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1 ium sulfate (MgSO4) has gained interest as a neuroprotective agent.
2 oprotective components may have utility as a neuroprotective agent.
3 mportant features necessary for an effective neuroprotective agent.
4 ng therapeutic potential for compound 1 as a neuroprotective agent.
5 unction of carnosine may be as an endogenous neuroprotective agent.
6 059, a MEK1-specific antagonist, is a potent neuroprotective agent.
7 the way toward its clinical development as a neuroprotective agent.
8 rs not to recruit activin A as an endogenous neuroprotective agent.
9 rentiation and has also been implicated as a neuroprotective agent.
10 nimine oxide (23) was shown as a very potent neuroprotective agent.
11 of its catabolic product adenosine, a potent neuroprotective agent.
12  were similar to those of memantine, a known neuroprotective agent.
13 ic-induced Parkinsonism and the discovery of neuroprotective agents.
14 ugs (NSAIDs) have been explored as potential neuroprotective agents.
15 ovide a useful system for screening putative neuroprotective agents.
16 on and that alpha7 antagonists may be useful neuroprotective agents.
17  gp120 causes cell death and to characterize neuroprotective agents.
18 elected four compounds to study as potential neuroprotective agents.
19 ideal clinical model for neuroprotection and neuroprotective agents.
20 ly used as anesthetics, anticonvulsants, and neuroprotective agents.
21 way, and PARG inhibitors may have promise as neuroprotective agents.
22 is therefore a target for the development of neuroprotective agents.
23 cers of apoptosis, photodynamic therapy, and neuroprotective agents.
24 ntageous when used in conjunction with other neuroprotective agents.
25 e remains an attractive target for potential neuroprotective agents.
26 mia, this model has been used for evaluating neuroprotective agents.
27  for biologic immunomodulatory treatments as neuroprotective agents.
28 hus, EphA2 targeted antagonists may serve as neuroprotective agents.
29 g of a novel generation of disease-modifying neuroprotective agents.
30 nds leading to development of more effective neuroprotective agents.
31 gents has hindered earlier phase 3 trials of neuroprotective agents.
32 nal swelling that consequently will serve as neuroprotective agents.
33 hus serve as a model for a new generation of neuroprotective agents.
34 test) nitrones 1-3, 6, 7, and 9 proved to be neuroprotective agents.
35 ic neuropathy and search for IOP-independent neuroprotective agents.
36 ggest the possible use of such inhibitors as neuroprotective agents.
37 ession and to determine efficacy of putative neuroprotective agents.
38 Parkinson's disease and for testing putative neuroprotective agents.
39 tration of the female sex steroid and potent neuroprotective agent, 17beta-estradiol, reduced ischemi
40 uopathies and, therefore, ideal for studying neuroprotective agents, 4R-tauopathies are still severe
41                             To develop novel neuroprotective agents, a library of novel arylalkenylpr
42 st that HB-EGF may function as an endogenous neuroprotective agent after seizure-induced neural activ
43                       However, its role as a neuroprotective agent after spinal cord injury (SCI), or
44 traumatic brain injury and may find use as a neuroprotective agent against acute and delayed neurodeg
45 light the potential of this bio-residue as a neuroprotective agent against AD in pharmaceutical and n
46 e potential of compound 37 as a BBB-permeant neuroprotective agent against H2O2-induced oxidative str
47 es CholesteroNitrone 2 as an antioxidant and neuroprotective agent against ischemic injury.
48 b behaves as a water-soluble, brain-permeant neuroprotective agent against oxidative insults without
49 erefore, betaxolol has the potential to be a neuroprotective agent against retinal degeneration in pa
50  the in vivo effectiveness of memantine as a neuroprotective agent against rotenone-induced retinal t
51  suggest that steroid hormones have roles as neuroprotective agents against demyelination and augment
52 inside the mitochondrial matrix and acted as neuroprotective agents against iron(III), hydrogen perox
53 ehensive drug discovery platform to identify neuroprotective agents against vincristine-induced neuro
54 trate that a small peptide can function as a neuroprotective agent and an activator of a beneficial s
55   The combined data show that betaxolol is a neuroprotective agent and attenuates the effects on the
56 tudy was to determine whether betaxolol is a neuroprotective agent and can therefore slow down the ch
57   Animal model studies suggest nicotine as a neuroprotective agent and nicotinic acetylcholine (ACh)
58   These findings extend the role of ANG as a neuroprotective agent and underscore its potential utili
59 alue of tetrahydrobenzothiazole analogues as neuroprotective agents and (ii) define the structural re
60              Additionally, several potential neuroprotective agents and strategies have been tested i
61 n of responses of the blood transcriptome to neuroprotective agents and subsequent stroke through the
62                         The search for ideal neuroprotective agents and techniques for timely injury
63 ing data showing that bexarotene is a potent neuroprotective agent, and identify a novel autophagy-mo
64 iety of agents such as volatile anesthetics, neuroprotective agents, and antidepressants.
65 gonists and inverse agonists have emerged as neuroprotective agents, and CB2R agonists have entered s
66 loads, including cytokines, toxins, enzymes, neuroprotective agents, and soluble factor traps.
67 ective HDAC8 inhibitor PCI-34051 is a potent neuroprotective agent; and by taking advantage of both p
68 , the topical administration of the selected neuroprotective agents appears useful in preventing the
69  regimen of the SMN2 inducer D156844 and the neuroprotective agent AR42 (REC-2282) on the disease pro
70 eurological disorders, and for how potential neuroprotective agents are screened for use in patients
71 cts of neural injury and that treatment with neuroprotective agents at the time of injury can reduce
72           There are many promising candidate neuroprotective agents based on pathological and laborat
73    We describe a novel role for gremlin as a neuroprotective agent both in vitro and in vivo and show
74  In the current study, it was found that the neuroprotective agent brain-derived neurotrophic factor
75 ially useful outcome measure in PD trials of neuroprotective agents, but further work is required to
76  levodopa, carbidopa, hyperbaric oxygen, and neuroprotective agents, but no proven effective treatmen
77 a beta(1)-adrenoceptor antagonist, acts as a neuroprotective agent by interacting with sodium and L-t
78 3-Arylcoumarins have already been studied as neuroprotective agents by our group.
79  detail through advanced imaging modalities, neuroprotective agents can and should be re-examined as
80                           Three experimental neuroprotective agents (clomethiazole, AR-R15896AR and N
81 orm, and mouse behavior models, an effective neuroprotective agent CN016 was discovered.
82 death could be studied and in which putative neuroprotective agents could be screened.
83 for the identification and implementation of neuroprotective agents could provide novel therapeutics
84 h appears to be a promising neurotrophic and neuroprotective agent deserving further investigation.
85 5 behaved as a safe and metabolically stable neuroprotective agent, devoid of cytochrome liability.
86 spheres (MSs) incorporating three recognised neuroprotective agents (dexamethasone (DX), melatonin (M
87 tency as a PARP-1 inhibitor and potency as a neuroprotective agent during MNNG incubations, with the
88 have been several small clinical trials with neuroprotective agents, early recognition and supportive
89 ogesterone, in its own right, is a potential neuroprotective agent following acute cerebral injury.
90  is currently under clinical assessment as a neuroprotective agent following acute ischemic stroke.
91 or isradipine is currently being tested as a neuroprotective agent for PD in a phase III clinical tri
92  is currently under clinical evaluation as a neuroprotective agent for stroke.
93  currently in clinical trials as a potential neuroprotective agent for the control of the cerebral da
94 lial activation, and MIF could be a valuable neuroprotective agent for the treatment of ICH.
95          VIP emerges as a potential valuable neuroprotective agent for the treatment of pathologic co
96         Therefore, VIP emerges as a valuable neuroprotective agent for the treatment of pathologic co
97  suggests that minocycline may be a valuable neuroprotective agent for the treatment of PD.
98 of clinical trials examining the benefits of neuroprotective agents for glaucoma currently limit the
99 these pathways, most importantly to identify neuroprotective agents for Parkinson's disease, and/or e
100 pport the use of VIPR2-selective agonists as neuroprotective agents for PD treatment.
101 vonoids can function as potent and effective neuroprotective agents for retinal ganglion cells.
102  need to be considered in the development of neuroprotective agents for stroke.
103  of using endothelin receptor antagonists as neuroprotective agents for the treatment of glaucoma.
104  of JNKs with the mitochondria may be useful neuroprotective agents for the treatment of Parkinson di
105                        However, its use as a neuroprotective agent has been hampered due to its low s
106                        Delayed initiation of neuroprotective agents has hindered earlier phase 3 tria
107                    Although many potentially neuroprotective agents have been investigated, the simpl
108                                Currently, no neuroprotective agents have been shown to impact the cli
109                            Although numerous neuroprotective agents have not shown benefit, trials of
110                          Estrogen is a known neuroprotective agent; however, the diverse mechanisms o
111 d thrombolysis; and 2) could be an efficient neuroprotective agent if given after tissue plasminogen
112                   Here we evaluate CNTF as a neuroprotective agent in a nonhuman primate model of Hun
113      However, C3 has not been evaluated as a neuroprotective agent in a Parkinson model in vivo.
114 he effectiveness of aminoguanidine (AG) as a neuroprotective agent in a rat model of transient middle
115     These results further establish EPO as a neuroprotective agent in acute neuronal ischemic injury.
116  been shown to be a cognition-preserving and neuroprotective agent in animal brain injury models, con
117 ate receptor-channel complex and a promising neuroprotective agent in animal models of focal brain is
118 vious studies support NGP1-01 as a promising neuroprotective agent in diseases involving calcium-rela
119     L-Carnosine has shown great promise as a neuroprotective agent in experimental stroke, but transl
120  neurotrophic factor (CNTF) acts as a potent neuroprotective agent in multiple retinal degeneration a
121  the potential of safinamide as an effective neuroprotective agent in multiple sclerosis, and implica
122 peptide provides the features of a promising neuroprotective agent in newborns with brain injury.
123 ort, enantioselective synthesis provides the neuroprotective agent in optically pure form.
124  In vivo efficacy of 15 makes it a promising neuroprotective agent in oxidative stress-related diseas
125  intestinal peptide (VIP) is an acknowledged neuroprotective agent in peripheral, including enteric,
126  responses, and CXCL10 may represent a novel neuroprotective agent in response to WNV infection in th
127   While haloperidol was found to be a potent neuroprotective agent in this in vitro cell assay, the p
128 ents, anticoagulants, antiplatelet drugs and neuroprotective agents in acute stroke patients.
129 semide and related agents might be useful as neuroprotective agents in alcohol abuse.
130 icularly 17beta-estradiol (E2), are powerful neuroprotective agents in animal models of cerebral isch
131 hy, and evaluating the efficacy of potential neuroprotective agents in clinical trials.
132  have relevance to researchers investigating neuroprotective agents in mixed sex experiments.
133 proposed as an outcome measure in studies of neuroprotective agents in multiple sclerosis, yet potent
134 erence to the potential development of novel neuroprotective agents in Parkinson's disease.
135 value for assessing the efficacy of putative neuroprotective agents in PD is considered.
136 hlight the potential of thiol peroxidases as neuroprotective agents in PD patients carrying LRRK2 mut
137 re promising candidates for further study as neuroprotective agents in PD.
138                                   The use of neuroprotective agents in stroke has been a notable fail
139 nvestigating the distribution and effects of neuroprotective agents in the brain.
140 tion may hold particular promise as powerful neuroprotective agents in the treatment of PD.
141  been re-investigated for their potential as neuroprotective agents, including beta-lactam antibiotic
142 nstant light by the application of exogenous neuroprotective agents, including brain-derived neurotro
143                                 Furthermore, neuroprotective agents, including fenofibrate and simvas
144      With the prospects of myelin repair and neuroprotective agents increasingly becoming recognized
145 t synthesis enables gram-scale access to the neuroprotective agent (+/-)-indanostatin.
146                             In addition, the neuroprotective agents KCl and chlorophenylthio-cAMP are
147 to examine a possible role of the endogenous neuroprotective agent kynurenate (KYNA) in this phenomen
148 ble to access the brain, CsA is an effective neuroprotective agent mainly due to its protection of mi
149 jury in preterm infants during a period when neuroprotective agents may be especially effective.
150 ommon pathways, raising the possibility that neuroprotective agents may have broad applicability in t
151 coma based on the premise that any potential neuroprotective agent must be administered orally, have
152 a support further evaluation of NGP1-01 as a neuroprotective agent, not only in diseases associated w
153 t that NXY-059 was by far the most effective neuroprotective agent of the three examined.
154                                      Several neuroprotective agents offer promise when combined with
155 ocampal neurons, and that treatment with the neuroprotective agent P7C3-A20 eradicates persistent rem
156 ially reported and revised structures of the neuroprotective agent palmyrolide A are reported.
157  the neurotoxin, quinolinic acid (QUIN), the neuroprotective agent, picolinic acid (PIC), the T(H)17/
158 to determine whether the glial modulator and neuroprotective agent propentofylline (PPF) modifies dru
159  Furthermore, M30, a derivative of VK-28 and neuroprotective agent rasagiline, may serve as a better
160 nsistent with a model of statins that act as neuroprotective agents rather than inhibitors of beta-am
161 s of lycibarbarines A and B which are potent neuroprotective agents recently isolated from the fruits
162        Bath application of compound T-588, a neuroprotective agent, reduced paired-pulse and repetiti
163 erebellar ataxia, and SK openers such as the neuroprotective agent riluzole may reduce neuronal hyper
164 racellular acidification, enhancement by the neuroprotective agent riluzole, and outward rectificatio
165 n assays and future evaluations of DIDS as a neuroprotective agent should incorporate multiple viabil
166                                          The neuroprotective agent sipatrigine (10 microM) inhibited
167 our findings demonstrate that NR is a better neuroprotective agent than NAD(+) in excitotoxicity-indu
168  which is a better anticonvulsant but weaker neuroprotective agent than sipatrigine, was a far less e
169             Erythropoietin (EPO) is a potent neuroprotective agent that could be developed as a new t
170 arbamylated erythropoietin (CEPO) is a novel neuroprotective agent that does not bind to the classica
171            Recombinant human VEGF-A165b is a neuroprotective agent that effectively protects both per
172   These findings support TAT-CBD3 as a novel neuroprotective agent that may increase neuronal surviva
173 research, and focus on a few key examples of neuroprotective agents that are showing newfound promise
174  reduce the potential side effect profile of neuroprotective agents that can influence neurotransmiss
175          This may lead to the development of neuroprotective agents that change the course of schizop
176 ved neurotrophic factor (BDNF) are potential neuroprotective agents that could be used in the treatme
177 zed, will set the stage for efficient use of neuroprotective agents that could slow down and alter th
178 mpared the therapeutic ratios of a number of neuroprotective agents that have undergone clinical tria
179 ave great potential to become a peripherally neuroprotective agent to prevent neurotoxicity caused by
180 rrhage rate, is particularly useful to study neuroprotective agents to attenuate embolism-induced hem
181 d be targeted in future clinical trials with neuroprotective agents to prevent the development of pro
182                                  Riluzole, a neuroprotective agent used clinically to slow the progre
183 gh this does not rule out a role for AG as a neuroprotective agent via its ability to inhibit iNOS, t
184            Because nicotine is known to be a neuroprotective agent, we propose that it can prevent ar
185                               Other putative neuroprotective agents were much less effective in this
186                       Estrogen is a powerful neuroprotective agent with the ability to induce trophic
187    Thus, Tat-N-dimer is a highly efficacious neuroprotective agent with therapeutic potential in stro

 
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