments, aged animals of both genders, and models with stroke comorbidities. Recent clinical trials demonstrate that 70%–80% of patients treated with endovascular thrombectomy achieve successful reperfusion. These successes revive the opportunity to retest previously failed approaches, including cocktail drugs that target multiple injury phases and different cell types. It is our hope that neurovascular protectants can be retested in future stroke research studies with specific criteria outlined in this review to increase translational successes.
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4

Sharkey, John, Paul A. Jones, Jennifer F. McCarter, and John S. Kelly. "Calcineurin Inhibitors as Neuroprotectants." CNS Drugs 13, no. 1 (January 2000): 1–13. http://dx.doi.org/10.2165/00023210-200013010-00001.

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5

Jeyaseelan, K., KY Lim, and A. Armugam. "Neuroprotectants in stroke therapy." Expert Opinion on Pharmacotherapy 9, no. 6 (April 2008): 887–900. http://dx.doi.org/10.1517/14656566.9.6.887.

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6

Štolc, Svorad. "Indole derivatives as neuroprotectants." Life Sciences 65, no. 18-19 (October 1999): 1943–50. http://dx.doi.org/10.1016/s0024-3205(99)00453-1.

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7

Kelly, J. S., and J. Sharkey. "Immunosuppressants-ligands as neuroprotectants." Transplantation Proceedings 33, no. 3 (May 2001): 2217–19. http://dx.doi.org/10.1016/s0041-1345(01)01945-5.

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8

Muir, K. W., and Ph A. Teal. "Why have neuroprotectants failed?" Journal of Neurology 252, no. 9 (August 25, 2005): 1011–20. http://dx.doi.org/10.1007/s00415-005-0933-6.

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9

&NA;. "Neuroprotectants for Parkinson's disease reviewed." Inpharma Weekly &NA;, no. 1389 (May 2003): 4. http://dx.doi.org/10.2165/00128413-200313890-00007.

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10

KLEIN, MICHAEL, SILVIA CALDERON, and BELINDA HAYES. "Abuse Liability Assessment of Neuroprotectants." Annals of the New York Academy of Sciences 890, no. 1 NEUROPROTECTI (December 1999): 515–25. http://dx.doi.org/10.1111/j.1749-6632.1999.tb08033.x.

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11

Elmer, Jonathan, and Jon C. Rittenberger. "Inhalational neuroprotectants: A noble cause." Resuscitation 107 (October 2016): A7—A8. http://dx.doi.org/10.1016/j.resuscitation.2016.08.003.

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12

Tizabi, Yousef. "Duality of Antidepressants and Neuroprotectants." Neurotoxicity Research 30, no. 1 (November 27, 2015): 1–13. http://dx.doi.org/10.1007/s12640-015-9577-1.

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13

Ahn, Young Hwan, Mia Emgård, and Patrik Brundin. "Ultrastructural Characterization of Dissociated Embryonic Ventral Mesencephalic Tissue Treated with Neuroprotectants." Cell Transplantation 12, no. 3 (April 2003): 235–41. http://dx.doi.org/10.3727/000000003108746795.

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Poor survival and differentiation of grafted dopamine neurons limits the application of clinical transplantation in Parkinson's disease. The survival of grafted dopamine neurons is only improved by a factor of 2–3 by adding neuroprotectants during tissue preparation. We used dye exclusion cell viability and electron microscopy to investigate the effects of the caspase inhibitor ac-YVAD-cmk and the lazaroid tirilazad mesylate on ultrastructural changes in dissociated embryonic mesencephalic cells. In addition, we examined whether the neuroprotectants selectively counteracted specific signs of neurodegeneration. Cell viability decreased significantly over time in both control and treated cell suspensions, but the number of viable cells remaining was significantly higher in tirilazad mesylate-treated cell suspensions. In control samples, the proportion of cells with an ultrastructure consistent with healthy cells decreased from 70%, immediately after dissociation, to 30% after 8 h of incubation. Similar changes were also observed in cell suspensions treated with neuroprotectants. Thus, the neuroprotectants examined did not block the development of specific morphological signs of neurodegeneration. However, when also taking into account that dead cells lysed and disappeared from each cell suspension with time, we found that the total number of remaining viable cells with healthy nuclear chromatin or intact membrane integrity was significantly higher in the tirilazad mesylate-treated group. The results indicate that tirilazad mesylate protects only a small subpopulation of embryonic mesencephalic cells from degeneration induced by mechanical trauma during tissue dissection and dissociation.
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14

FLOYD, ROBERT A., KENNETH HENSLEY, MICHAEL J. FORSTER, JUDITH A. KELLEHER-ANDERSON, and PAUL L. WOOD. "Nitrones as Neuroprotectants and Antiaging Drugs." Annals of the New York Academy of Sciences 959, no. 1 (April 2002): 321–29. http://dx.doi.org/10.1111/j.1749-6632.2002.tb02103.x.

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15

Dawson, V. L. "Potent neuroprotectants linked to bifunctional inhibition." Proceedings of the National Academy of Sciences 96, no. 19 (September 14, 1999): 10557–58. http://dx.doi.org/10.1073/pnas.96.19.10557.

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16

Kandela, Peter. "Apply neuroprotectants rapidly for best results." Lancet 350, no. 9082 (September 1997): 936. http://dx.doi.org/10.1016/s0140-6736(05)63276-x.

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17

Bhardwaj, Anish. "Statins as neuroprotectants after subarachnoid hemorrhage*." Critical Care Medicine 40, no. 2 (February 2012): 695–97. http://dx.doi.org/10.1097/ccm.0b013e318236e307.

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18

Alonso de Leciñana, María, and Jose Antonio Egido. "Estrogens as Neuroprotectants against Ischemic Stroke." Cerebrovascular Diseases 21, no. 2 (2006): 48–53. http://dx.doi.org/10.1159/000091703.

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19

Lobine, D., M.-J. R. Howes, I. Cummins, J. Govinden-Soulange, M. Ranghoo-Sanmukhiya, K. Lindsey, and P. L. Chazot. "Bio-prospecting endemic MascareneAloesfor potential neuroprotectants." Phytotherapy Research 31, no. 12 (October 11, 2017): 1926–34. http://dx.doi.org/10.1002/ptr.5941.

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20

Babadjouni, Robin Moshe, Ryan E. Radwanski, Brian P. Walcott, Arati Patel, Ramon Durazo, Drew M. Hodis, Benjamin A. Emanuel, and William J. Mack. "Neuroprotective strategies following intraparenchymal hemorrhage." Journal of NeuroInterventional Surgery 9, no. 12 (July 14, 2017): 1202–7. http://dx.doi.org/10.1136/neurintsurg-2017-013197.

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Intracerebral hemorrhage and, more specifically, intraparenchymal hemorrhage, are devastating disease processes with poor clinical outcomes. Primary injury to the brain results from initial hematoma expansion while secondary hemorrhagic injury occurs from blood-derived products such as hemoglobin, heme, iron, and coagulation factors that overwhelm the brains natural defenses. Novel neuroprotective treatments have emerged that target primary and secondary mechanisms of injury. Nonetheless, translational application of neuroprotectants from preclinical to clinical studies has yet to show beneficial clinical outcomes. This review summarizes therapeutic agents and neuroprotectants in ongoing clinical trials aimed at targeting primary and secondary mechanisms of injury after intraparenchymal hemorrhage.
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21

Redivo, Luca, Rozalia-Maria Anastasiadi, Marco Pividori, Federico Berti, Maria Peressi, Devis Di Tommaso, and Marina Resmini. "Prediction of self-assembly of adenosine analogues in solution: a computational approach validated by isothermal titration calorimetry." Physical Chemistry Chemical Physics 21, no. 8 (2019): 4258–67. http://dx.doi.org/10.1039/c8cp05647a.

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22

Chamorro, Ángel. "Neuroprotectants in the Era of Reperfusion Therapy." Journal of Stroke 20, no. 2 (May 31, 2018): 197–207. http://dx.doi.org/10.5853/jos.2017.02901.

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23

Thauerer, Bettina, Stephanie zur Nedden, and Gabriele Baier‐Bitterlich. "Purine nucleosides: endogenous neuroprotectants in hypoxic brain." Journal of Neurochemistry 121, no. 3 (March 14, 2012): 329–42. http://dx.doi.org/10.1111/j.1471-4159.2012.07692.x.

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24

Penkowa, Milena. "Metallothioneins are multipurpose neuroprotectants during brain pathology." FEBS Journal 273, no. 9 (April 5, 2006): 1857–70. http://dx.doi.org/10.1111/j.1742-4658.2006.05207.x.

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25

Lyden, Patrick, and Nils Gunnar Wahlgren. "Mechanisms of action of neuroprotectants in stroke." Journal of Stroke and Cerebrovascular Diseases 9, no. 6 (November 2000): 9–14. http://dx.doi.org/10.1053/jscd.2000.19316.

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26

Bankhead, Charles. "Neuroprotectants not up to scratch in stroke." Inpharma Weekly &NA;, no. 1228 (March 2000): 3–4. http://dx.doi.org/10.2165/00128413-200012280-00003.

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27

&NA;. "'Doom and gloom' for neuroprotectants in stroke?" Inpharma Weekly &NA;, no. 1241 (June 2000): 3. http://dx.doi.org/10.2165/00128413-200012410-00004.

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28

Callaway, Jennifer. "Acute Stroke Therapy: Combination Drugs and Multifunctional Neuroprotectants." Current Neuropharmacology 2, no. 3 (July 1, 2004): 277–94. http://dx.doi.org/10.2174/1570159043359602.

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29

Wahlgren, Nils Gunnar. "Neuroprotectants in Late Clinical Development – A Status Report." Cerebrovascular Diseases 7, no. 2 (1997): 13–17. http://dx.doi.org/10.1159/000108238.

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30

Parng, Chuenlei, Christopher Ton, Ying-Xin Lin, Nicole Marie Roy, and Patricia McGrath. "A zebrafish assay for identifying neuroprotectants in vivo." Neurotoxicology and Teratology 28, no. 4 (July 2006): 509–16. http://dx.doi.org/10.1016/j.ntt.2006.04.003.

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31

Danino, O., N. Giladi, S. Grossman, and B. Fischer. "Nucleoside 5′-phosphorothioate derivatives are highly effective neuroprotectants." Biochemical Pharmacology 88, no. 3 (April 2014): 384–92. http://dx.doi.org/10.1016/j.bcp.2014.02.001.

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32

Wahlgren, Nils Gunnar, and Patrick Lyden. "Neuroprotectants in the treatment of stroke—An overview." Journal of Stroke and Cerebrovascular Diseases 9, no. 6 (November 2000): 32–35. http://dx.doi.org/10.1053/jscd.2000.19320.

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33

LoPachin, Richard M., Terrence Gavin, Brian C. Geohagen, Lihai Zhang, Diana Casper, Rukmani Lekhraj, and David S. Barber. "β-Dicarbonyl enolates: a new class of neuroprotectants." Journal of Neurochemistry 116, no. 1 (December 2, 2010): 132–43. http://dx.doi.org/10.1111/j.1471-4159.2010.07091.x.

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34

Yuen, P. W., and K. W. Wang. "Calpain inhibitors: Novel neuroprotectants and potential anticataract agents." Drugs of the Future 23, no. 7 (1998): 741. http://dx.doi.org/10.1358/dof.1998.023.07.858362.

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35

Abed, Edoardo, Giovanni Corbo, and Benedetto Falsini. "Neurotrophin Family Members as Neuroprotectants in Retinal Degenerations." BioDrugs 29, no. 1 (November 19, 2014): 1–13. http://dx.doi.org/10.1007/s40259-014-0110-5.

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36

Mitka, Mike. "News About Neuroprotectants for the Treatment of Stroke." JAMA 287, no. 10 (March 13, 2002): 1253. http://dx.doi.org/10.1001/jama.287.10.1253-jmn0313-2-1.

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37

Velpandian, Thirumurthy. "Closed Gateways — Can Neuroprotectants Shield the Retina in Glaucoma?" Drugs in R&D 10, no. 2 (July 2010): 93–96. http://dx.doi.org/10.2165/11539310-000000000-00000.

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38

Carlson, Robert H. "Rough road to development for neuroprotectants in acute stroke." Inpharma Weekly &NA;, no. 1027 (March 1996): 9–10. http://dx.doi.org/10.2165/00128413-199610270-00015.

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39

Yang, Nan, Qi-Wen Guan, Fang-Hui Chen, Qin-Xuan Xia, Xi-Xi Yin, Hong-Hao Zhou, and Xiao-Yuan Mao. "Antioxidants Targeting Mitochondrial Oxidative Stress: Promising Neuroprotectants for Epilepsy." Oxidative Medicine and Cellular Longevity 2020 (November 25, 2020): 1–14. http://dx.doi.org/10.1155/2020/6687185.

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Mitochondria are major sources of reactive oxygen species (ROS) within the cell and are especially vulnerable to oxidative stress. Oxidative damage to mitochondria results in disrupted mitochondrial function and cell death signaling, finally triggering diverse pathologies such as epilepsy, a common neurological disease characterized with aberrant electrical brain activity. Antioxidants are considered as promising neuroprotective strategies for epileptic condition via combating the deleterious effects of excessive ROS production in mitochondria. In this review, we provide a brief discussion of the role of mitochondrial oxidative stress in the pathophysiology of epilepsy and evidences that support neuroprotective roles of antioxidants targeting mitochondrial oxidative stress including mitochondria-targeted antioxidants, polyphenols, vitamins, thiols, and nuclear factor E2-related factor 2 (Nrf2) activators in epilepsy. We point out these antioxidative compounds as effectively protective approaches for improving prognosis. In addition, we specially propose that these antioxidants exert neuroprotection against epileptic impairment possibly by modulating cell death interactions, notably autophagy-apoptosis, and autophagy-ferroptosis crosstalk.
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40

Leker, R. R., and M. Y. Neufeld. "Anti-epileptic drugs as possible neuroprotectants in cerebral ischemia." Brain Research Reviews 42, no. 3 (June 2003): 187–203. http://dx.doi.org/10.1016/s0165-0173(03)00170-x.

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41

Shen, J., K. Ghai, P. Sompol, X. Liu, X. Cao, P. M. Iuvone, and K. Ye. "N-acetyl serotonin derivatives as potent neuroprotectants for retinas." Proceedings of the National Academy of Sciences 109, no. 9 (February 13, 2012): 3540–45. http://dx.doi.org/10.1073/pnas.1119201109.

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42

Fukuta, Tatsuya, Naoto Oku, and Kentaro Kogure. "Application and Utility of Liposomal Neuroprotective Agents and Biomimetic Nanoparticles for the Treatment of Ischemic Stroke." Pharmaceutics 14, no. 2 (February 4, 2022): 361. http://dx.doi.org/10.3390/pharmaceutics14020361.

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Ischemic stroke is still one of the leading causes of high mortality and severe disability worldwide. Therapeutic options for ischemic stroke and subsequent cerebral ischemia/reperfusion injury remain limited due to challenges associated with drug permeability through the blood-brain barrier (BBB). Neuroprotectant delivery with nanoparticles, including liposomes, offers a promising solution to address this problem, as BBB disruption following ischemic stroke allows nanoparticles to pass through the intercellular gaps between endothelial cells. To ameliorate ischemic brain damage, a number of nanotherapeutics encapsulating neuroprotective agents, as well as surface-modified nanoparticles with specific ligands targeting the injured brain regions, have been developed. Combination therapy with nanoparticles encapsulating neuroprotectants and tissue plasminogen activator (t-PA), a globally approved thrombolytic agent, has been demonstrated to extend the narrow therapeutic time window of t-PA. In addition, the design of biomimetic drug delivery systems (DDS) employing circulating cells (e.g., leukocytes, platelets) with unique properties has recently been investigated to overcome the injured BBB, utilizing these cells’ inherent capability to penetrate the ischemic brain. Herein, we review recent findings on the application and utility of nanoparticle DDS, particularly liposomes, and various approaches to developing biomimetic DDS functionalized with cellular membranes/membrane proteins for the treatment of ischemic stroke.
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43

Pattarachotanant, Nattaporn, Anchalee Prasansuklab, and Tewin Tencomnao. "Momordica charantia L. Extract Protects Hippocampal Neuronal Cells against PAHs-Induced Neurotoxicity: Possible Active Constituents Include Stigmasterol and Vitamin E." Nutrients 13, no. 7 (July 10, 2021): 2368. http://dx.doi.org/10.3390/nu13072368.

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Polycyclic aromatic hydrocarbons (PAHs) have been recognized to cause neurobehavioral dysfunctions and disorder of cognition and behavioral patterns in childhood. Momordica charantia L. (MC) has been widely known for its nutraceutical and health-promoting properties. To date, the effect of MC for the prevention and handling of PAHs-induced neurotoxicity has not been reported. In the current study, the neuroprotective effects of MC and its underlying mechanisms were investigated in mouse hippocampal neuronal cell line (HT22); moreover, in silico analysis was performed with the phytochemicals MC to decipher their potential function as neuroprotectants. MC was demonstrated to possess neuroprotective effect by reducing reactive oxygen species’ (ROS’) production and down-regulating cyclin D1, p53, and p38 mitogen-activated protein kinase (MAPK) protein expressions, resulting in the inhibition of cell apoptosis and the normalization of cell cycle progression. Additionally, 28 phytochemicals of MC and their competence on inhibiting cytochrome P450 (CYP: CYP1A1, CYP1A2, and CYP1B1) functions were resolved. In silico analysis of vitamin E and stigmasterol revealed that their binding to either CYP1A1 or CYP1A2 was more efficient than the binding of each positive control (alizarin or purpurin). Together, MC is potentially an interesting neuroprotectant including vitamin E and stigmasterol as probable active components for the prevention for PAHs-induced neurotoxicity.
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44

Kaur, Prameet, Fujia Liu, Jun Tan, Kai Lim, Sugunavathi Sepramaniam, Dwi Karolina, Arunmozhiarasi Armugam, and Kandiah Jeyaseelan. "Non-Coding RNAs as Potential Neuroprotectants against Ischemic Brain Injury." Brain Sciences 3, no. 4 (March 20, 2013): 360–95. http://dx.doi.org/10.3390/brainsci3010360.

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45

A. Sutherland, Brad, Joanne C. Harrison, Shiva M. Nair, and Ivan A. Sammut. "Inhalation Gases or Gaseous Mediators As Neuroprotectants for Cerebral Ischaemia." Current Drug Targets 14, no. 1 (December 1, 2012): 56–73. http://dx.doi.org/10.2174/1389450111314010007.

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46

A. Sutherland, Brad, Joanne C. Harrison, Shiva M. Nair, and Ivan A. Sammut. "Inhalation Gases or Gaseous Mediators As Neuroprotectants for Cerebral Ischaemia." Current Drug Targets 14, no. 1 (January 1, 2013): 56–73. http://dx.doi.org/10.2174/138945013804806433.

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47

FUKUTA, Tatsuya, Tomohiro ASAI, and Naoto OKU. "Usefulness of Liposomal Neuroprotectants for the Treatment of Ischemic Stroke." Oleoscience 17, no. 8 (2017): 359–66. http://dx.doi.org/10.5650/oleoscience.17.359.

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48

Pei, Zhang, Chen Jie-Si, Li Qi-Ye, Sheng Long-Xiang, Gao Yi-Xing, Lu Bing-Zheng, Zhu Wen-Bo, et al. "Neuroprotectants attenuate hypobaric hypoxia-induced brain injuries in cynomolgus monkeys." Zool. Res. 41, no. 1 (2020): 3–19. http://dx.doi.org/10.24272/j.issn.2095-8137.2020.012.

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49

Singh, Meharvan. "Estrogens and progesterone as neuroprotectants: what animal models teach us." Frontiers in Bioscience 13, no. 13 (2008): 1083. http://dx.doi.org/10.2741/2746.

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50

Steiner, Thorsten, and Werner Hacke. "Combination Therapy with Neuroprotectants and Thrombolytics in Acute Ischaemic Stroke." European Neurology 40, no. 1 (1998): 1–8. http://dx.doi.org/10.1159/000007947.

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