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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 ative states, and potentially intervene with neuroprotective therapy.
5 nts a critical opportunity to intervene with neuroprotective therapy.
6 s closer to realizing ATP13A2's potential in neuroprotective therapy.
7 dria will therefore be central to developing neuroprotective therapies.
8 or the development of disease biomarkers and neuroprotective therapies.
9 unities to evaluate potential alphaSYN-based neuroprotective therapies.
10 ell as the PTP, as a potential target for MS neuroprotective therapies.
11 vestigation to identify novel candidates for neuroprotective therapies.
12 lso have the potential to form the basis for neuroprotective therapies.
13 t to intervene for the purpose of evaluating neuroprotective therapies.
14 otential anti-inflammatory, remyelinating or neuroprotective therapies.
15 enesis of Parkinson's disease and developing neuroprotective therapies.
16  desirable for developing the most effective neuroprotective therapies.
17  and who would thus be suitable for putative neuroprotective therapies.
18 ity of any given group forecasted to provide neuroprotective therapies.
19 e unlikely to be as successful as multimodal neuroprotective therapies.
20 toxicity is crucial for developing effective neuroprotective therapies against ADC.
21  Abeta-mediated oxidative stress, supporting neuroprotective therapies aimed at ameliorating defects
22 ent AB-mediated oxidative stress, supporting neuroprotective therapies aimed at ameliorating defects
23       These data open the possibility of new neuroprotective therapies aimed at SPN synapse function,
24     This study may prompt development of new neuroprotective therapies aimed at the immune system, to
25  an important but often overlooked effect of neuroprotective therapy, analogous to the protective eff
26                                  The lack of neuroprotective therapies and the limited treatment stra
27 ents recent advances in the understanding of neuroprotective therapy and brain-specific monitoring fo
28 ioning (IPC) is gaining attention as a novel neuroprotective therapy and could provide an improved me
29 clinical efficacy of new treatments, such as neuroprotective therapies, and help stratify this hetero
30             A major hurdle in development of neuroprotective therapies are due to limited understandi
31 mptoms but induce dyskinesias over time, and neuroprotective therapies are nonexistent.
32 fficacy of new treatments; however, previous neuroprotective therapies, based on systemic delivery in
33 potentially ideal targets for development of neuroprotective therapies, because candidate drugs can b
34 m of P5B ATPases, thereby paving the way for neuroprotective therapy by activating ATP13A2.
35 rmal SSH1 catalytic function may provide new neuroprotective therapies for AD and related dementias.
36 tion could be used to advance the search for neuroprotective therapies for Parkinson's disease.
37                                 New powerful neuroprotective therapies for PD might be considered by
38 e coming decade for developing and achieving neuroprotective therapies for PD.
39            Current glaucoma research targets neuroprotective therapies for retinal ganglion cells (RG
40 X pathway could become a promising target of neuroprotective therapies for the aging brain.
41 e MHCII signaling complex may be a target of neuroprotective therapies for the disease.
42  the design of clinical trials investigating neuroprotective therapies for the disease.
43 efully will lead to the development of novel neuroprotective therapies for the disorder.
44 dying etiopathogenic mechanisms and putative neuroprotective therapies for the illness.
45 mplications for the development of effective neuroprotective therapies for these incurable illnesses.
46                               The concept of neuroprotective therapy for acute ischemic stroke to sal
47 ility of targeting the JAK/STAT pathway as a neuroprotective therapy for neurodegenerative diseases.
48 lore potential use of these compounds in the neuroprotective therapy for PD.
49 tive agent rasagiline, may serve as a better neuroprotective therapy for PD.
50  blood-brain barrier, DbetaHB may be a novel neuroprotective therapy for PD.
51 R Stat3 expression has potential as a common neuroprotective therapy for these disorders, and (iii) i
52                   To evaluate this potential neuroprotective therapy further, we determined the effec
53 t challenges in the development of potential neuroprotective therapies has been the lack of reliable
54                                              Neuroprotective therapies have been proposed but none ha
55                                     Although neuroprotective therapies have been suggested to have th
56 diabetes mellitus, are emerging as promising neuroprotective therapies in Alzheimer's disease (AD) an
57 e could have potential therapeutic value for neuroprotective therapies in ischemic stroke and other n
58 on astrocytes may represent a new target for neuroprotective therapies in MS.
59 spose to greater responsiveness to metabolic neuroprotective therapies in OAG.
60 and 60%, respectively, of studies evaluating neuroprotective therapies in preclinical models.
61 val pathways that could serve as targets for neuroprotective therapies in preventing this disabling n
62            Obstacles to the development of a neuroprotective therapy in PD include: (1) uncertainty a
63 pt should be further evaluated as a possible neuroprotective therapy in PD.
64 eta2 may represent a target for prophylactic neuroprotective therapy in populations at high risk of s
65 hat ET(B) receptor activation may be a novel neuroprotective therapy in the treatment of focal ischem
66 ogression, there is a need for an adjunctive neuroprotective therapy in this population.
67 polarization (CSD) is a promising target for neuroprotective therapy in traumatic brain injury (TBI).
68  axonal toxicity may provide new targets for neuroprotective therapy in WM diseases.
69              The main obstacle to developing neuroprotective therapies is a limited understanding of
70 nce the discovery of L-dopa in the 1960s, no neuroprotective therapy is yet available.
71 o understand the utility of new and presumed neuroprotective therapies like hypothermia and avoidance
72        These results suggest that adjunctive neuroprotective therapy may reduce collateral damage to
73 mpared with treating injured brain tissue in neuroprotective therapy might more readily help with tra
74                                Recently, the neuroprotective therapy of hypothermia has emerged as th
75 e CaN-Drp1 complex as a potential target for neuroprotective therapy of ischemic stroke.
76 gonists has implications for symptomatic and neuroprotective therapy of various neuropsychiatric dise
77                                              Neuroprotective therapy primarily targets the biochemica
78                                              Neuroprotective therapy remains an elusive goal for the
79 gesting that the implementation of trials of neuroprotective therapies should focus on people with th
80  and ON pathology, undermining our candidate neuroprotective therapy, siCASP2.
81 tion after ischemia as a possible target for neuroprotective therapy.SIGNIFICANCE STATEMENT Brain isc
82 nts an exciting opportunity to develop novel neuroprotective therapies that can prevent or halt the d
83 ese findings have important implications for neuroprotective therapies that directly target OL surviv
84 d death worldwide, yet there are no approved neuroprotective therapies that improve neurological outc
85 gic agents with a relatively long half-life, neuroprotective therapies that prevent the loss of dopam
86                           The development of neuroprotective therapies that target these mechanisms m
87  solid basis for the development of rational neuroprotective therapies that we hope will halt the pro
88                         The development of a neuroprotective therapy that slows, stops, or reverses n
89 esearch are now beginning to bring candidate neuroprotective therapies to clinical trials.
90 er of insult severity is desirable to target neuroprotective therapies to patients most likely to ben
91 rogression, there is an unmet need for novel neuroprotective therapies to support RGC survival.
92  to translate emerging repair promyelinating/neuroprotective therapies to the clinic for myelin disor
93                                          For neuroprotective therapy to be effective, it is important
94  efficacy of erythropoietin as an adjunctive neuroprotective therapy to therapeutic hypothermia.
95           These data provide new targets for neuroprotective therapies via optimizing AC-driven plast
96                    In anticipation of future neuroprotective therapies, we present a classifier to im
97 n particular forced exercise, as a potential neuroprotective therapy when implemented before and afte
98                               Development of neuroprotective therapies will require elucidation of th
99 rtant therapeutic target for postreperfusion neuroprotective therapies, with treatment efficacy monit
100  that it could provide the basis for a novel neuroprotective therapy worthy of further investigation.