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Source: Molecular Neurobiology

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Total 278 results found since Jan 2013.

Neuroprotective Effects of Acetyl-L-Carnitine Against Oxygen-Glucose Deprivation-Induced Neural Stem Cell Death
Abstract Deprivation of oxygen and glucose is the main cause of neuronal cell death during cerebral infarction and can result in severe morbidity and mortality. In general, the neuroprotective therapies that are applied after ischemic stroke have been unsuccessful, despite many investigations. Acetyl-L-carnitine (ALCAR) plays an important role in mitochondrial metabolism and in modulating the coenzyme A (CoA)/acyl-CoA ratio. We investigated the protective effects of ALCAR against oxygen-glucose deprivation (OGD) in neural stem cells (NSCs). We measured cell viability, proliferation, apoptosis, and intracellular si...
Source: Molecular Neurobiology - December 8, 2015 Category: Neurology Source Type: research

Posterior Reversible Encephalopathy Syndrome After Transplantation: a Review
Abstract Posterior reversible encephalopathy syndrome (PRES) is a rare neurological disease. Recently, an increase in the number of transplantations has led to more cases being associated with PRES than what was previously reported. Calcineurin inhibitors (CNIs) are major risk factors for PRES in posttransplantation patients. The mechanisms of the development of PRES remain to be unclear. The typical clinical symptoms of PRES include seizures, acute encephalopathy syndrome, and visual symptoms. The hyperintense signal on fluid-attenuated inversion recovery image is the characteristic of the imaging appearance in t...
Source: Molecular Neurobiology - December 14, 2015 Category: Neurology Source Type: research

Deletion of Nuclear Localizing Signal Attenuates Proinflammatory Activity of Prothymosin-Alpha and Enhances Its Neuroprotective Effect on Transient Ischemic Stroke
In conclusion, ProT has pro-inflammatory effect that may counteract its neuroprotective effect. Deletion of NLS from ProT may attenuate post-ischemic inflammation and enhance the neuroprotective effects of ProT.
Source: Molecular Neurobiology - January 9, 2016 Category: Neurology Source Type: research

Leukemia Inhibitory Factor Protects Neurons from Ischemic Damage via Upregulation of Superoxide Dismutase 3
Abstract Leukemia inhibitory factor (LIF) has been shown to protect oligodendrocytes from ischemia by upregulating endogenous antioxidants. The goal of this study was to determine whether LIF protects neurons during stroke by upregulating superoxide dismutase 3 (SOD3). Animals were administered phosphate-buffered saline (PBS) or 125 μg/kg LIF at 6, 24, and 48 h after middle cerebral artery occlusion or sham surgery. Neurons were isolated from rat pups on embryonic day 18 and used between 7 and 15 days in culture. Cells were treated with LIF and/or 10 μM Akt inhibitor IV with PBS and 0.1 % DMSO acting as veh...
Source: Molecular Neurobiology - January 9, 2016 Category: Neurology Source Type: research

Upregulating the Expression of Survivin-HBXIP Complex Contributes to the Protective Role of IMM-H004 in Transient Global Cerebral Ischemia/Reperfusion
Abstract IMM-H004, a 3-piperazinylcoumarin compound derived from coumarin, has been proved effective against CA1 cell loss and spatial learning impairments resulting from transient global ischemia/reperfusion (TGCI/R), while the mechanism is still largely unknown. Here, we confirmed that treatment of rats with IMM-H004 immediately after TGCI/R ameliorated delayed neuronal death (DND) in the CA1 of hippocampus and cortex. Further study suggested that IMM-H004 contributed to the expression of antiapoptotic protein survivin through the activation of PI3K-dependent protein kinase B (PKB/Akt), which led to the phosphor...
Source: Molecular Neurobiology - January 7, 2016 Category: Neurology Source Type: research

A Tale of the Good and Bad: Remodeling of the Microtubule Network in the Brain by Cdk5
Abstract Cdk5, a cyclin-dependent kinase family member, is a global orchestrator of neuronal cytoskeletal dynamics. During embryogenesis, Cdk5 is indispensable for brain development. In adults, it is essential for numerous neuronal processes, including higher cognitive functions such as learning and memory formation, drug addiction, pain signaling, and long-term behavior changes through long-term potentiation and long-term depression, all of which rely on rapid alterations in the cytoskeleton. Cdk5 activity becomes deregulated in various brain disorders, including Alzheimer’s disease, Parkinson’s disease, Hunt...
Source: Molecular Neurobiology - March 5, 2016 Category: Neurology Source Type: research

Amikacin Inhibits miR-497 Maturation and Exerts Post-ischemic Neuroprotection
In this study, we present a systematic computational approach that includes 3D modeling, docking-based virtual screening, and molecular dynamics simulation to identify small-molecule inhibitors of pre-miR-497 maturation. The top hit, aminoglycosidic antibiotic, amikacin, formed a stable complex with pre-miR-497. Later, the protective efficacy of amikacin was evaluated against oxygen-glucose deprivation (OGD) and reoxygenation-induced neuronal cell death in SH-SY5Y cells and mouse organotypic hippocampal slice cultures. To confirm the inhibitory potential of amikacin on miR-497 maturation, quantitative real-time PCR was per...
Source: Molecular Neurobiology - May 20, 2016 Category: Neurology Source Type: research

Profiling of Signaling Proteins in Penumbra After Focal Photothrombotic Infarct in the Rat Brain Cortex
AbstractIn ischemic stroke, cell damage propagates from infarct core to surrounding tissue. To reveal proteins involved in neurodegeneration and neuroprotection, we explored the protein profile in penumbra surrounding the photothrombotic infarct core induced in rat cerebral cortex by local laser irradiation after Bengal Rose administration. Using antibody microarrays, we studied changes in expression of 224 signaling proteins 1, 4, or 24  h after photothrombotic infarct compared with untreated contralateral cortex. Changes in protein expression were greatest at 4 h after photothrombotic impact. These included over-expres...
Source: Molecular Neurobiology - October 21, 2016 Category: Neurology Source Type: research

Enriched Endogenous Omega-3 Polyunsaturated Fatty Acids Protect Cortical Neurons from Experimental Ischemic Injury
AbstractOmega-3 polyunsaturated fatty acids (n-3 PUFAs) exert therapeutic potential in a variety of neurological disorders, including ischemic stroke. However, the underlying mechanisms still lack investigation. Here, we report that cultured cortical neurons isolated fromfat-1 mice with high endogenous n-3 PUFAs were tolerant to oxygen-glucose deprivation/reperfusion (OGD/R) injury.Fat-1 neurons exhibited significantly attenuated reactive oxygen species (ROS) activation induced by OGD/R injury, upregulated antiapoptotic proteins Bcl-2 and Bcl-xL, and reduced cleaved caspase-3. Exogenous administration of docosahexaenoic ac...
Source: Molecular Neurobiology - October 28, 2016 Category: Neurology Source Type: research

TRPC3/6/7 Knockdown Protects the Brain from Cerebral Ischemia Injury via Astrocyte Apoptosis Inhibition and Effects on NF- кB Translocation
AbstractIschemia contributes significantly to morbidity and mortality associated with many common neurological diseases. Calcium overload is an important mechanism of cerebral ischemia and reperfusion (I/R) injury. Despite decades of intense research, an effective beneficial treatment of stroke remains limited; few therapeutic strategies exist to combat the consequences of cerebral ischemia. Traditionally, a “neurocentric” view has dominated research in this field. Evidence is now accumulating that glial cells, especially astrocytes, play an important role in the pathophysiology of cerebral ischemia. Here, we show that...
Source: Molecular Neurobiology - November 7, 2016 Category: Neurology Source Type: research

Direct Conversion of Somatic Cells into Induced Neurons
AbstractThe progressive loss and degeneration of neurons in the central nervous system (CNS), as a result of traumas or diseases including Alzheimer ’s, Parkinson’s, Huntington’s disease, stroke, and traumatic injury to the brain and spinal cord, can usually have devastating effects on quality of life. The current strategies available for treatments are described including drug delivery, surgery, electrical stimulation, and cell-based tiss ue engineering approaches. However, apart from cell-based therapy, other attempts are limited in improving clinical outcomes. Recently, stem cell and neural stem cell (NSC) in part...
Source: Molecular Neurobiology - December 15, 2016 Category: Neurology Source Type: research

Erratum to: LncRNA-N1LR Enhances Neuroprotection Against Ischemic Stroke Probably by Inhibiting p53 Phosphorylation
Source: Molecular Neurobiology - January 3, 2017 Category: Neurology Source Type: research

The Role of GluN2A in Cerebral Ischemia: Promoting Neuron Death and Survival in the Early Stage and Thereafter
AbstractOver-activation of NMDA receptors is a crucial step required for brain damage following a stroke. Although clinical trials for NMDA receptor blockers have failed, the role of GluN2A subunit in cerebral ischemia has been extensively evaluated in recent years. However, the effect of GluN2A on neuron damage induced by cerebral ischemia remains a matter of controversy. The underlying reason may be that GluN2A mediates both pro-death and pro-survival effects. These two effects result from two mutually excluding pathways, Ca2+ overload-dependent pro-death signaling and C-terminal-dependent pro-survival signaling, respect...
Source: Molecular Neurobiology - January 18, 2017 Category: Neurology Source Type: research

MMP-12, a Promising Therapeutic Target for Neurological Diseases
AbstractThe role of matrix metalloproteinase-12 (MMP-12) in the pathogenesis of several inflammatory diseases such as chronic obstructive pulmonary disease, emphysema, and asthma is well established. Several new studies and recent reports from our laboratory and others highlighted the detrimental role of MMP-12 in the pathogenesis of several neurological diseases. In this review, we discuss in detail the pathological role of MMP-12 and the possible underlying molecular mechanisms that contribute to disease pathogenesis in the context of central nervous system diseases such as stroke, spinal cord injury, and multiple sclero...
Source: Molecular Neurobiology - February 1, 2017 Category: Neurology Source Type: research

Cofilin Mediates LPS-Induced Microglial Cell Activation and Associated Neurotoxicity Through Activation of NF- κB and JAK–STAT Pathway
In conclusion, we demonstrated that cofilin is involved in the cascade of microglial cell activation and further validates our previous study on cofilin’s role in mediating neuronal apoptosis. Together, our results sug gest that cofilin could present a common target in neurons and microglial cells and might prove to be a promising therapy for different brain injury mechanisms including stroke.
Source: Molecular Neurobiology - February 12, 2017 Category: Neurology Source Type: research