ライフサイエンスコーパス: neuroprotective therapy

1 61) as a valid target for the development of neuroprotective therapy.

2 h greater than that from currently available neuroprotective therapy.

3 ting a novel avenue of anti-inflammatory and neuroprotective therapy.

4 or the development of disease biomarkers and neuroprotective therapies.

5 ell as the PTP, as a potential target for MS neuroprotective therapies.

6 vestigation to identify novel candidates for neuroprotective therapies.

7 lso have the potential to form the basis for neuroprotective therapies.

8 unities to evaluate potential alphaSYN-based neuroprotective therapies.

9 otential anti-inflammatory, remyelinating or neuroprotective therapies.

10 enesis of Parkinson's disease and developing neuroprotective therapies.

11 desirable for developing the most effective neuroprotective therapies.

12 and who would thus be suitable for putative neuroprotective therapies.

13 toxicity is crucial for developing effective neuroprotective therapies against ADC.

14 This study may prompt development of new neuroprotective therapies aimed at the immune system, to

15 an important but often overlooked effect of neuroprotective therapy, analogous to the protective eff

16 The lack of neuroprotective therapies and the limited treatment stra

17 ents recent advances in the understanding of neuroprotective therapy and brain-specific monitoring fo

18 ioning (IPC) is gaining attention as a novel neuroprotective therapy and could provide an improved me

19 clinical efficacy of new treatments, such as neuroprotective therapies, and help stratify this hetero

20 A major hurdle in development of neuroprotective therapies are due to limited understandi

21 mptoms but induce dyskinesias over time, and neuroprotective therapies are nonexistent.

22 potentially ideal targets for development of neuroprotective therapies, because candidate drugs can b

23 tion could be used to advance the search for neuroprotective therapies for Parkinson's disease.

24 New powerful neuroprotective therapies for PD might be considered by

25 e coming decade for developing and achieving neuroprotective therapies for PD.

26 Current glaucoma research targets neuroprotective therapies for retinal ganglion cells (RG

27 X pathway could become a promising target of neuroprotective therapies for the aging brain.

28 e MHCII signaling complex may be a target of neuroprotective therapies for the disease.

29 the design of clinical trials investigating neuroprotective therapies for the disease.

30 efully will lead to the development of novel neuroprotective therapies for the disorder.

31 dying etiopathogenic mechanisms and putative neuroprotective therapies for the illness.

32 mplications for the development of effective neuroprotective therapies for these incurable illnesses.

33 The concept of neuroprotective therapy for acute ischemic stroke to sal

34 ility of targeting the JAK/STAT pathway as a neuroprotective therapy for neurodegenerative diseases.

35 lore potential use of these compounds in the neuroprotective therapy for PD.

36 tive agent rasagiline, may serve as a better neuroprotective therapy for PD.

37 blood-brain barrier, DbetaHB may be a novel neuroprotective therapy for PD.

38 R Stat3 expression has potential as a common neuroprotective therapy for these disorders, and (iii) i

39 To evaluate this potential neuroprotective therapy further, we determined the effec

40 Neuroprotective therapies have been proposed but none ha

41 e could have potential therapeutic value for neuroprotective therapies in ischemic stroke and other n

42 on astrocytes may represent a new target for neuroprotective therapies in MS.

43 val pathways that could serve as targets for neuroprotective therapies in preventing this disabling n

44 Obstacles to the development of a neuroprotective therapy in PD include: (1) uncertainty a

45 pt should be further evaluated as a possible neuroprotective therapy in PD.

46 hat ET(B) receptor activation may be a novel neuroprotective therapy in the treatment of focal ischem

47 ogression, there is a need for an adjunctive neuroprotective therapy in this population.

48 axonal toxicity may provide new targets for neuroprotective therapy in WM diseases.

49 The main obstacle to developing neuroprotective therapies is a limited understanding of

50 nce the discovery of L-dopa in the 1960s, no neuroprotective therapy is yet available.

51 o understand the utility of new and presumed neuroprotective therapies like hypothermia and avoidance

52 These results suggest that adjunctive neuroprotective therapy may reduce collateral damage to

53 mpared with treating injured brain tissue in neuroprotective therapy might more readily help with tra

54 Recently, the neuroprotective therapy of hypothermia has emerged as th

55 e CaN-Drp1 complex as a potential target for neuroprotective therapy of ischemic stroke.

56 gonists has implications for symptomatic and neuroprotective therapy of various neuropsychiatric dise

57 Neuroprotective therapy primarily targets the biochemica

58 Neuroprotective therapy remains an elusive goal for the

59 ese findings have important implications for neuroprotective therapies that directly target OL surviv

60 gic agents with a relatively long half-life, neuroprotective therapies that prevent the loss of dopam

61 The development of neuroprotective therapies that target these mechanisms m

62 The development of a neuroprotective therapy that slows, stops, or reverses n

63 esearch are now beginning to bring candidate neuroprotective therapies to clinical trials.

64 er of insult severity is desirable to target neuroprotective therapies to patients most likely to ben

65 For neuroprotective therapy to be effective, it is important

66 These data provide new targets for neuroprotective therapies via optimizing AC-driven plast

67 n particular forced exercise, as a potential neuroprotective therapy when implemented before and afte

68 Development of neuroprotective therapies will require elucidation of th

69 rtant therapeutic target for postreperfusion neuroprotective therapies, with treatment efficacy monit

70 that it could provide the basis for a novel neuroprotective therapy worthy of further investigation.