Results 51 to 60 of about 82,251 (326)
Refractory status epilepticus (RSE) is a life‐threatening neurological emergency with high rates of death and long‐term disability, but treatments for it are often based on limited evidence. RSE is now understood to involve neuroinflammation, which has led to the exploration of anti‐inflammatory and immunomodulatory agents like Tocilizumab. Traditional
Shanika Samarasekera +12 more
wiley +1 more source
Effect of glutamate antagonists on nitric oxide production in rat brain following intrahippocampal injection [PDF]
Stimulation of glutamate receptors induces neuronal nitric oxide (NO) release, which in turn modulates glutamate transmission. The involvement of ionotropic glutamate NMDA and AMPA/kainate receptors in induction of NO production in the rat brain was ...
Radenović Lidija +3 more
doaj +1 more source
Mitochondria and neuroprotection in stroke: Cationic arginine-rich peptides (CARPs) as a novel class of mitochondria-targeted neuroprotective therapeutics [PDF]
Stroke is the second leading cause of death globally and represents a major cause of devastating long-term disability. Despite sustained efforts to develop clinically effective neuroprotective therapies, presently there is no clinically available ...
Anderton, Ryan S +4 more
core +1 more source
Therapeutic potential of co-enzyme Q10 in retinal diseases [PDF]
Coenzyme Q10 (CoQ10) plays a critical role in mitochondrial oxidative phosphorylation by serving as an electron carrier in the respiratory electron transport chain.
Marcheggiani, Fabio +6 more
core +1 more source
Hippocampal single ‐nucleus transcriptomes and chromatin accessibility after mild traumatic brain injury reveal dentate granule neuron vulnerability driven by ferroptosis. The c‐Jun–Tmsb4x–Slc2a2 axis modulates lipid peroxidation and iron dysregulation.
Manrui Li +13 more
wiley +1 more source
Excitotoxicity due to excessive glutamate release causes oxidative stress and neuronal death, and is a feature of many brain diseases. Here the authors show that protein kinase D1 is inactivated by excitotoxicity in a model of stroke and that its ...
Julia Pose-Utrilla +18 more
doaj +1 more source
Background Hyperexcitability of neuronal networks can lead to excessive release of the excitatory neurotransmitter glutamate, which in turn can cause neuronal damage by overactivating NMDA-type glutamate receptors and related signaling pathways.
Takashi Miyamoto +7 more
doaj +1 more source
Transport of BMAA into Neurons and Astrocytes by System x\u3csub\u3ec\u3c/sub\u3e- [PDF]
The study of the mechanism of β-N-methylamino-l-alanine (BMAA) neurotoxicity originally focused on its effects at the N-methyl-d-aspartate (NMDA) receptor. In recent years, it has become clear that its mechanism of action is more complicated.
Albano, Rebecca, Lobner, Doug
core +1 more source
This study demonstrates that polyC‐RNA‐binding protein 1 (PCBP1) in ventral hippocampal astrocytes modulates depressive‐like behaviors by regulating glutathione peroxidase 4‐mediated ferroptosis and synaptic glutamatergic transmission. PCBP1 overexpression intervention in the chronic unpredictable mild stress model rescues behavioral deficits ...
Jinyu Zhang +15 more
wiley +1 more source
The essential role of AMPA receptor GluR2 subunit RNA editing in the normal and diseased brain
AMPA receptors are comprised of different combinations of GluR1-GluR4 (also known as GluA1-GluA4 and GluR-A to GluR-D) subunits. The GluR2 subunit is subject to Q/R site RNA editing by the ADAR2 enzyme, which converts a codon for glutamine (Q), present ...
Amanda Lorraine Wright +3 more
doaj +1 more source

