ライフサイエンスコーパス: neuroprotective agent

1 ng therapeutic potential for compound 1 as a neuroprotective agent.

2 unction of carnosine may be as an endogenous neuroprotective agent.

3 059, a MEK1-specific antagonist, is a potent neuroprotective agent.

4 rs not to recruit activin A as an endogenous neuroprotective agent.

5 rentiation and has also been implicated as a neuroprotective agent.

6 of its catabolic product adenosine, a potent neuroprotective agent.

7 were similar to those of memantine, a known neuroprotective agent.

8 ium sulfate (MgSO4) has gained interest as a neuroprotective agent.

9 oprotective components may have utility as a neuroprotective agent.

10 mportant features necessary for an effective neuroprotective agent.

11 gp120 causes cell death and to characterize neuroprotective agents.

12 ideal clinical model for neuroprotection and neuroprotective agents.

13 ly used as anesthetics, anticonvulsants, and neuroprotective agents.

14 way, and PARG inhibitors may have promise as neuroprotective agents.

15 is therefore a target for the development of neuroprotective agents.

16 cers of apoptosis, photodynamic therapy, and neuroprotective agents.

17 ntageous when used in conjunction with other neuroprotective agents.

18 e remains an attractive target for potential neuroprotective agents.

19 mia, this model has been used for evaluating neuroprotective agents.

20 gents has hindered earlier phase 3 trials of neuroprotective agents.

21 nal swelling that consequently will serve as neuroprotective agents.

22 hus, EphA2 targeted antagonists may serve as neuroprotective agents.

23 hus serve as a model for a new generation of neuroprotective agents.

24 test) nitrones 1-3, 6, 7, and 9 proved to be neuroprotective agents.

25 ic neuropathy and search for IOP-independent neuroprotective agents.

26 ggest the possible use of such inhibitors as neuroprotective agents.

27 ession and to determine efficacy of putative neuroprotective agents.

28 Parkinson's disease and for testing putative neuroprotective agents.

29 ugs (NSAIDs) have been explored as potential neuroprotective agents.

30 ovide a useful system for screening putative neuroprotective agents.

31 on and that alpha7 antagonists may be useful neuroprotective agents.

32 tration of the female sex steroid and potent neuroprotective agent, 17beta-estradiol, reduced ischemi

33 To develop novel neuroprotective agents, a library of novel arylalkenylpr

34 st that HB-EGF may function as an endogenous neuroprotective agent after seizure-induced neural activ

35 However, its role as a neuroprotective agent after spinal cord injury (SCI), or

36 traumatic brain injury and may find use as a neuroprotective agent against acute and delayed neurodeg

37 e potential of compound 37 as a BBB-permeant neuroprotective agent against H2O2-induced oxidative str

38 es CholesteroNitrone 2 as an antioxidant and neuroprotective agent against ischemic injury.

39 b behaves as a water-soluble, brain-permeant neuroprotective agent against oxidative insults without

40 erefore, betaxolol has the potential to be a neuroprotective agent against retinal degeneration in pa

41 the in vivo effectiveness of memantine as a neuroprotective agent against rotenone-induced retinal t

42 suggest that steroid hormones have roles as neuroprotective agents against demyelination and augment

43 trate that a small peptide can function as a neuroprotective agent and an activator of a beneficial s

44 The combined data show that betaxolol is a neuroprotective agent and attenuates the effects on the

45 tudy was to determine whether betaxolol is a neuroprotective agent and can therefore slow down the ch

46 Animal model studies suggest nicotine as a neuroprotective agent and nicotinic acetylcholine (ACh)

47 alue of tetrahydrobenzothiazole analogues as neuroprotective agents and (ii) define the structural re

48 Additionally, several potential neuroprotective agents and strategies have been tested i

49 n of responses of the blood transcriptome to neuroprotective agents and subsequent stroke through the

50 The search for ideal neuroprotective agents and techniques for timely injury

51 ing data showing that bexarotene is a potent neuroprotective agent, and identify a novel autophagy-mo

52 iety of agents such as volatile anesthetics, neuroprotective agents, and antidepressants.

53 gonists and inverse agonists have emerged as neuroprotective agents, and CB2R agonists have entered s

54 ective HDAC8 inhibitor PCI-34051 is a potent neuroprotective agent; and by taking advantage of both p

55 eurological disorders, and for how potential neuroprotective agents are screened for use in patients

56 cts of neural injury and that treatment with neuroprotective agents at the time of injury can reduce

57 There are many promising candidate neuroprotective agents based on pathological and laborat

58 We describe a novel role for gremlin as a neuroprotective agent both in vitro and in vivo and show

59 In the current study, it was found that the neuroprotective agent brain-derived neurotrophic factor

60 ially useful outcome measure in PD trials of neuroprotective agents, but further work is required to

61 levodopa, carbidopa, hyperbaric oxygen, and neuroprotective agents, but no proven effective treatmen

62 a beta(1)-adrenoceptor antagonist, acts as a neuroprotective agent by interacting with sodium and L-t

63 detail through advanced imaging modalities, neuroprotective agents can and should be re-examined as

64 Three experimental neuroprotective agents (clomethiazole, AR-R15896AR and N

65 death could be studied and in which putative neuroprotective agents could be screened.

66 h appears to be a promising neurotrophic and neuroprotective agent deserving further investigation.

67 tency as a PARP-1 inhibitor and potency as a neuroprotective agent during MNNG incubations, with the

68 have been several small clinical trials with neuroprotective agents, early recognition and supportive

69 ogesterone, in its own right, is a potential neuroprotective agent following acute cerebral injury.

70 is currently under clinical assessment as a neuroprotective agent following acute ischemic stroke.

71 or isradipine is currently being tested as a neuroprotective agent for PD in a phase III clinical tri

72 is currently under clinical evaluation as a neuroprotective agent for stroke.

73 currently in clinical trials as a potential neuroprotective agent for the control of the cerebral da

74 lial activation, and MIF could be a valuable neuroprotective agent for the treatment of ICH.

75 VIP emerges as a potential valuable neuroprotective agent for the treatment of pathologic co

76 Therefore, VIP emerges as a valuable neuroprotective agent for the treatment of pathologic co

77 suggests that minocycline may be a valuable neuroprotective agent for the treatment of PD.

78 of clinical trials examining the benefits of neuroprotective agents for glaucoma currently limit the

79 these pathways, most importantly to identify neuroprotective agents for Parkinson's disease, and/or e

80 pport the use of VIPR2-selective agonists as neuroprotective agents for PD treatment.

81 vonoids can function as potent and effective neuroprotective agents for retinal ganglion cells.

82 need to be considered in the development of neuroprotective agents for stroke.

83 of using endothelin receptor antagonists as neuroprotective agents for the treatment of glaucoma.

84 of JNKs with the mitochondria may be useful neuroprotective agents for the treatment of Parkinson di

85 However, its use as a neuroprotective agent has been hampered due to its low s

86 Delayed initiation of neuroprotective agents has hindered earlier phase 3 tria

87 Although many potentially neuroprotective agents have been investigated, the simpl

88 Although numerous neuroprotective agents have not shown benefit, trials of

89 d thrombolysis; and 2) could be an efficient neuroprotective agent if given after tissue plasminogen

90 Here we evaluate CNTF as a neuroprotective agent in a nonhuman primate model of Hun

91 However, C3 has not been evaluated as a neuroprotective agent in a Parkinson model in vivo.

92 he effectiveness of aminoguanidine (AG) as a neuroprotective agent in a rat model of transient middle

93 These results further establish EPO as a neuroprotective agent in acute neuronal ischemic injury.

94 been shown to be a cognition-preserving and neuroprotective agent in animal brain injury models, con

95 ate receptor-channel complex and a promising neuroprotective agent in animal models of focal brain is

96 vious studies support NGP1-01 as a promising neuroprotective agent in diseases involving calcium-rela

97 neurotrophic factor (CNTF) acts as a potent neuroprotective agent in multiple retinal degeneration a

98 the potential of safinamide as an effective neuroprotective agent in multiple sclerosis, and implica

99 peptide provides the features of a promising neuroprotective agent in newborns with brain injury.

100 ort, enantioselective synthesis provides the neuroprotective agent in optically pure form.

101 intestinal peptide (VIP) is an acknowledged neuroprotective agent in peripheral, including enteric,

102 responses, and CXCL10 may represent a novel neuroprotective agent in response to WNV infection in th

103 While haloperidol was found to be a potent neuroprotective agent in this in vitro cell assay, the p

104 ents, anticoagulants, antiplatelet drugs and neuroprotective agents in acute stroke patients.

105 semide and related agents might be useful as neuroprotective agents in alcohol abuse.

106 icularly 17beta-estradiol (E2), are powerful neuroprotective agents in animal models of cerebral isch

107 hy, and evaluating the efficacy of potential neuroprotective agents in clinical trials.

108 have relevance to researchers investigating neuroprotective agents in mixed sex experiments.

109 proposed as an outcome measure in studies of neuroprotective agents in multiple sclerosis, yet potent

110 erence to the potential development of novel neuroprotective agents in Parkinson's disease.

111 value for assessing the efficacy of putative neuroprotective agents in PD is considered.

112 hlight the potential of thiol peroxidases as neuroprotective agents in PD patients carrying LRRK2 mut

113 re promising candidates for further study as neuroprotective agents in PD.

114 The use of neuroprotective agents in stroke has been a notable fail

115 nvestigating the distribution and effects of neuroprotective agents in the brain.

116 tion may hold particular promise as powerful neuroprotective agents in the treatment of PD.

117 been re-investigated for their potential as neuroprotective agents, including beta-lactam antibiotic

118 nstant light by the application of exogenous neuroprotective agents, including brain-derived neurotro

119 With the prospects of myelin repair and neuroprotective agents increasingly becoming recognized

120 In addition, the neuroprotective agents KCl and chlorophenylthio-cAMP are

121 to examine a possible role of the endogenous neuroprotective agent kynurenate (KYNA) in this phenomen

122 ble to access the brain, CsA is an effective neuroprotective agent mainly due to its protection of mi

123 jury in preterm infants during a period when neuroprotective agents may be especially effective.

124 ommon pathways, raising the possibility that neuroprotective agents may have broad applicability in t

125 coma based on the premise that any potential neuroprotective agent must be administered orally, have

126 a support further evaluation of NGP1-01 as a neuroprotective agent, not only in diseases associated w

127 t that NXY-059 was by far the most effective neuroprotective agent of the three examined.

128 Several neuroprotective agents offer promise when combined with

129 ially reported and revised structures of the neuroprotective agent palmyrolide A are reported.

130 the neurotoxin, quinolinic acid (QUIN), the neuroprotective agent, picolinic acid (PIC), the T(H)17/

131 to determine whether the glial modulator and neuroprotective agent propentofylline (PPF) modifies dru

132 Furthermore, M30, a derivative of VK-28 and neuroprotective agent rasagiline, may serve as a better

133 nsistent with a model of statins that act as neuroprotective agents rather than inhibitors of beta-am

134 Bath application of compound T-588, a neuroprotective agent, reduced paired-pulse and repetiti

135 erebellar ataxia, and SK openers such as the neuroprotective agent riluzole may reduce neuronal hyper

136 racellular acidification, enhancement by the neuroprotective agent riluzole, and outward rectificatio

137 n assays and future evaluations of DIDS as a neuroprotective agent should incorporate multiple viabil

138 The neuroprotective agent sipatrigine (10 microM) inhibited

139 our findings demonstrate that NR is a better neuroprotective agent than NAD(+) in excitotoxicity-indu

140 which is a better anticonvulsant but weaker neuroprotective agent than sipatrigine, was a far less e

141 Erythropoietin (EPO) is a potent neuroprotective agent that could be developed as a new t

142 arbamylated erythropoietin (CEPO) is a novel neuroprotective agent that does not bind to the classica

143 Recombinant human VEGF-A165b is a neuroprotective agent that effectively protects both per

144 These findings support TAT-CBD3 as a novel neuroprotective agent that may increase neuronal surviva

145 research, and focus on a few key examples of neuroprotective agents that are showing newfound promise

146 reduce the potential side effect profile of neuroprotective agents that can influence neurotransmiss

147 This may lead to the development of neuroprotective agents that change the course of schizop

148 ved neurotrophic factor (BDNF) are potential neuroprotective agents that could be used in the treatme

149 zed, will set the stage for efficient use of neuroprotective agents that could slow down and alter th

150 mpared the therapeutic ratios of a number of neuroprotective agents that have undergone clinical tria

151 rrhage rate, is particularly useful to study neuroprotective agents to attenuate embolism-induced hem

152 d be targeted in future clinical trials with neuroprotective agents to prevent the development of pro

153 Riluzole, a neuroprotective agent used clinically to slow the progre

154 gh this does not rule out a role for AG as a neuroprotective agent via its ability to inhibit iNOS, t

155 Because nicotine is known to be a neuroprotective agent, we propose that it can prevent ar

156 Other putative neuroprotective agents were much less effective in this

157 Estrogen is a powerful neuroprotective agent with the ability to induce trophic

158 Thus, Tat-N-dimer is a highly efficacious neuroprotective agent with therapeutic potential in stro