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1 th the goal to decipher its critical role in neuronal protection.
2 tine (ALC) is a natural compound involved in neuronal protection.
3 ependent transcriptional activity to promote neuronal protection.
4 e attenuation of glial Ca2+ signals leads to neuronal protection.
5 ve been implicated in leukocyte adhesion and neuronal protection.
6 es and is involved in growth factor-mediated neuronal protection.
7 normal clearance of glutamate and providing neuronal protection.
8 atment with human albumin may provide direct neuronal protection.
9 of optimum exercise conditions for effective neuronal protection, a key characteristic of healthy agi
10 e whether endogenous BDNF may play a role in neuronal protection after ganglion cell trauma, BDNF exp
12 at delta-opioid receptors may play a role in neuronal protection against hypoxic/ischemic or glutamat
13 w that pan-HDAC inhibition not only promotes neuronal protection against oxidative stress, a common m
14 ropose that pTHRB2 has a fundamental role in neuronal protection against ROS cellular damage, and mit
16 .Akt(K179A)) resulted in loss of PS-mediated neuronal protection, Akt activation, and Bad and Mdm2 ph
17 mice may serve as a useful model system for neuronal protection and apoptosis in traumatic brain inj
18 um physical exercise conditions that provide neuronal protection and exercise-related factors remain
25 dy also indicates the role OAA could play in neuronal protection by suppressing excessive neuroinflam
28 noids are involved in synaptic signaling and neuronal protection; however, our understanding of the m
31 tination may be a signal for aggregation and neuronal protection in PD, which may be relevant for oth
32 age chains, leading to LRRK2 aggregation and neuronal protection in primary neurons and a Drosophila
33 tial for therapeutic exploitation to provide neuronal protection in situations of oxidative stress.
37 nfluenced the degree of plaque clearance and neuronal protection; (iv) high affinity of the antibody
39 se antagonists after SE provided significant neuronal protection raising the potential for a glial co
40 t 17beta-estradiol may also directly mediate neuronal protection, suggesting pleiotropic mechanisms o
41 receptor (beta(2)-AR) signaling and mediated neuronal protection through an arginase 1-polyamine axis
42 ing correlated with a clearance response and neuronal protection, whereas the ability of antibodies t