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Journal articles on the topic 'Neuroprotective agents'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 August 2024

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1

Sunjoyo, Ageng, and Andy Nugroho. "Neuroprotective Agents: A Simple Overview." Open Access Macedonian Journal of Medical Sciences 10, F (September 2, 2022): 578–82. http://dx.doi.org/10.3889/oamjms.2022.10329.

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Neuroprotective agents are medications that can alter the course of metabolic events and have neuroprotective function. Neuroprotective agents are needed in patients undergoing a surgical procedure and clinical conditions that correspond with the central nervous system (CNS); also, in intensive care, the neuroprotective agents are often used to prevent complications and patient deterioration. Over the years, there is still no clear understanding of the potential for neuroprotection and the interactions between various drugs that serve a crucial role in anesthetic care and critical illness. This literature review will discuss further the mechanism of neuronal damage and various neuroprotective agents.

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2

Richardson, J. Steven. "Neuroprotective Agents." Physical Medicine and Rehabilitation Clinics of North America 10, no. 2 (May 1999): 447–61. http://dx.doi.org/10.1016/s1047-9651(18)30205-5.

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3

Hilton, Genell. "Experimental Neuroprotective Agents." Dimensions Of Critical Care Nursing 14, no. 4 (July 1995): 181–88. http://dx.doi.org/10.1097/00003465-199507000-00004.

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4

Sánchez, A. J., and A. García-Merino. "Neuroprotective agents: Cannabinoids." Clinical Immunology 142, no. 1 (January 2012): 57–67. http://dx.doi.org/10.1016/j.clim.2011.02.010.

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5

Yanık, Tuğra, and Burcu Yanık. "Current neuroprotective agents in stroke." Turkish Journal of Physical Medicine and Rehabilitation 70, no. 2 (May 16, 2024): 157–63. http://dx.doi.org/10.5606/tftrd.2024.15287.

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What is expected from neuroprotection is to inhibit neuronal death and halt or decelerate the neuronal loss to lower the mortality rates, decrease disability, and improve the quality of life following an acute ischemic stroke. Several agents were described as neuroprotective up to date; however, there is still debate which to use in the neurorehabilitation of stroke patients, in terms of both efficacy and also safety. In this review, we discuss the agents, citicoline, cerebrolysin and MLC901 (NeuroAiD II), the three agents which have started to be used frequently in neurorehabilitation clinics recently in the light of the current literature.

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6

Douna, H., B. M. Bavelaar, H. Pellikaan, B. Olivier, and T. Pieters. "Neuroprotection in Parkinson's Disease: A Systematic Review of the Preclinical Data." Open Pharmacology Journal 6, no. 1 (May 9, 2012): 12–26. http://dx.doi.org/10.2174/1874143601206010012.

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Aim: This study aimed to systematically review the preclinical data of neuroprotective agents for Parkinson’s disease (PD) to support the translation of these compounds. Methods: The study consisted of two phases. In phase I, Pubmed and Scopus were systematically searched for neuroprotective agents for PD. In phase II, a systematic search was conducted for each substance identified in phase I. Articles were included if they used MPTP, 6-OHDA, rotenone or paraquat injury models. Results: Phase I led to the identification of 168 putative neuroprotective agents. Eventually ten compounds were included: melatonin, estrogen, nicotine, caffeine, riluzole, curcumin, coenzyme Q10, aspirin, EGCG and resveratrol. Phase II revealed 113 experimental studies and three reviews. Conclusion: This study clearly depicts the preclinical data of ten promising neuroprotective agents. While some of these compounds have already been tested in clinical use, none of them was studied in an appropriately designed trial to determine a neuroprotective effect. In expectation of qualitatively improved neuroprotection trials, the data from this study provide a firm foundation for future research.

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7

Dugan, L. L., D. M. Turetsky, C. Du, D. Lobner, M. Wheeler, C. R. Almli, C. K. F. Shen, T. Y. Luh, D. W. Choi, and T. S. Lin. "Carboxyfullerenes as neuroprotective agents." Proceedings of the National Academy of Sciences 94, no. 17 (August 19, 1997): 9434–39. http://dx.doi.org/10.1073/pnas.94.17.9434.

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8

Cores, Ángel, Noelia Carmona-Zafra, José Clerigué, Mercedes Villacampa, and J. Carlos Menéndez. "Quinones as Neuroprotective Agents." Antioxidants 12, no. 7 (July 20, 2023): 1464. http://dx.doi.org/10.3390/antiox12071464.

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Quinones can in principle be viewed as a double-edged sword in the treatment of neurodegenerative diseases, since they are often cytoprotective but can also be cytotoxic due to covalent and redox modification of biomolecules. Nevertheless, low doses of moderately electrophilic quinones are generally cytoprotective, mainly due to their ability to activate the Keap1/Nrf2 pathway and thus induce the expression of detoxifying enzymes. Some natural quinones have relevant roles in important physiological processes. One of them is coenzyme Q10, which takes part in the oxidative phosphorylation processes involved in cell energy production, as a proton and electron carrier in the mitochondrial respiratory chain, and shows neuroprotective effects relevant to Alzheimer’s and Parkinson’s diseases. Additional neuroprotective quinones that can be regarded as coenzyme Q10 analogues are idobenone, mitoquinone and plastoquinone. Other endogenous quinones with neuroprotective activities include tocopherol-derived quinones, most notably vatiquinone, and vitamin K. A final group of non-endogenous quinones with neuroprotective activity is discussed, comprising embelin, APX-3330, cannabinoid-derived quinones, asterriquinones and other indolylquinones, pyrroloquinolinequinone and its analogues, geldanamycin and its analogues, rifampicin quinone, memoquin and a number of hybrid structures combining quinones with amino acids, cholinesterase inhibitors and non-steroidal anti-inflammatory drugs.

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9

Ali Esmail Al-Snafi. "Medicinal Plants with neuroprotective effects." GSC Biological and Pharmaceutical Sciences 17, no. 1 (October 30, 2021): 213–31. http://dx.doi.org/10.30574/gscbps.2021.17.1.0319.

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Neuroprotection is the preservation of the structure and function of neurons from insults from cellular injuries caused by a variety of agents or neurodegenerative diseases. Medicinal plants possess neuroprotective effects via mechanisms that include inhibiting protein-based deposit accumulation, oxidative stress, and neuroinflammation, and correcting defects of neurotransmitters such as acetylcholine and dopamine [1-3]. The current review will highlight the neuroprotective effects of medicinal plants.

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10

O'Mara, Keliana, and Christopher McPherson. "Neuroprotective Agents for Neonates with Hypoxic-Ischemic Encephalopathy." Neonatal Network 40, no. 6 (November 1, 2021): 406–13. http://dx.doi.org/10.1891/11-t-755.

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Hypoxic-ischemic encephalopathy (HIE) remains a significant source of long-term neurodevelopmental impairment despite overall improvements in survival without disability in neonates who undergo therapeutic hypothermia. Each phase in the evolution of hypoxic-ischemic injury presents potential pharmacologic targets for neuroprotective agents. Melatonin is a promising emerging therapy for early phases of ischemic injury, but utility is currently limited by the lack of pharmaceutical-grade products. Magnesium has been extensively studied for its neuroprotective effects in the preterm population. Studies in neonates with HIE have produced mixed outcomes. Erythropoietin use in HIE with or without therapeutic hypothermia appears to be safe and may provide additional benefit. Dexmedetomidine, N-acetylcysteine, xenon, and topiramate all have promising animal data, but need additional human trials to elucidate what role they may play in HIE. Frequent review of existing literature is required to ensure provision of evidence-based pharmacologic agents for neuroprotection following HIE.

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11

Yang, Fan, Wei-Ping He, Jia-Qi Yao, Dong Zou, Pu Chen, and Jie Li. "Synthesis and Neuroprotective Biological Evaluation of Quinazolinone Derivatives via Scaffold Hopping." Current Organic Synthesis 16, no. 5 (October 17, 2019): 772–75. http://dx.doi.org/10.2174/1570179416666190328233501.

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Objective: To develop efficient method for the synthesis of quinazolinone derivatives bearing different functional groups on ring A and ring B and evaluation as neuroprotective agents. Methods: Synthetic route to quinazolinone derivatives was furnished by condensation/cyclocondensation/ reduction sequence of the activated N-acylbenzotriazoles. The structures of the targets compounds have been deduced upon their spectral data (1HNMR, 13CNMR and Mass spectroscopy). The neuroprotective activities of the synthesized compounds are also evaluated. Results: Preliminary screening on a MPP+ induced SH-SY5Y cell injury model of the synthesized compounds resulted in four compounds (6q, 6r, 6u, and 8e) showed promising neural cell protection activities. The action mechanisms of these compounds on neuroprotection were then analyzed by docking and reverse docking modeling. Conclusion: A series of quinazolinone derivatives, including different substitution types on rings A and B were designed and synthesized via scaffold hopping. With the help of neuroprotective biological evaluation, several efficient therapeutic neuroprotective agents were found for further evaluation as drug candidate against neurodegenerative disorder.

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12

Konaklieva, Monika, Balbina Plotkin, and Terena Herbert. "β-Lactams as Neuroprotective Agents." Anti-Infective Agents in Medicinal Chemistry 8, no. 1 (January 1, 2009): 28–35. http://dx.doi.org/10.2174/187152109787047823.

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13

KAWAGUCHI, Masahiko, and Hitoshi FURUYA. "Neuroprotective Effects of Anesthetic Agents." JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 29, no. 4 (2009): 358–63. http://dx.doi.org/10.2199/jjsca.29.358.

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14

Levi, M., and M. Brimble. "A Review of Neuroprotective Agents." Current Medicinal Chemistry 11, no. 18 (September 1, 2004): 2383–97. http://dx.doi.org/10.2174/0929867043364522.

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15

Cornacchia, C., I. Cacciatore, L. Baldassarre, A. Mollica, F. Feliciani, and F. Pinnen. "2,5-Diketopiperazines as Neuroprotective Agents." Mini-Reviews in Medicinal Chemistry 12, no. 1 (January 1, 2012): 2–12. http://dx.doi.org/10.2174/138955712798868959.

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16

Pandey, Achyut, Parul Singh, Ameeta Kaul, and P. Sharma. "Glaucoma: role of neuroprotective agents." International Journal of Basic & Clinical Pharmacology 3, no. 5 (2014): 755. http://dx.doi.org/10.5455/2319-2003.ijbcp20141016.

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17

Gulyaeva, N., M. Stepanichev, M. Onufriev, N. Lazareva, and H. Fliss. "Zinc ionophores as neuroprotective agents." Journal of Neurochemistry 85 (May 8, 2003): 27. http://dx.doi.org/10.1046/j.1471-4159.85.s2.28.x.

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18

MARCHIONNI, MARK A., JUDITH B. GRINSPAN, PETER D. CANOLL, NAGESH K. MAHANTHAPPA, JAMES L. SALZER, and STEVEN S. SCHERER. "Neuregulins as Potential Neuroprotective Agents." Annals of the New York Academy of Sciences 825, no. 1 Neuroprotecti (October 1997): 348–65. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48446.x.

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19

Choi, Dennis. "Neuroprotective Agents and Cerebral Ischaemia." Trends in Neurosciences 21, no. 8 (August 1998): 363. http://dx.doi.org/10.1016/s0166-2236(98)01257-0.

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20

Kawaguchi, Masahiko, Hitoshi Furuya, and Piyush M. Patel. "Neuroprotective effects of anesthetic agents." Journal of Anesthesia 19, no. 2 (April 25, 2005): 150–56. http://dx.doi.org/10.1007/s00540-005-0305-5.

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21

Legos, Jeffrey J., Dennis Lee, and Joseph A. Erhardt. "Caspase inhibitors as neuroprotective agents." Emerging Drugs 6, no. 1 (April 2001): 81–94. http://dx.doi.org/10.1517/14728214.6.1.81.

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22

Ravishankar, Divyashree, Giulia Corona, Stephanie M. Hogan, Jeremy P. E. Spencer, Francesca Greco, and Helen M. I. Osborn. "Thioflavones as novel neuroprotective agents." Bioorganic & Medicinal Chemistry 24, no. 21 (November 2016): 5513–20. http://dx.doi.org/10.1016/j.bmc.2016.09.006.

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23

Wood, Thomas R., Brianna J. Stubbs, and Sandra E. Juul. "Exogenous Ketone Bodies as Promising Neuroprotective Agents for Developmental Brain Injury." Developmental Neuroscience 40, no. 5-6 (2018): 451–62. http://dx.doi.org/10.1159/000499563.

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Ketone bodies are a promising area of neuroprotection research that may be ideally suited to the injured newborn. During normal development, the human infant is in significant ketosis for at least the first week of life. Ketone uptake and metabolism is upregulated in the both the fetus and neonate, with ketone bodies providing at least 10% of cerebral metabolic energy requirements, as well as being the preferred precursors for the synthesis of fatty acids and cholesterol. At the same time, ketone bodies have been shown to have multiple neuroprotective effects, including being anticonvulsant, decreasing oxidative stress and inflammation, and epigenetically upregulating the production of neurotrophic factors. While ketogenic diets and exogenous ketosis are largely being investigated in the setting of adult brain injury, the adaptation of the neonate to ketosis suggests that developmental brain injury may be the area most suited to the use of ketones for neuroprotection. Here, we describe the mechanisms by which ketone bodies exert their neuroprotective effects, and how these may translate to benefits within each of the phases of neonatal asphyxial brain injury.

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24

Burlacu, Codrin-Constantin, Maria-Adriana Neag, Andrei-Otto Mitre, Alexandru-Constantin Sirbu, Andrei-Vlad Badulescu, and Anca-Dana Buzoianu. "The Role of miRNAs in Dexmedetomidine’s Neuroprotective Effects against Brain Disorders." International Journal of Molecular Sciences 23, no. 10 (May 13, 2022): 5452. http://dx.doi.org/10.3390/ijms23105452.

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There are limited neuroprotective strategies for various central nervous system conditions in which fast and sustained management is essential. Neuroprotection-based therapeutics have become an intensively researched topic in the neuroscience field, with multiple novel promising agents, from natural products to mesenchymal stem cells, homing peptides, and nanoparticles-mediated agents, all aiming to significantly provide neuroprotection in experimental and clinical studies. Dexmedetomidine (DEX), an α2 agonist commonly used as an anesthetic adjuvant for sedation and as an opioid-sparing medication, stands out in this context due to its well-established neuroprotective effects. Emerging evidence from preclinical and clinical studies suggested that DEX could be used to protect against cerebral ischemia, traumatic brain injury (TBI), spinal cord injury, neurodegenerative diseases, and postoperative cognitive disorders. MicroRNAs (miRNAs) regulate gene expression at a post-transcriptional level, inhibiting the translation of mRNA into functional proteins. In vivo and in vitro studies deciphered brain-related miRNAs and dysregulated miRNA profiles after several brain disorders, including TBI, ischemic stroke, Alzheimer’s disease, and multiple sclerosis, providing emerging new perspectives in neuroprotective therapy by modulating these miRNAs. Experimental studies revealed that some of the neuroprotective effects of DEX are mediated by various miRNAs, counteracting multiple mechanisms in several disease models, such as lipopolysaccharides induced neuroinflammation, β-amyloid induced dysfunction, brain ischemic-reperfusion injury, and anesthesia-induced neurotoxicity models. This review aims to outline the neuroprotective mechanisms of DEX in brain disorders by modulating miRNAs. We address the neuroprotective effects of DEX by targeting miRNAs in modulating ischemic brain injury, ameliorating the neurotoxicity of anesthetics, reducing postoperative cognitive dysfunction, and improving the effects of neurodegenerative diseases.

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25

Barreiro, Sandra, Bárbara Silva, Solida Long, Madalena Pinto, Fernando Remião, Emília Sousa, and Renata Silva. "Fiscalin Derivatives as Potential Neuroprotective Agents." Pharmaceutics 14, no. 7 (July 12, 2022): 1456. http://dx.doi.org/10.3390/pharmaceutics14071456.

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Neurodegenerative diseases (ND) share common molecular/cellular mechanisms that contribute to their progression and pathogenesis. In this sense, we are here proposing new neuroprotection strategies by using marine-derived compounds as fiscalins. This work aims to evaluate the protective effects of fiscalin derivatives towards 1-methyl-4-phenylpyridinium (MPP+)- and iron (III)-induced cytotoxicity in differentiated SH-SY5Y cells, an in vitro disease model to study ND; and on P-glycoprotein (P-gp) transport activity, an efflux pump of drugs and neurotoxins. SH-SY5Y cells were simultaneously exposed to MPP+ or iron (III), and noncytotoxic concentrations of 18 fiscalin derivatives (0–25 μM), being the cytotoxic effect of both MPP+ and iron (III) evaluated 24 and 48 h after exposure. Fiscalins 1a and 1b showed a significant protective effect against MPP+-induced cytotoxicity and fiscalins 1b, 2b, 4 and 5 showed a protective effect against iron (III)-induced cytotoxicity. Fiscalins 4 and 5 caused a significant P-gp inhibition, while fiscalins 1c, 2a, 2b, 6 and 11 caused a modest increase in P-gp transport activity, thus suggesting a promising source of new P-gp inhibitors and activators, respectively. The obtained results highlight fiscalins with promising neuroprotective effects and with relevance for the synthesis of new derivatives for the treatment/prevention of ND.

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26

Diez-Iriepa, Daniel, Beatriz Chamorro, Marta Talaván, Mourad Chioua, Isabel Iriepa, Dimitra Hadjipavlou-Litina, Francisco López-Muñoz, José Marco-Contelles, and María Jesús Oset-Gasque. "Homo-Tris-Nitrones Derived from α-Phenyl-N-tert-butylnitrone: Synthesis, Neuroprotection and Antioxidant Properties." International Journal of Molecular Sciences 21, no. 21 (October 26, 2020): 7949. http://dx.doi.org/10.3390/ijms21217949.

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Herein we report the synthesis, antioxidant and neuroprotective power of homo-tris-nitrones (HTN) 1-3, designed on the hypothesis that the incorporation of a third nitrone motif into our previously identified homo-bis-nitrone 6 (HBN6) would result in an improved and stronger neuroprotection. The neuroprotection of HTNs 1-3, measured against oligomycin A/rotenone, showed that HTN2 was the best neuroprotective agent at a lower dose (EC50 = 51.63 ± 4.32 μM), being similar in EC50 and maximal activity to α-phenyl-N-tert-butylnitrone (PBN) and less potent than any of HBNs 4-6. The results of neuroprotection in an in vitro oxygen glucose deprivation model showed that HTN2 was the most powerful (EC50 = 87.57 ± 3.87 μM), at lower dose, but 50-fold higher than its analogous HBN5, and ≈1.7-fold less potent than PBN. HTN3 had a very good antinecrotic (IC50 = 3.47 ± 0.57 μM), antiapoptotic, and antioxidant (EC50 = 6.77 ± 1.35 μM) profile, very similar to that of its analogous HBN6. In spite of these results, and still being attractive neuroprotective agents, HTNs 2 and 3 do not have better neuroprotective properties than HBN6, but clearly exceed that of PBN.

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27

Maskery, Mark P., Christian Holscher, Stephanie P. Jones, Christopher I. Price, W. David Strain, Caroline L. Watkins, David J. Werring, and Hedley CA Emsley. "Glucagon-like peptide-1 receptor agonists as neuroprotective agents for ischemic stroke: a systematic scoping review." Journal of Cerebral Blood Flow & Metabolism 41, no. 1 (September 20, 2020): 14–30. http://dx.doi.org/10.1177/0271678x20952011.

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Stroke mortality and morbidity is expected to rise. Despite considerable recent advances within acute ischemic stroke treatment, scope remains for development of widely applicable neuroprotective agents. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), originally licensed for the management of Type 2 Diabetes Mellitus, have demonstrated pre-clinical neuroprotective efficacy in a range of neurodegenerative conditions. This systematic scoping review reports the pre-clinical basis of GLP-1RAs as neuroprotective agents in acute ischemic stroke and their translation into clinical trials. We included 35 pre-clinical studies, 11 retrospective database studies, 7 cardiovascular outcome trials and 4 prospective clinical studies. Pre-clinical neuroprotection was demonstrated in normoglycemic models when administration was delayed by up to 24 h following stroke induction. Outcomes included reduced infarct volume, apoptosis, oxidative stress and inflammation alongside increased neurogenesis, angiogenesis and cerebral blood flow. Improved neurological function and a trend towards increased survival were also reported. Cardiovascular outcomes trials reported a significant reduction in stroke incidence with semaglutide and dulaglutide. Retrospective database studies show a trend towards neuroprotection. Prospective interventional clinical trials are on-going, but initial indicators of safety and tolerability are favourable. Ultimately, we propose that repurposing GLP-1RAs is potentially advantageous but appropriately designed trials are needed to determine clinical efficacy and cost-effectiveness.

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28

Sanders, Robert D., Helen J. Manning, Nicola J. Robertson, Daqing Ma, A. David Edwards, Henrik Hagberg, and Mervyn Maze. "Preconditioning and Postinsult Therapies for Perinatal Hypoxic–Ischemic Injury at Term." Anesthesiology 113, no. 1 (July 1, 2010): 233–49. http://dx.doi.org/10.1097/aln.0b013e3181dc1b84.

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Perinatal hypoxic-ischemic encephalopathy can be a devastating complication of childbirth. Herein, the authors review the pathophysiology of hypoxic-ischemic encephalopathy and the current status of neuroprotective strategies to ameliorate the injury centering on four themes: (1) monitoring in the perinatal period, (2) rapid identification of affected neonates to allow timely institution of therapy, (3) preconditioning therapy (a therapeutic that reduces the brain vulnerability) before hypoxic-ischemic encephalopathy, and (4) prompt institution of postinsult therapies to ameliorate the evolving injury. Recent clinical trials have demonstrated the significant benefit for hypothermic therapy in the postnatal period; furthermore, there is accumulating preclinical evidence that adjunctive therapies can enhance hypothermic neuroprotection. Advances in the understanding of preconditioning may lead to the administration of neuroprotective agents earlier during childbirth. Although most of these neuroprotective strategies have not yet entered clinical practice, there is a significant hope that further developments will enhance hypothermic neuroprotection.

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29

Jia, Xiaohui, Menglu Jia, Yuqin Yang, Di Wang, Fei Zhou, Wenxi Zhang, Xuemei Huang, et al. "Synthesis of Novel Baicalein Amino Acid Derivatives and Biological Evaluation as Neuroprotective Agents." Molecules 24, no. 20 (October 9, 2019): 3647. http://dx.doi.org/10.3390/molecules24203647.

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Baicalein, a famously effective component of the traditional Chinese medicine Rhizoma Huang Qin (Scutellaria altissima L.), has been proved to have potent neuroprotection and anti-platelet aggregation effects with few side effects. Meanwhile, recent studies have revealed that the introduction of amino acid to baicalein could improve its neuroprotective activity. In the present study, a series of novel baicalein amino acid derivatives were designed, synthesized, and screened for their neuroprotective effect against tert-butyl, hydroperoxide-induced, SH-SY5Y neurotoxicity cells and toxicity on the normal H9C2 cell line by standard methylthiazol tetrazolium (MTT) assay. In addition, all of the newly synthesized compounds were characterized by 1H-NMR, 13C-NMR, and high resolution mass spectrometry (HR-MS). The results showed that most of the compounds provided more potent neuroprotection than baicalein, and were equivalent to the positive drug edaravin. They showed no obvious cytotoxicity on normal H9C2 cells. Notably, the most active compound 8 displayed the highest protective effect (50% effective concentration (EC50) = 4.31 μM) against tert-butyl, hydroperoxide-induced, SH-SY5Y neurotoxicity cells, which was much better than the baicalein (EC50 = 24.77 μM) and edaravin (EC50 = 5.62 μM). Further research on the chick chorioallantoic membrane (CAM) model indicated that compound 8 could significantly increase angiogenesis, which might promote neurovascular proliferation. The detection of apoptosis analysis showed that compound 8 could dramatically alleviate morphological manifestations of cell damage. Moreover, the benzyloxycarbonyl (cbz)-protected baicalein amino acid derivatives showed better neuroprotective activity than the t-Butyloxy carbonyl (boc)-protected derivatives.

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Kyrychenko, O. V., and S. P. Moskovko. "A modern view of approaches of neuroprotective therapy in patients with ischemic stroke. Review." Ukrainian Neurological Journal, no. 1—2 (July 1, 2022): 12–16. http://dx.doi.org/10.30978/unj2022-1-12.

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Timely use of neuroprotectors for treatment of ischemic stroke should prevent or inhibit the pathogenetic mechanisms that lead to apoptosis of brain cells, both in the nucleus of the infarct and in the ischemic penumbra. The concept of neuroprotection has a sufficient scientific basis, but the questions of its effectiveness, safety and optimal points of application remain controversial, taking into account the available results of clinical trials. Currently, two pharmacological agents are most commonly used as neuroprotective agents in ischemic stroke (IS) — Cerebrolysin and Edaravon (in the Ukrainian pharmaceuзtical market — Xavron). They have the broadest evidence base and are favored by practitioners to provide the potential for recovery in the poststroke period. Objective — to investigate the available evidence base of results of admission and effectiveness of neuroprotective agents — Cerebrolysin and Edaravon in treatment of IS: the impact to the outcome of treatment during hospita period and in the medium term. A search was conducted for studies and metaanilysis for the Key words «schemic stroke», «neuroprotection», «edaravon», «cerebrolysin» in the PubMed database and the Cochrane Library, published between 2010 and 2022.The selection criteria for publications were the availability of a full text or a detailed summary in English. Given the results of research, the clinical effects of neuroprotective therapy are significant. However, there are reports of questionable results, the probable causes of which may be: failure to take into account the level of neurological deficit at the time of hospitalization, as well as the therapeutic window for the appointment of the drug and the dosage regimen. The outcome on the 90th day of treatment could be influenced by factors such as comorbid pathology, complications of the hospital period, as well as different approaches to rehabilitation measures. Large clinical trials with more sophisticated patient selection criteria are needed to determine the importance of neuroprotective agents in the complex intensive care of patients with IS.

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31

GOYAGI, Toru. "Neuroprotective Effects of Anesthetic-Related Agents." JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 29, no. 4 (2009): 364–76. http://dx.doi.org/10.2199/jjsca.29.364.

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32

Kelsey, Natalie A., Heather M. Wilkins, and Daniel A. Linseman. "Nutraceutical Antioxidants as Novel Neuroprotective Agents." Molecules 15, no. 11 (November 3, 2010): 7792–814. http://dx.doi.org/10.3390/molecules15117792.

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33

&NA;. "Can statins operate as neuroprotective agents?" Inpharma Weekly &NA;, no. 1305 (September 2001): 2. http://dx.doi.org/10.2165/00128413-200113050-00002.

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34

Hock, Nanette H. "Neuroprotective Agents in Acute Ischemic Stroke." Topics in Stroke Rehabilitation 7, no. 1 (April 2000): 53–61. http://dx.doi.org/10.1310/c36f-yq82-hgvp-7r1r.

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35

Fearnside, Michael. "NEUROPROTECTIVE AGENTS IN SEVERE HEAD INJURY." Clinical and Experimental Pharmacology and Physiology 23, s2 (November 1996): s54—s55. http://dx.doi.org/10.1111/j.1440-1681.1996.tb03047.x.

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36

Maas, Andrew IR. "Neuroprotective agents in traumatic brain injury." Expert Opinion on Investigational Drugs 10, no. 4 (April 2001): 753–67. http://dx.doi.org/10.1517/13543784.10.4.753.

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37

Hock, Nanette H. "Neuroprotective Agents in Acute Ischemic Stroke." Journal of Cardiovascular Nursing 13, no. 1 (October 1998): 17–25. http://dx.doi.org/10.1097/00005082-199810000-00003.

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38

Dodd, Seetal, Michael Maes, George Anderson, Olivia M. Dean, Steven Moylan, and Michael Berk. "Putative neuroprotective agents in neuropsychiatric disorders." Progress in Neuro-Psychopharmacology and Biological Psychiatry 42 (April 2013): 135–45. http://dx.doi.org/10.1016/j.pnpbp.2012.11.007.

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Toner, Christopher C., and Jonathan A. Stamford. "8 General anaesthetics as neuroprotective agents." Baillière's Clinical Anaesthesiology 10, no. 3 (September 1996): 515–33. http://dx.doi.org/10.1016/s0950-3501(96)80032-8.

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SLIKKER, WILLIAM, and DAVID W. GAYLOR. "Risk Assessment Strategies for Neuroprotective Agents." Annals of the New York Academy of Sciences 765, no. 1 Neuroprotecti (September 1995): 198–208. http://dx.doi.org/10.1111/j.1749-6632.1995.tb16576.x.

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Salsabila, Syifa Fitriyanda, Widhya Aligita, and Yani Mulyani. "Review: Neuroprotective effect of herbal plant extracts against Parkinson's disease." Jurnal Ilmiah Farmasi 17, no. 2 (December 28, 2021): 198–209. http://dx.doi.org/10.20885/jif.vol17.iss2.art9.

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Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder caused by the loss of dopaminergic neurons and the exist of alpha-synuclein aggregates in the substantia nigra pars compacta (SNpc). Among the various types of neuroprotective therapy, natural products are potential therapeutic agents for PD. Objective: The aim of this study is to describe the neuroprotective effect of herbal plant extracts against Parkinson's Disease (PD). Method: The search strategy was carried out on electronic databases, namely Google Scholar, ScienceDirect, and PubMed. There are 111 scientific journals that have been filtered into 20 scientific journals which are international journals published in the last 5 years (2015-2020). The keywords used include Parkinson's Disease, Neuroprotective Effects, Neuroprotection, Plant Extracts, Natural Products and Parkinson's Disease Model. Results: Several experimental studies have shown the neuroprotective ability of various plant extracts to protect against neurotoxicity, through several neuroprotective pathways including antioxidant activity, anti-inflammatory activity, and antiapoptotic activity. Conclusion: Herbal plant extracts have been shown to have strong neuroprotective effects, making them as potential drug candidates for prevention or treatment of Parkinson's Disease (PD). There are Mucuna pruriens, Centella asiatica, Camellia sinensis, Ginkgo biloba, and Uncaria rhynchophylla. Keywords: Parkinson's Disease (PD), neuroprotective, extract.

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Tator, Charles H., Robin Hashimoto, Annie Raich, Daniel Norvell, Michael G. Fehlings, James S. Harrop, James Guest, Bizhan Aarabi, and Robert G. Grossman. "Translational potential of preclinical trials of neuroprotection through pharmacotherapy for spinal cord injury." Journal of Neurosurgery: Spine 17, Suppl1 (September 2012): 157–229. http://dx.doi.org/10.3171/2012.5.aospine12116.

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There is a need to enhance the pipeline of discovery and evaluation of neuroprotective pharmacological agents for patients with spinal cord injury (SCI). Although much effort and money has been expended on discovering effective agents for acute and subacute SCI, no agents that produce major benefit have been proven to date. The deficiencies of all aspects of the pipeline, including the basic science input and the clinical testing output, require examination to determine remedial strategies. Where has the neuroprotective/pharmacotherapy preclinical process failed and what needs to be done to achieve success? These are the questions raised in the present review, which has 2 objectives: 1) identification of articles that address issues related to the translational readiness of preclinical SCI pharmacological therapies; and 2) examination of the preclinical studies of 5 selected agents evaluated in animal models of SCI (including blunt force trauma, penetrating trauma, or ischemia). The 5 agents were riluzole, glyburide, magnesium sulfate, nimodipine, and minocycline, and these were selected because of their promise of translational readiness as determined by the North American Clinical Trials Network Consortium. The authors found that there are major deficiencies in the effort that has been extended to coordinate and conduct preclinical neuroprotection/pharmacotherapy trials in the SCI field. Apart from a few notable exceptions such as the NIH effort to replicate promising strategies, this field has been poorly coordinated. Only a small number of articles have even attempted an overall evaluation of the neuroprotective/pharmacotherapy agents used in preclinical SCI trials. There is no consensus about how to select the agents for translation to humans on the basis of their preclinical performance and according to agreed-upon preclinical performance criteria. In the absence of such a system and to select the next agent for translation, the Consortium has developed a Treatment Strategy Selection Committee, and this committee selected the most promising 5 agents for potential translation. The results show that the preclinical work on these 5 agents has left numerous gaps in knowledge about their preclinical performance and confirm the need for significant changes in preclinical neuroprotection/pharmacotherapy trials in SCI. A recommendation is made for the development and validation of a preclinical scoring system involving worldwide experts in preclinical and clinical SCI.

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da Silva, Geisa Gabriela, Lúcia Pinheiro Santos Pimenta, Júlio Onésio Ferreira Melo, Henrique de Oliveira Prata Mendonça, Rodinei Augusti, and Jacqueline Aparecida Takahashi. "Phytochemicals of Avocado Residues as Potential Acetylcholinesterase Inhibitors, Antioxidants, and Neuroprotective Agents." Molecules 27, no. 6 (March 15, 2022): 1892. http://dx.doi.org/10.3390/molecules27061892.

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Avocado (Persea americana) is a widely consumed fruit and a rich source of nutrients and phytochemicals. Its industrial processing generates peels and seeds which represent 30% of the fruit. Environmental issues related to these wastes are rapidly increasing and likely to double, according to expected avocado production. Therefore, this work aimed to evaluate the potential of hexane and ethanolic peel (PEL-H, PEL-ET) and seed (SED-H, SED-ET) extracts from avocado as sources of neuroprotective compounds. Minerals, total phenol (TPC), total flavonoid (TF), and lipid contents were determined by absorption spectroscopy and gas chromatography. In addition, phytochemicals were putatively identified by paper spray mass spectrometry (PSMS). The extracts were good sources of Ca, Mg, Fe, Zn, ω-6 linoleic acid, and flavonoids. Moreover, fifty-five metabolites were detected in the extracts, consisting mainly of phenolic acids, flavonoids, and alkaloids. The in vitro antioxidant capacity (FRAP and DPPH), acetylcholinesterase inhibition, and in vivo neuroprotective capacity were evaluated. PEL-ET was the best acetylcholinesterase inhibitor, with no significant difference (p > 0.05) compared to the control eserine, and it showed neither preventive nor regenerative effect in the neuroprotection assay. SED-ET demonstrated a significant protective effect compared to the control, suggesting neuroprotection against rotenone-induced neurological damage.

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Prakash, Samay, and Wayne G. Carter. "The Neuroprotective Effects of Cannabis-Derived Phytocannabinoids and Resveratrol in Parkinson’s Disease: A Systematic Literature Review of Pre-Clinical Studies." Brain Sciences 11, no. 12 (November 28, 2021): 1573. http://dx.doi.org/10.3390/brainsci11121573.

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Currently, there are no pharmacological treatments able to reverse nigral degeneration in Parkinson’s disease (PD), hence the unmet need for the provision of neuroprotective agents. Cannabis-derived phytocannabinoids (CDCs) and resveratrol (RSV) may be useful neuroprotective agents for PD due to their anti-oxidative and anti-inflammatory properties. To evaluate this, we undertook a systematic review of the scientific literature to assess the neuroprotective effects of CDCs and RSV treatments in pre-clinical in vivo animal models of PD. The literature databases MEDLINE, EMBASE, PsychINFO, PubMed, and Web of Science core collection were systematically searched to cover relevant studies. A total of 1034 publications were analyzed, of which 18 met the eligibility criteria for this review. Collectively, the majority of PD rodent studies demonstrated that treatment with CDCs or RSV produced a significant improvement in motor function and mitigated the loss of dopaminergic neurons. Biochemical analysis of rodent brain tissue suggested that neuroprotection was mediated by anti-oxidative, anti-inflammatory, and anti-apoptotic mechanisms. This review highlights the neuroprotective potential of CDCs and RSV for in vivo models of PD and therefore suggests their potential translation to human clinical trials to either ameliorate PD progression and/or be implemented as a prophylactic means to reduce the risk of development of PD.

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Pereira, Leonel, and Ana Valado. "Red Algae Compounds: Potential Neuroprotective Agents for Neurodegenerative Disorders." OBM Neurobiology 08, no. 02 (May 10, 2024): 1–27. http://dx.doi.org/10.21926/obm.neurobiol.2402223.

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This review explores the potential of compounds derived from red algae (Rhodophyta) as promising neuroprotective agents for treating neurodegenerative disorders. Red algae, abundant in marine environments, contain bioactive compounds with diverse chemical structures and functionalities. Sulfated polysaccharides, primarily agar and carrageenans, stand out as the predominant and widely utilized compounds derived from red algae. Additionally, red algae harbor a spectrum of potential molecules such as essential fatty acids, phycobiliproteins, vitamins, minerals, and secondary metabolites. Extensive research has highlighted the diverse biological activities exhibited by these compounds, including anti-oxidative and anti-inflammatory properties. These compounds show various biological activities that have garnered interest in their therapeutic potential for neurodegenerative diseases. This comprehensive review aims to summarize the current knowledge regarding the extraction, characterization, mechanisms of action, and therapeutic applications of Rhodophyta-derived compounds in the context of neuroprotection and treatment of neurodegenerative disorders.

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Li, Jun, and Louise D. McCullough. "Sex Differences in Minocycline-Induced Neuroprotection after Experimental Stroke." Journal of Cerebral Blood Flow & Metabolism 29, no. 4 (February 4, 2009): 670–74. http://dx.doi.org/10.1038/jcbfm.2009.3.

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Minocycline is neuroprotective in clinical and experimental stroke studies, due in part to its ability to inhibit poly (ADP-ribose) polymerase. Previous preclinical data have shown that interference with poly (ADP-ribose) polymerase signaling leads to sex-specific neuroprotection, reducing stroke injury only in males. In this study, we show that minocycline is ineffective at reducing ischemic damage in females after middle cerebral artery occlusion, likely due to effects on poly (ADP-ribose) polymerase signaling. Clinical trials must consider possible sex differences in the response to neuroprotective agents, if we hope to translate promising therapies to stroke patients of both sexes.

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O'Collins, Victoria E., Malcolm R. Macleod, Susan F. Cox, Leena Van Raay, Elena Aleksoska, Geoffrey A. Donnan, and David W. Howells. "Preclinical Drug Evaluation for Combination Therapy in Acute Stroke Using Systematic Review, Meta-Analysis, and Subsequent Experimental Testing." Journal of Cerebral Blood Flow & Metabolism 31, no. 3 (October 27, 2010): 962–75. http://dx.doi.org/10.1038/jcbfm.2010.184.

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There is some evidence that in animal models of acute ischaemic stroke, combinations of neuroprotective agents might be more efficacious than the same agents administered alone. Hence, we developed pragmatic, empirical criteria based on therapeutic target, cost, availability, efficacy, administration, and safety to select drugs for testing in combination in animal models of acute stroke. Magnesium sulphate, melatonin, and minocycline were chosen from a library of neuroprotective agents, and were tested in a more ‘realistic’ model favoured by the STAIR (Stroke Therapy Academic Industry Roundtable). Outcome was assessed with infarct volume, neurologic score, and two newly developed scales measuring general health and physiologic homeostasis. Owing to the failure to achieve neuroprotection in aged, hypertensive animals with drug delivery at 3 hours, the bar was lowered in successive experiments to determine whether neuroprotection could be achieved under conditions more conducive to recovery. Testing in younger animals showed more favourable homeostasis and general health scores than did testing in older animals, but infarct volume and neurologic scores did not differ with age, and treatment efficacy was again not shown. Testing with shorter occlusions resulted in smaller infarct volumes; nevertheless, treatment efficacy was still not observed. It was concluded that this combination, in these stroke models, was not effective.

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Zaa, César A., Clara Espitia, Karen L. Reyes-Barrera, Zhiqiang An, and Marco A. Velasco-Velázquez. "Neuroprotective Agents with Therapeutic Potential for COVID-19." Biomolecules 13, no. 11 (October 27, 2023): 1585. http://dx.doi.org/10.3390/biom13111585.

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COVID-19 patients can exhibit a wide range of clinical manifestations affecting various organs and systems. Neurological symptoms have been reported in COVID-19 patients, both during the acute phase of the illness and in cases of long-term COVID. Moderate symptoms include ageusia, anosmia, altered mental status, and cognitive impairment, and in more severe cases can manifest as ischemic cerebrovascular disease and encephalitis. In this narrative review, we delve into the reported neurological symptoms associated with COVID-19, as well as the underlying mechanisms contributing to them. These mechanisms include direct damage to neurons, inflammation, oxidative stress, and protein misfolding. We further investigate the potential of small molecules from natural products to offer neuroprotection in models of neurodegenerative diseases. Through our analysis, we discovered that flavonoids, alkaloids, terpenoids, and other natural compounds exhibit neuroprotective effects by modulating signaling pathways known to be impacted by COVID-19. Some of these compounds also directly target SARS-CoV-2 viral replication. Therefore, molecules of natural origin show promise as potential agents to prevent or mitigate nervous system damage in COVID-19 patients. Further research and the evaluation of different stages of the disease are warranted to explore their potential benefits.

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Tan, Shih Jen, and Intan Safinar Ismail. "Potency of Selected Berries, Grapes, and Citrus Fruit as Neuroprotective Agents." Evidence-Based Complementary and Alternative Medicine 2020 (May 30, 2020): 1–12. http://dx.doi.org/10.1155/2020/3582947.

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A healthy diet should nourish the brain with essential nutrients, including bioactive compounds, for normal brain functioning and to protect it from the negative effects of inflammation and oxidative stress. In this review, a concise summation of the protective effects of selected fruits, namely, berries, grapes, and citrus fruits, against neurological disorder is presented. The focus is on the neuroprotective potential of these fruits against neurodegenerative and mental disorders. The fruits selection was based on the vast reported pharmacological studies on their neuroprotection efficacies. Hence, the respective knowledge and limitations are discussed based on the biological and pharmacological evidence compiled from the previously reported laboratory, epidemiology, and intervention trials.

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Pryce, Gareth, Sofia Sisay, Gavin Giovannoni, David L. Selwood, and David Baker. "Neuroprotection in an Experimental Model of Multiple Sclerosis via Opening of Big Conductance, Calcium-Activated Potassium Channels." Pharmaceuticals 16, no. 7 (July 7, 2023): 972. http://dx.doi.org/10.3390/ph16070972.

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Big conductance calcium-activated (BK) channel openers can inhibit pathologically driven neural hyperactivity to control symptoms via hyperpolarizing signals to limit neural excitability. We hypothesized that BK channel openers would be neuroprotective during neuroinflammatory, autoimmune disease. The neurodegenerative disease was induced in a mouse experimental autoimmune encephalomyelitis model with translational value to detect neuroprotection in multiple sclerosis. Following the treatment with the BK channel openers, BMS-204253 and VSN16R, neuroprotection was assessed using subjective and objective clinical outcomes and by quantitating spinal nerve content. Treatment with BMS-204253 and VSN16R did not inhibit the development of relapsing autoimmunity, consistent with minimal channel expression via immune cells, nor did it change leukocyte levels in rodents or humans. However, it inhibited the accumulation of nerve loss and disability as a consequence of autoimmunity. Therefore, in addition to symptom control, BK channel openers have the potential to save nerves from excitotoxic damage and could be useful as either stand-alone neuroprotective agents or as add-ons to current disease-modifying treatments that block relapsing MS but do not have any direct neuroprotective activity.

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