Relevant bibliographies by topics / Neuroprotective agents

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Neuroprotective agents'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 August 2024

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Journal articles on the topic "Neuroprotective agents"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Neuroprotective agents"

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Nilsson, Olov. "Cannabinoids as neuroprotective agents : a mechanistic study." Doctoral thesis, Umeå : Umeå universitet, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-873.

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Badenhorst, Hester Elizabeth. "Antihistamines as neuroprotective agents / Hester Elizabeth Badenhorst." Thesis, North-West University, 2004. http://hdl.handle.net/10394/95.

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Biomolecules are continuously exposed to potentially harmful oxidative stress as a consequence of free radical formation. Increased free radical generation has been associated with aging as well as neurodegenerative disorders. Antioxidants affect processes associated with oxidative stress by quenching free radicals and acting as oxygen scavengers. Parkinson's disease results from a deficiency in the neurotransmitter, dopamine and it is also evident that damage caused by free radicals play an important role in the progression of this neurodegenerative disorder. The histamine HI antagonist, diphenhydramine is used to treat mild cases of Parkinson's disease and cimetidine can scavenge hydroxyl radicals. The histamine H3 antagonists are known to promote the release of dopamine. Together with a free radical scavenging activity, these compounds might have a dual therapeutic effect in the reduction of the progression of Parkinson's disease. The aim of this study was thus to determine whether histamine antagonists could act as free radical scavengers and to compare the results with aspirin, a known free radical scavenger. Ibuprofen was included to compare the free radical scavenging activities of aspirin to another non-steroidal anti-inflammatory drug. The free radical scavenging activities of the following compounds were determined and compared: diphenhydramine; cimetidine; roxatidine; clobenpropit; impentarnine; thioperamide; aspirin and ibuprofen. The ORAC assay was used to determine whether the test compounds were able to scavenge peroxyl radicals and the FRAP assay was used to determine the reducing abilities of the compounds. No meaningll results were obtained from these two assays, suggesting that the compounds were not able to act as direct antioxidants or as peroxyl radical scavengers. The comet assay was used to determine whether the compounds were able to reduce oxidative damage after MPTP administration. No damage was however obtained after a single dose of MPTP and it is suggested that one year old mice and chronic rather than acute treatment is used. Using a cyanide model to induce neurotoxic effects in rat brain homogenates, the neuroprotective properties of the histamine antagonists were examined and compared to aspirin. Superoxide anion levels and malondialdehyde concentrations were assessed using the nitrobluetetrazolium and lipid peroxidation assays. Clobenpropit and thioperamide significantly reduced superoxide anion generation and lipid peroxidation. At a concentration of lmM, these two histamine Hj antagonists reduced lipid peroxidation to values lower than that of the control. Impentamine reduced lipid peroxidation at all concentrations used and superoxide anion generation at a concentration of 1mM. Diphenhydramine (0.25 and 0.5mM) significantly reduced both variables at lower concentrations. Cimetidine (1mM) was able to reduce superoxide anion generation and significantly reduced lipid peroxidation at all concentrations Abstract used. Roxatidine (0.5mM and 1mM) significantly reduced the rise in superoxide anion generation and significantly reduced malondialdehyde concentration in a dose dependent manner. Ibuprofen significantly decreased superoxide anions in a dose dependant manner and lipid peroxidation at a concentration of 1mM. In the lipid peroxidation assay, all the drugs compared favourably to aspirin. The in vivo free radical scavenging effects of the selected compounds were also examined with the nitroblue tetrazoliurn and lipid peroxidation assays. MPP' was used to induce a Parkinsonian like condition. Diphenhydramine, ibuprofen, thioperamide and clobenpropit significantly reduced free radical generation in both assays. Thioperamide and clobenpropit were able to reduce lipid peroxidation and superoxide anion generation to values lower than that of the control, suggesting that these two compounds could be able to attenuate normal free radical processes in the brain. Cimetidine did not have the expected in vivo scavenging effects and it is suggested that blood-brain barrier permeability might play a role. All the compounds, except diphenhydramine had significantly lower in vivo values than aspirin. The superoxide anion plays an important role in the formation of further free radicals. It leads to the formation of peroxyl radicals during the inititation step of lipid peroxidation and also leads to the generation of hydroxyl radicals, where transition metals like iron, is a key factor. Diphenhydramine at lower concentrations, and the newly discovered histamine Hj antagonists, clobenpropit and thioperamide significantly reduced superoxide anion generation and lipid peroxidation. Although the compounds did not have meaningful effects in the FRAY and ORAC assay, their significant ability to reduce lipid peroxidation and superoxide levels make them promising tools to attenuate oxidative damage. This study demonstrates the potential of these agents to be neuroprotective with a dual therpeutic effect by exerting a scavenging effect on superoxide anions and increasing dopamine levels.
Thesis (M.Sc. (Pharmaceutical Chemistry))--North-West University, Potchefstroom Campus, 2005.
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Egunlusi, Ayodeji Olatunde. "Novel norbornane derivatives as potential neuroprotective agents." University of Western Cape, 2020. http://hdl.handle.net/11394/7339.

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Philosophiae Doctor - PhD
Neurodegenerative disorders are characterised by progressive loss of the brain’s physiological functions as a result of gradual degeneration of neurons in the central nervous system. Even though they are classified as diseases of the elderly, occurrence earlier in life is possible, but that would suggest the influence of genetic and/or environmental factors. Due to the continuous rise in modernisation and industrialisation over the years, there has been an increase in incidence and prevalence of neurodegenerative disorders. With the advances in technology and life expectancy, the rates of the common forms (Alzheimer’s disease and Parkinson’s disease), are expected to increase exponentially by 2050. Unfortunately, there is still no clinically approved treatment or therapy to slow down or halt the degenerative process as most registered drugs only offer symptomatic relief. Confounding this issue is the lack of definite mechanism of neurodegeneration, which is still poorly defined and not completely understood. Nonetheless, the pathology of most neurodegenerative disorders is believed to be a combination of interrelated processes that eventually leads to neuronal cell death. Among the postulated processes, the impact of excitotoxicity mediated by NMDA receptor over-activation is prominent and it is implicated in virtually all neurodegenerative disorders. With this basic insight, it is believed that molecules capable of inhibiting NMDA receptors and associated calcium channels, without affecting the normal physiological functions of the brain, could potentially serve as good neuroprotective drugs. Competitive and uncompetitive blockers (MK-801 and ketamine) have been explored, but none were clinically accepted due to undesirable side effects such as hallucinations, sedation and depression. However, NGP1-01, a polycyclic cage molecule, has been shown to be neuroprotective through modulation of NMDA receptors and voltage gated calcium channels and attenuation of MPP+ -induced toxicity. A similar approach could be useful in the design and development of new neuroprotective drugs. The aim of this study was to synthesise a series of open and rearranged cage-like molecules and explore their neuroprotective potential in neuroblastoma SH-SY5Y cells. The proposed structures, with norbornane scaffolds that contained different moieties, were designed to structurally resemble NGP1-01 and MK-801. Once synthesised, the compounds were purified and characterised, and were evaluated for their biological activities. Compounds were first screened for cytotoxicity at different concentrations. Thereafter, they were evaluated for neuroprotective effects against MPP+ -induced excitotoxicity and for calcium flux modulatory effects on NMDA receptor and voltage gated calcium channels. The norbornane derivatives were synthesised and characterised, and all final products were afforded in sufficient yields. All compounds with the exception of two compounds displayed good cytotoxic profiles towards the SH-SY5Y neuroblastoma cells at 10 µM, 50 µM and 100 µM concentrations as they demonstrated percentage cell viabilities close to 100% (control treated cells). Only two compounds showed percentage cell viability of 51% and 59% at 100 µM. Utilising the same cell line, all compounds, tested at 10 µM, attenuated MPP+ -induced toxicity after 24 hours of exposure to a neurotoxin. This was evident in the 23% to 53% enhancement (significant with p < 0.05) in cell viability when compared to the MPP+ only treated cells. In comparison to known NMDA receptor and/or voltage gated calcium channel blockers (MK-801, NGP1-01 or nimodipine), the synthesised compounds demonstrated mono or dual inhibition of calcium channels as they effectively attenuated calcium influx by blocking NMDA receptors and/or voltage gated calcium channels expressed in neuroblastoma SHSY5Y cells. This group of compounds were found to be more potent NMDA receptor inhibitors, probably due to similarities with MK-801 and memantine, than voltage gated calcium channel inhibitors. All compounds demonstrated moderate to good calcium inhibitory effects at NMDA receptors in the range of 23% to 70% while a selected few displayed very little or no activity at the voltage gated calcium channels. In conclusion, 27 compounds with norbornane scaffolds were successfully synthesised and evaluated for cytotoxicity and neuroprotection. The abilities of the synthesised compounds to protect neurons from the neurotoxin MPP+ and reduce calcium flux into neuronal cells were successfully demonstrated. These characteristics are essential in neuroprotection as they may prove significant in halting or slowing down the disease progression. The compounds showing a good cytotoxicity profile, neuroprotective effects and ability to reduce calcium overload, could potentially act as neuroprotective agents with good safety profiles or contribute as lead structures to the development and design of structurally related molecules that could clinically benefit people with neurodegenerative disorders.
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Kadernani, Yakub Esmail Y. E. "Novel adamantane derivatives as multifunctional neuroprotective agents." University of the Western Cape, 2013. http://hdl.handle.net/11394/4256.

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>Magister Scientiae - MSc
The pathology of neurodegenerative disorders involves multiple steps, and it is probably for this reason that targeting one particular step in a multi-step process has only yielded limited results. Nitric oxide (NO) is synthesised from L-Arginine by an enzyme known as nitric oxide synthase (NOS). Three isoforms of NOS exist, including endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS). In the central nervous system (CNS), nNOS is involved in the synthesis of NO, which is involved in various neurological functions. NO is a free radical and this probably explains why an excess amount of it has been implicated in the development of neurodegenerative disorders. In the CNS, the Nmethyl- D-aspartate (NMDA) receptor in its active state allows the influx of calcium ions which activate nNOS thus increasing the amount of NO and other detrimental reactive nitrogen species within neuronal cells. Calcium entry through voltage-gated calcium channels (VGCC) may also contribute to this. Although calcium ions are important for physiological functioning, an excess is responsible for excitotoxicity, which can ultimately lead to neurodegeneration. Our aim was to synthesise a series of adamantane-derived compounds that act at multiple target sites in the neurodegenerative pathway. By conjugating benzyl and phenylethyl moieties with different functional groups (-H, -NO2, -NH2, -NHC(NH)NH2, -OCH3) to the amantadine structure, we aimed to synthesise compounds that display calcium channel and NMDA receptor (NMDAR) channel inhibition, as well as selective inhibition of nNOS. A series of compounds (-H, -NO2, -NH2, -OCH3) were obtained in yields that varied between 16.5 % and 90.25 %. These novel compounds were tested for calcium influx through VGCC and NMDAR inhibition using synaptoneurosomes isolated from rat brain homogenate against the reference compounds MK-801, NGP1-01, amantadine, memantine and nimodipine. A lack of success with the synthesis of the guanidine compounds prevented the use of the oxyhemoglobin capture assay for the determination of nNOS inhibitory activity of these compounds. The novel synthesised compounds display inhibitory activity towards VGCC and the NMDAR in the micromolar range. Further tests are recommended on compounds SE-1, SE-4, SE-11 and SE-12 as they displayed good inhibitory activity against both NMDAR- as well as ii KCl-mediated calcium influx. These novel compounds may be better therapeutic options than amantadine and memantine as they inhibit both NMDAR and VGCC-mediated calcium influx, whereas amantadine and memantine only inhibit NMDA-mediated calcium influx. These novel adamantane derived compounds may possibly serve as novel leads or potential therapeutic agents for the treatment of neurodegenerative disorders.
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Zindo, Frank T. "Polycyclic propargylamine derivatives as multifunctional neuroprotective agents." University of the Western Cape, 2018. http://hdl.handle.net/11394/6748.

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Philosophiae Doctor - PhD
The abnormal death of neurons in the central nervous system of individuals suffering from neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease and amyotrophic lateral sclerosis, takes place by an intrinsic cell suicide programme known as apoptosis. This process is triggered by several stimuli, and consists of numerous pathways and cascades which lead to the death of neuronal cells. It is this multifactorial nature of neurodegenerative diseases that has over the years seen many researchers develop compounds that may serve as multi-target directed ligands (MTDLs) which could potentially confer neuroprotection by acting simultaneously on different receptors and target sites implicated in neurodegeneration. This study was aimed at developing MTDLs that may serve as neuroprotective agents by simultaneously (a) inhibiting N-methyl D-aspartate receptors (NMDAR) and blocking L-type voltage gated calcium channels (VGCC) thus regulating the Ca2+ influx mediated excitotoxic process; (b) inhibiting the monoamine oxidase enzymes A and -B (MAO-A/B) thus allowing increase in dopamine levels in the central nervous system and reducing the levels of the highly oxidative products produced by the activity of these enzymes; (c) possessing anti-apoptotic activity to halt the neuronal cell death process. In designing the compounds we focused on the structures of rasagiline and selegiline, two well-known MAO-B inhibitors and proposed neuroprotective agents, and of NGP1-01, a known VGCC blocker and NMDAR antagonist. The first series of compounds (reported in research article 1, Chapter 3), comprised polycyclic propargylamine and acetylene derivatives. Compounds 12, 15 and 16 from this series showed promising VGCC and NMDA receptor channel inhibitory activity ranging from 18 % to 59 % in micromolar concentrations, and compared favourably to the reference compounds. In the MAO-B assay, compound 10 exhibited weak MAO-B inhibition of 73.32 % at 300 μM. The rest of the series showed little to no activity on these target sites, despite showing significant anti-apoptotic activity. This suggested the compounds in this series to be exhibiting their neuroprotective action through some other mechanism(s) unexplored in this study.
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Saathoff, John. "Curcumin/Melatonin Hybrids as Neuroprotective Agents for Alzheimer's disease." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4586.

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia, affecting ~5.2 million Americans. Current FDA approved medications provide mainly symptomatic relief and there are no agents available to delay or cure this disease. Multiple factors such as amyloid-β aggregates, dyshomeostasis of biometals, oxidative stress, and neuroinflammation have been implicated in the development of AD. Even though significant advances have been made in understanding the mechanisms leading to AD, the exact etiology still remains elusive. Given AD’s multifactorial nature, a multifunctional strategy of small molecule design would help to identify novel chemical templates. Recently our lab has developed hybrid molecules of curcumin and melatonin that exhibited potent neuroprotective ability in various AD models. Further modifications identified a lead compound with potent neuroprotective and antioxidative activity in MC65 cells, while also establishing the hybrid strategy as a viable approach in providing unique chemotypes with novel pharmacology. Further preliminary biological studies suggest that the lead is orally available and exhibits multifunctional properties both in vitro and in vivo on AD pathologies, thus strongly encouraging further structural examination. Herein, we report the structural exploration of this chemical template through structure-activity relationship studies at three domains: the phenyl domain, α,β-unsaturated β-ketone amide domain, and the indole domain. Collectively, the results show that the chemical space around the curcumin portion doesn’t favor electronic or steric/hydrophobic interactions, but might favor pi-pi (π-π) and hydrogen-bond interactions. Additionally, the α,β-unsaturated β-ketone amide domain is not as important as the linearity of the β-ketone acetamide. Moreover, the results indicate that a free rotatable β-OH might be the actual moiety that is important for the observed biological activity through favorable hydrogen bonds. Finally, steric interactions are not favored in the chemical space surrounding the indole nitrogen, suggesting that hydrogen bond interactions are required for the observed neuroprotective activity. Conversely, a hydrogen bond acceptor is necessary at the 5-position of the indole ring and bulky substitutions can be accommodated, with restrictions, suggesting steric tolerance and hydrophobic interactions at this position. These modifications have yielded a series of novel compounds that are capable of modifying AD pathology while shedding further light onto the chemical scaffold thus warranting future investigations into the development, optimization, and characterization of these curcumin/melatonin hybrids as potential treatments for AD.
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Hobbs, Catherine E., and n/a. "Perinatal hypoxia-ischaemia : neuroprotective strategies." University of Otago. Department of Anatomy & Structural Biology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070221.145910.

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Perinatal hypoxia-ischaemia is a major cause of disability, including cerebral palsy, yet a neuroprotectant which fully protects the brain remains elusive. Following a hypoxic-ischaemic insult, striatal medium-spiny neurons and hippocampal CA1 neurons are vulnerable to a complex cascade of neurotoxic events. This cascade includes energy failure, a massive release of glutamate, the formation of free radicals and caspase activation. The overall aim of this thesis was to assess the efficacy of three potential neuroprotective strategies that target this cascade from different directions. Short-term, and where appropriate, long-term, neuroprotection was investigated. The first treatment strategy aimed to suppress the generation of free radicals through treatment with the potent free radical spin trap, N-tertbutyl-(2-sulphophenyl)-nitrone (S-PBN). The second compound tested was the caspase-3 inhibitor, minocycline. Finally, the third treatment strategy combined a series of S-PBN injections with 6 hours of moderate hypothermia immediately after hypoxia-ischaemia. Hypothermia is suggested to slow the rate of the neurotoxic cascade, thus potentially allowing other neuroprotective agents greater efficacy. Using an adaptation of the Rice et al. (1981) model, hypoxia-ischaemia was induced on postnatal day (PN) 8 in the right cerebral hemisphere. For the short-term studies, the rats were perfused at 14 days-of-age. The brains were dissected out and embedded in Technovit. Forty [mu]m serial sections were cut through the right striatum and hippocampus. The total number of medium-spiny neurons in the striatum and where appropriate, the total number of neurons in the hippocampal CA1 pyramidal layer, were stereologically determined using the optical disector/Cavalieri method. For the long-term study, fine motor control was assessed in half of the animals through the staircase test from 9-11 weeks-of-age. Neuroprotection was assessed in the remaining animals. All animals were sacrificed at 12 weeks-of-age. The total number of striatal medium-spiny neurons was stereologically determined in the non-behavioural animals as described above. A series of seven injections of S-PBN (100mg/kg) did not offer statistically significant neuroprotection to the striatum at one week after perinatal hypoxia-ischaemia. Similarly, a single injection of minocycline (45mg/kg) immediately after the insult did not offer significant neuroprotection to the striatum nor the CA1 region of the hippocampus at this early time-point. In contrast, when the series of S-PBN injections was combined with 6 hours of moderate hypothermia post-hypoxia-ischaemia, sterelogical analysis revealed significant neuroprotection of the striatal medium-spiny neurons to normal levels at one week after the injury. No significant neuroprotection was seen in the CA1 region of the same animals. To assess whether this impressive striatal neuroprotection was long-lasting and whether it represented functional rescue, the final experiment in this thesis investigated rat pups at 12 weeks-of-age after exposure to hypoxia-ischaemia at PN8. Treatment with S-PBN/hypothermia offered persistent neuroprotection of striatal medium-spiny neurons and preservation of fine motor skills compared to diluent-normothermia-treated controls. The long-term behavioural outcomes were compared with normal, uninjured controls and the total number of medium-spiny neurons was compared with normal numbers from the literature. These comparisons revealed that the histological and functional integrity of the striatum was rescued to normal levels. This is the first study to identify a treatment strategy that offers complete and long-lasting preservation of striatal neuronal numbers, by accurate and unbiased stereological methods, paired with persistent preservation of fine motor control following perinatal hypoxia-ischaemia.
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Singer, Cherie A. "Neurotrophic and neuroprotective effects of estrogen /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/6301.

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Musakwa, Lovetone. "Chalcone and curcumin hybrids of indole propargylamines as multifunctional neuroprotective agents." University of the Western Cape, 2020. http://hdl.handle.net/11394/7959.

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Magister Pharmaceuticae - MPharm
Neurodegenerative disorders (NDs) are a range of chronic brain disorders that includes amongst others motor function loss. Parkinson’s disease (PD) is one of the common NDs that has an insidious onset and diagnosed when dopaminergic neurons in the substantia nigra are already lost. The loss creates a deficiency of the dopamine (neurotransmitter) thereby causing neurochemical imbalance resulting in the signs and symptoms of PD. NDs overlap at multiple levels so some of the symptoms overlap as well. NDs currently have no cure yet and current drug therapies only improve the quality of life of the patients by targeting the symptoms mainly. Treatment of PD currently involves different classes of drugs and depending on the stages of the disease, some drugs can be only used as an adjunct therapy. Anti-oxidants and monoamine oxidase inhibitors (MAO-I) are part of the treatment options.
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Janis, Kelly Lynn. "Investigation of the efficacy of various neuroprotection agents for their potential use in the treatment of Parkinson's disease." Diss., Connect to online resource - MSU authorized users, 2008.

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Books on the topic "Neuroprotective agents"

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International Conference on Neuroprotective Agents: Clinical and Experimental Aspects (8th 2006 Mackinac Island, Mich.). Neuroprotective agents. Edited by Slikker William, Andrews Russell J, Trembly Bruce, and New York Academy of Sciences. Malden, MA: Blackwell Pub. on behalf of the New York Academy of Sciences, 2007.

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William, Slikker, Trembly Bruce, and International Conference on Neuroprotective Agents: Clinical and Experimental Aspects (5th ; : 2000 : Lake Tahoe, Nev.), eds. Neuroprotective agents: Fifth international conference. New York, N.Y: New York Academy of Sciences, 2001.

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William, Slikker, and Trembly Bruce, eds. Neuroprotective agents: Third international conference. New York: New York Academy of Sciences, 1997.

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International Conference on Neuroprotective Agents: Clinical and Experimental Aspects (9th 2008 Woods Hole, Mass.). Neuroprotective agents: Ninth international conference. Edited by Andrews Russell J. New York: New York Academy of Sciences, 2010.

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López-Muñoz, Francisco, Venkataramanujam Srinivasan, Domenico de Berardis, Cecilio Álamo, and Takahiro A. Kato, eds. Melatonin, Neuroprotective Agents and Antidepressant Therapy. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2803-5.

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Bruce, Trembly, Slikker William, and International Conference on Neuroprotective Agents: Clinical and Experimental Aspects (2nd : 1994 : Lake George, N.Y.), eds. Neuroprotective agents: Clinical and experimental aspects. New York: New York Academy of Sciences, 1995.

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V, Borlongan Cesario, Isacson Ole, and Sanberg Paul R, eds. Immunosuppressant analogs in neuroprotection. Totowa, N.J: Humana Press, 2003.

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V, Borlongan Cesario, Isacson Ole, and Sanberg Paul R, eds. Immunosuppressant analogs in neuroprotection. Totowa, N.J: Humana Press, 2003.

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V, Borlongan Cesario, Isacson Ole, and Sanberg Paul R, eds. Immunosuppressant analogs in neuroprotection. Totowa, N.J: Humana Press, 2003.

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Jain, K. K. The handbook of neuroprotection. New York: Humana Press, 2011.

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Book chapters on the topic "Neuroprotective agents"

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Jain, Kewal K. "Neuroprotective Agents." In The Handbook of Neuroprotection, 25–139. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-049-2_2.

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Jain, Kewal K. "Neuroprotective Agents." In Springer Protocols Handbooks, 45–173. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9465-6_2.

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Caltana, Laura R., and Alicia Brusco. "Cannabinoids: A Group of Promising Neuroprotective Agents." In Neuroprotective Natural Products, 321–39. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527803781.ch13.

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Dev, Kapil, and Rakesh Maurya. "Marine-Derived Anti-Alzheimer's Agents of Promise." In Neuroprotective Natural Products, 153–84. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527803781.ch7.

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Burlakova, Elena B. "Antioxidant Drugs as Neuroprotective Agents." In Alzheimer Disease, 313–17. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4615-8149-9_52.

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Volsko, Christina, and Ranjan Dutta. "Neuroprotective Agents: An Overview on the General Modes of Action." In Neuroprotective Natural Products, 7–21. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527803781.ch2.

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Pita, René, Eva Ramos, José Luis Marco-Contelles, and Alejandro Romero. "Melatonin as a Novel Therapeutic Agent Against Chemical Warfare Agents." In Melatonin, Neuroprotective Agents and Antidepressant Therapy, 177–91. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2803-5_14.

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Mahadik, Sahebarao P. "Gangliosides: New Generation of Neuroprotective Agents." In Emerging Strategies in Neuroprotection, 187–223. Boston, MA: Birkhäuser Boston, 1992. http://dx.doi.org/10.1007/978-1-4684-6796-3_10.

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Festoff, Barry W. "Clinical Potential of Agents That Affect Thrombin Signaling in Degenerative and Traumatic Neurologic Disorders." In Neuroprotective Signal Transduction, 221–41. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-475-7_12.

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Fernández-Moriano, Carlos, Elena González-Burgos, and Maria Pilar Gómez-Serranillos. "Lipid Peroxidation and Mitochondrial Dysfunction in Alzheimer's and Parkinson's Diseases: Role of Natural Products as Cytoprotective Agents." In Neuroprotective Natural Products, 107–51. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527803781.ch6.

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Conference papers on the topic "Neuroprotective agents"

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Merrill, Thomas L., Denise R. Merrill, and Jennifer E. Akers. "Localized Brain Tissue Cooling for Use During Intracranial Thrombectomy." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80083.

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The primary goal of current ischemic stroke treatment is quickly restoring blood perfusion. Recanalization is linked to improved neurological outcomes [1]. Resulting tissue necrosis, however, following a stroke has two causes: 1) ischemic injury and 2) reperfusion injury. Therefore, development of neuroprotective agents specifically beneficial against reperfusion injury are required.
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Alza, Natalia, Valeria Cavallaro, Oriana Benzi Juncos, Ana Murray, and Gabriela Salvador. "&lt;em&gt;Cyclolepis genistoides&lt;/em&gt; aqueous extract as source of neuroprotective agents." In 7th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11536.

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Taraboletti, Alexandra, and Albert J. Fornace. "Abstract 3744: Repurposing the neuroprotective agent dimethyl fumarate against white matter damage and cognitive decline after radiotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3744.

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Taraboletti, Alexandra, and Albert J. Fornace. "Abstract 3744: Repurposing the neuroprotective agent dimethyl fumarate against white matter damage and cognitive decline after radiotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3744.

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Tosatti, Jéssica, Adriana Fontes, Paulo Caramelli, and Karina Gomes. "EFFECTS OF RESVERATROL SUPPLEMENTATION ON THE COGNITIVE FUNCTION OF PATIENTS WITH ALZHEIMER’S DISEASE: A META-ANALYSIS OF RANDOMIZED CONTROLLED TRIALS." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda026.

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Background: Alzheimer’s disease (AD) is characterized by a deposition of β-amyloid peptide and the neurofibrillary tangles of tau protein. Resveratrol is a neuroprotective agent, acting in the prevention of redox impairment, and could reduce neuronal damage in patients with AD. Objectives: Systematic review and meta-analysis about the effects of resveratrol supplementation on cognitive and functional performance in patients with AD. Methods: Databases were searched for primary studies that reported cognitive and functional performance based on ADAS-cog, ADCS-ADL or MMSE instruments in AD patients treated with resveratrol. Primary studies published up to May 2021 and without language and publication date restrictions were included. The measure of effect of the meta-analysis was presented as weighted mean difference (WMD). decrease in ADAS-cog scores [WMD: -3.69 points], and significant increases in ADCS-ADL [WMD: 5.65 points] and MMSE scores [WMD: 2.03 points] in the resveratrol intervention group, when compared to the placebo group. Conclusions: Resveratrol supplementation may result in improving cognitive and functional performance in AD patients.
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Abd. Aziz, N. A. W., R. Agarwal, A. Abd Latiff, and N. M. Ismail. "RESVERATROL AS A POTENTIAL AGENT FOR NEUROPROTECTION AGAINST INTRACEREBRAL HEMORRHAGE: INSIGHT ON THE ROLE OF ADENOSINE A1 RECEPTORS." In MedChem-Russia 2021. 5-я Российская конференция по медицинской химии с международным участием «МедХим-Россия 2021». Издательство Волгоградского государственного медицинского университета, 2021. http://dx.doi.org/10.19163/medchemrussia2021-2021-88.

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Smith, Katisha D., and Liang Zhu. "Theoretical Evaluation of a Simple Cooling Pad Inducing Hypothermia in the Spinal Cord Following Traumatic Injury." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206190.

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Although significant damage is caused by the mechanics of the traumatic spinal cord injury (SCI), secondary injury that follows is often times even more dangerous. It occurs within the first 12–24 hours following the injury and can last up to 5–10 days, depending on the severity of the injury [1]. Secondary injury causes physiological disturbances that disrupt the body’s homeostasis like initiating a cellular inflammatory response at the injury site and increasing the release of free radicals. An overabundance of free radicals contributes to tissue ischemia, cerebral edema, and disruption of the spine-blood barrier. The use of hypothermia (<35°C) as a therapeutic agent has been shown effective in providing neuroprotection from secondary injury [2]. Research has shown the benefits of hypothermia include decreasing oxygen consumption, free radical generation, neurotransmitter release, inflammation, and metabolic demands [3–5]. Even a temperature decrease of 1–2°C can be beneficial at the cellular level [4,6]. However, these studies use techniques that can be invasive. This research evaluates the effectiveness of using a non-invasive cooling pad on the torso to reduce the spinal cord temperature by at least 2°C.
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Reports on the topic "Neuroprotective agents"

1

Shih, Tsung-Ming A., Steven M. Duniho, and John H. McDonough. Control of Nerve Agent-Induced Seizures is Critical for Neuroprotection and Survival. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada417799.

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Luan, Sisi, Wenke Cheng, Chenglong Wang, Hongjian Gong, and Jianbo Zhou. Impact of glucagon-like peptide 1 analogs on cognitive function among patients with type 2 diabetes mellitus. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0015.

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Review question / Objective: Diabetes is an independent risk factor for cognitive impairment. Little is known regarding the neuroprotective effects of glucagon-like peptide 1 (GLP-1) analogs on type 2 diabetes mellitus (T2DM).Here, the study aim to assess the impact of GLP-1 on general cognition function among patients with T2DM. Eligibility criteria: Inclusion criteria were as follows: (1) an original article was recently published in English, (2) the population included subjects diagnosed with diabetes at baseline, (3) GLP-1 analogs is a single formulation rather than a fixed dose combination, (4) GLP-1 analogs were compared with no GLP-1 use or placebo or self-control before treatment, (5) the duration of antidiabetic agent use was 12 weeks or more, and (6) it provided quantitative measures of general cognitive function assessed by MMSE or MoCA. Exclusion criteria were as follows: (1) the publication was a review, case report, animal study, or letter to the editor, (2) the study did not clearly define clinical outcomes, (3) the authors could not provide valid data after being contacted, (4) duplicated data.
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