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Source: Molecular Neurobiology
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Total 278 results found since Jan 2013.
Docosanoids Promote Neurogenesis and Angiogenesis, Blood-Brain Barrier Integrity, Penumbra Protection, and Neurobehavioral Recovery After Experimental Ischemic Stroke
AbstractDocosahexaenoic acid (DHA) and neuroprotectin D1 (NPD1) are neuroprotective after experimental ischemic stroke. To explore underlying mechanisms, SD rats underwent 2 h of middle cerebral artery occlusion (MCAo) and treated with DHA (5 mg/kg, IV) or NPD1 (5 μg/per rat, ICV) and vehicles 1 h after. Neuro-behavioral assessments was conducted on days 1, 2, and 3, and on week 1, 2, 3, or 4. BrdU was injected on days 4, 5, and 6, immunohistochemistry was perform ed on week 2 or 4, MRI on day 7, and lipidomic analysis at 4 and 5 h after onset of stroke. DHA improved short- and long-term behavioral functions and red...
Source: Molecular Neurobiology - June 1, 2018 Category: Neurology Source Type: research
Angiotensin Receptor Blockade by Inhibiting Glial Activation Promotes Hippocampal Neurogenesis Via Activation of Wnt/ β-Catenin Signaling in Hypertension
AbstractHypertension is one of the major risk factors for central nervous system (CNS) disorders like stroke and Alzheimer ’s disease (AD). On the other hand, CNS diseases like AD have been associated with gliosis and impaired neurogenesis. Further, renin angiotensin system (RAS) is intricately associated with hypertension; however, the accumulating evidences suggest that over-activity of RAS may perpetuate the brain inflammation related with AD. Therefore, in the present study, we examined the effect of hypertension and RAS on glial (astrocytes and microglia) activation and hippocampal neurogenesis in a rat model of chr...
Source: Molecular Neurobiology - May 11, 2018 Category: Neurology Source Type: research
JM-20 Treatment After MCAO Reduced Astrocyte Reactivity and Neuronal Death on Peri-infarct Regions of the Rat Brain
In this study, we look into plausible molecular and cellular targets for JM-20, a new hybrid molecule, against ischemic stroke in vivo. Male Wistar rats were subjected to 90 min middle cerebral artery occlusion (MCAO) following 23 h of reperfusion. Animals treated with 8 mg/kg JM-20 (p.o., 1 h after reperfusion) showed minimal neurological impairment and lower GABA and IL-1β levels in CSF when compared to damaged rats that received vehicle. Immunocontent of pro-su rvival, phosphorylated Akt protein decreased in the cortex after 24 h as result of the ischemic insult, accompanied by decreased number of NeuN+ cells in ...
Source: Molecular Neurobiology - May 3, 2018 Category: Neurology Source Type: research
Apoptosis Following Cortical Spreading Depression in Juvenile Rats
AbstractRepetitive cortical spreading depression (CSD) can lead to cell death in immature brain tissue. Caspases are involved in neuronal cell death in several CSD-related neurological disorders, such as stroke and epilepsy. Yet, whether repetitive CSD itself can induce caspase activation in adult or juvenile tissue remains unknown. Inducing repetitive CSD in somatosensory cortices of juvenile and adult rats in vivo, we thus aimed to investigate the effect of repetitive CSD on the expression caspase-3, caspase-8, caspase-9, and caspase-12 in different brain regions using immunohistochemistry and western blotting techniques...
Source: Molecular Neurobiology - April 4, 2018 Category: Neurology Source Type: research
TRPV4 Activation Contributes Functional Recovery from Ischemic Stroke via Angiogenesis and Neurogenesis
In conclusion, our data suggest that TRPV4 activation by 4α-PDD may improve poststroke functional improvement through angiogenesis and neurogenesis.
Source: Molecular Neurobiology - April 4, 2018 Category: Neurology Source Type: research
Combination of High-Sensitivity C-Reactive Protein and Homocysteine Predicts the Post-Stroke Depression in Patients with Ischemic Stroke
In this study, we examined the changes in high-sensitivity C-reactive protein (Hs-CRP) and homocysteine (HCY) levels, two of the risk factors, during the acute period of ischemic stroke (IS) and evaluated the relationship between these two factors and long-term post-stroke depression (PSD). In this study, 259 patients with IS had finished the follow-up and were included. Based on the symptoms, diagnoses of depression were made in accordance with DSM-IV criteria for depression at 1 year after stroke. The influence of Hs-CRP/CHY levels on PSD was performed by binary logistic regression analysis and receiver operating chara...
Source: Molecular Neurobiology - March 8, 2018 Category: Neurology Source Type: research
Genetic Deletion of Kr üppel-Like Factor 11 Aggravates Ischemic Brain Injury
AbstractKr üppel-like factors (KLFs) belong to the zinc finger family of transcription factors, and their function in the CNS is largely unexplored. KLF11 is a member of the KLF family, and we have previously demonstrated that peroxisome proliferator-activated receptor gamma-mediated cerebral protection durin g ischemic insults needs recruitment of KLF11 as its critical coactivator. Here, we sought to determine the role of KLF11 itself in cerebrovascular function and the pathogenesis of ischemic stroke. Transient middle cerebral artery occlusion (MCAO) was performed in KLF11 knockout and wild-type contro l mice, and brain...
Source: Molecular Neurobiology - March 8, 2018 Category: Neurology Source Type: research
Genetic Mutation of GluN2B Protects Brain Cells Against Stroke Damages
AbstractImmediately following ischemia, glutamate accumulates in the extracellular space and results in extensive stimulation of its receptors including N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors. A large amount of Ca2+ influx directly through the receptor-gated ion channels which leads to Ca2+ overload and triggers several downstream lethal reactions. As a result, cell dies via apoptosis or necrosis, or both. Death-associated protein kinase 1 (DAPK1) physically and functionally interacts with the NMDA receptor GluN2B subunit at extra-synaptic sites and this inte...
Source: Molecular Neurobiology - March 8, 2018 Category: Neurology Source Type: research
Thioredoxin-Interacting Protein (TXNIP) in Cerebrovascular and Neurodegenerative Diseases: Regulation and Implication
AbstractNeurological diseases, including acute attacks (e.g., ischemic stroke) and chronic neurodegenerative diseases (e.g., Alzheimer ’s disease), have always been one of the leading cause of morbidity and mortality worldwide. These debilitating diseases represent an enormous disease burden, not only in terms of health suffering but also in economic costs. Although the clinical presentations differ for these diseases, a growing body of evidence suggests that oxidative stress and inflammatory responses in brain tissue significantly contribute to their pathology. However, therapies attempting to prevent oxidative damage o...
Source: Molecular Neurobiology - February 27, 2018 Category: Neurology Source Type: research
Early Treatment with Poly(ADP-Ribose) Polymerase-1 Inhibitor (JPI-289) Reduces Infarct Volume and Improves Long-Term Behavior in an Animal Model of Ischemic Stroke
AbstractIn patients with stroke and neurodegenerative diseases, overactivation of poly(ADP-ribose) polymerase-1 (PARP-1) causes harmful effects by inducing apoptosis, necrosis, neuroinflammation, and immune dysregulation. The current study investigated the neuroprotective effect of a novel PARP-1 inhibitor, JPI-289, in an animal model of ischemic stroke. A transient middle cerebral artery occlusion (tMCAO, 2 h) model was used to determine the therapeutic effect and the most effective dose and time window of administration of JPI-289. We also investigated the long-term outcomes of treatment with JPI-289 by diffusion-weigh...
Source: Molecular Neurobiology - January 30, 2018 Category: Neurology Source Type: research
Brain Photobiomodulation Therapy: a Narrative Review
This article reviews the state-of-the-art preclinical and clinical evidence regarding the efficacy of brain PBM therapy.
Source: Molecular Neurobiology - January 11, 2018 Category: Neurology Source Type: research
Inhibition of Peroxynitrite-Induced Mitophagy Activation Attenuates Cerebral Ischemia-Reperfusion Injury
AbstractActivated autophagy/mitophagy has been intensively observed in ischemic brain, but its roles remain controversial. Peroxynitrite (ONOO−), as a representative of reactive nitrogen species, is considered as a critical neurotoxic factor in mediating cerebral ischemia-reperfusion (I/R) injury, but its roles in autophagy/mitophagy activation remain unclear. Herein, we hypothesized that ONOO− could induce PINK1/Parkin-mediated mitophagy activation via triggering dynamin-related protein 1 (Drp1) recruitment to damaged mitochondria, contributing to cerebral I/R injury. Firstly, we found PINK1/Parkin-mediated mitophagy ...
Source: Molecular Neurobiology - January 6, 2018 Category: Neurology Source Type: research
Metabolomic Estimation of the Diagnosis and Onset Time of Permanent and Transient Cerebral Ischemia
AbstractDetermining the time of stroke onset in order to apply recanalization therapies within the accepted therapeutic window and the correct diagnosis of transient ischemic attack (TIA) are two common clinical problems in acute cerebral ischemia management. Therefore, biomarkers helping in this conundrum could be very helpful. We developed mouse models of distal middle cerebral artery occlusion mimicking TIA and ischemic stroke (IS), respectively. Plasma samples were analyzed by metabolomics at 6, 12, 24, and 48 h post onset in order to find TIA- and time-related stroke biomarkers. The results were validated in a secon...
Source: Molecular Neurobiology - December 21, 2017 Category: Neurology Source Type: research
Age-Related Upregulation of Carboxyl Terminal Modulator Protein Contributes to the Decreased Brain Ischemic Tolerance in Older Rats
AbstractStroke remains one of the leading causes of death worldwide. The underlying neuropathology for stroke is ischemic brain injury. Carboxyl terminal modulator protein (CTMP), an endogenous inhibitor of the prosurvival Akt, may increase brain ischemic injury in young animals. Aging decreases brain ischemic tolerance. We hypothesize that CTMP is increased with aging and that this increase contributes to the decreased brain ischemic tolerance. To address these hypotheses, we determined the expression of CTMP and its downstream proteins in the brain of various ages of rats (Fischer 344 and Sprague-Dawley rats). The role o...
Source: Molecular Neurobiology - December 18, 2017 Category: Neurology Source Type: research
Erratum to: Neuroprotection by Chlorpromazine and Promethazine in Severe Transient and Permanent Ischemic Stroke
Source: Molecular Neurobiology - November 14, 2017 Category: Neurology Source Type: research
