13,299 results match your criteria Experimental neurology[Journal]


Combining molecular intervention with in vivo imaging to untangle mechanisms of axon pathology and outgrowth following spinal cord injury.

Exp Neurol 2019 Apr 13. Epub 2019 Apr 13.

Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians University Munich, Munich 81377, Germany; Biomedical Center, Medical Faculty, Ludwig-Maximilians University Munich, Martinsried 82152, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich 81377, Germany. Electronic address:

In vivo imaging of the spinal cord has allowed the observation of single axons over relatively long periods in the living mouse. After spinal cord injury, this methodology has helped to differentiate several pathological stages and tissue processes which impact axon morphology. In addition, the combination of in vivo imaging techniques with specific molecular intervention has shown that specific pathological axon changes can respond to distinct treatments. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.04.003DOI Listing

Understanding the axonal response to injury by in vivo imaging in the mouse spinal cord: A tale of two branches.

Exp Neurol 2019 Apr 12. Epub 2019 Apr 12.

Department of Neuroscience, Jefferson Synaptic Biology Center, Vickie and Jack Farber Institute for Neuroscience, Sydney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.

Understanding the basic properties of how axons respond to injury in the mammalian central nervous system (CNS) is of fundamental value for developing strategies to promote neural repair. Axons possess complex morphologies with stereotypical branching patterns. However, current knowledge of the axonal response to injury gives little consideration to axonal branches, nor do strategies to promote axon regeneration. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.04.008DOI Listing
April 2019
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Improved memory and reduced anxiety in δ-catenin transgenic mice.

Exp Neurol 2019 Apr 11. Epub 2019 Apr 11.

College of Pharmacy and Research Institute for Drug Development, Chonnam National University, Gwangju 61186, Republic of Korea. Electronic address:

δ-Catenin is abundant in the brain and affects its synaptic plasticity. Furthermore, loss of δ-catenin is related to the deficits of learning and memory, mental retardation (cri-du-chat syndrome), and autism. A few studies about δ-catenin deficiency mice were performed. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00144886193006
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http://dx.doi.org/10.1016/j.expneurol.2019.04.006DOI Listing
April 2019
2 Reads

Detection of brain specific cardiolipins in plasma after experimental pediatric head injury.

Exp Neurol 2019 Apr 11. Epub 2019 Apr 11.

Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, PA, USA; Center for Free Radical and Antioxidant Health, University of Pittsburgh, Pittsburgh, PA, USA; Children's Neuroscience Institute, Children's Hospital of Pittsburgh, Pittsburgh, PA, USA; Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address:

Cardiolipin (CL) is a mitochondria-specific phospholipid that is central to maintenance and regulation of mitochondrial bioenergetic and metabolic functions. CL molecular species display great tissue variation with brain exhibiting a distinct, highly diverse CL population. We recently showed that the appearance of unique brain-type CLs in plasma could serve as a brain-specific marker of mitochondrial/tissue injury in patients after cardiac arrest. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.04.007DOI Listing
April 2019
1 Read

OCT4B-190 protects against ischemic stroke by modulating GSK-3β/HDAC6.

Exp Neurol 2019 Apr 11. Epub 2019 Apr 11.

Department of Neurology, Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing 210008, China; Institute of Brain Science, Nanjing University, Nanjing 210008, China. Electronic address:

OCT4 is a key regulator in maintaining the pluripotency and self-renewal of embryonic stem cells (ESCs). Human OCT4 gene has three mRNA isoforms, termed OCT4A, OCT4B and OCT4B1. The 190-amino-acid protein isoform (OCT4B-190) is one of the major products of OCT4B mRNA, the biological function of which is still not well defined. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.04.005DOI Listing
April 2019
3 Reads

Depletion of microglia immediately following traumatic brain injury in the pediatric rat: Implications for cellular and behavioral pathology.

Exp Neurol 2019 Apr 10. Epub 2019 Apr 10.

Department of Anesthesiology and Critical Care, Children's Hospital of Philadelphia, Philadelphia, PA, United States of America. Electronic address:

The inflammatory response is a significant component of the pathophysiology of pediatric traumatic brain injury. High levels of inflammatory mediators have been found in the cerebrospinal fluid of brain-injured children which have been linked to poor prognosis. Targeting aspects of the inflammatory response in the hopes of finding a viable post-injury therapeutic option has gained attention. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.04.004DOI Listing

Excess glutamate secreted from astrocytes drives upregulation of P-glycoprotein in endothelial cells in amyotrophic lateral sclerosis.

Exp Neurol 2019 Apr 9. Epub 2019 Apr 9.

Jefferson Weinberg ALS Center, Vickie and Jack Farber Institute for Neuroscience, Department of Neuroscience, Thomas Jefferson University, 900 Walnut Street, Philadelphia, PA 19107, USA. Electronic address:

In amyotrophic lateral sclerosis (ALS), upregulation in expression and activity of the ABC transporter P-glycoprotein (P-gp) driven by disease advancement progressively reduces CNS penetration and efficacy of the ALS drug, riluzole. Post-mortem spinal cord tissues from ALS patients revealed elevated P-gp expression levels in endothelial cells of the blood-spinal cord barrier compared to levels measured in control, non-diseased individuals. We recently found that astrocytes expressing familial ALS-linked SOD1 mutations regulate expression levels of P-gp in endothelial cells, which also exhibit a concomitant, significant increase in reactive oxygen species production and NFκB nuclear translocation when exposed to mutant SOD1 astrocyte conditioned media. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.04.002DOI Listing
April 2019
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4.696 Impact Factor

Insulin resistance: Genetic associations with depression and cognition in population based cohorts.

Exp Neurol 2019 Apr 6. Epub 2019 Apr 6.

Division of Psychiatry, Royal Edinburgh Hospital, University of Edinburgh, Edinburgh, UK; Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK; Department of Psychology, University of Edinburgh, Edinburgh, UK.

Insulin resistance, broadly defined as the reduced ability of insulin to exert its biological action, has been associated with depression and cognitive dysfunction in observational studies. However, it is unclear whether these associations are causal and whether they might be underpinned by other shared factors. To address this knowledge gap, we capitalized on the stability of genetic biomarkers through the lifetime, and on their unidirectional relationship with depression and cognition. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.04.001DOI Listing

Metabolic perturbations after pediatric TBI: It's not just about glucose.

Exp Neurol 2019 Apr 3. Epub 2019 Apr 3.

Anesthesiology & Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, United States. Electronic address:

Improved patient survival following pediatric traumatic brain injury (TBI) has uncovered a currently limited understanding of both the adaptive and maladaptive metabolic perturbations that occur during the acute and long-term phases of recovery. While much is known about the redundancy of metabolic pathways that provide adequate energy and substrates for normal brain growth and development, the field is only beginning to characterize perturbations in these metabolic pathways after pediatric TBI. To date, the majority of studies have focused on dysregulated oxidative glucose metabolism after injury; however, the immature brain is well-equipped to use alternative substrates to fuel energy production, growth, and development. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.018DOI Listing
April 2019
5 Reads

MicroRNA-132 attenuates cerebral injury by protecting blood-brain-barrier in MCAO mice.

Exp Neurol 2019 Mar 28. Epub 2019 Mar 28.

Discipline of Neuroscience, Department of Anatomy, Histology and Embryology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address:

MicroRNAs (miRNAs) have been widely reported to induce posttranscriptional gene silencing and led to an explosion of new strategies for the treatment of human disease. It has been reported that the expression of MicroRNA-132 (miR-132) are altered both in the blood and brain after stroke. However, the effect of miR-132 on blood-brain barrier (BBB) disruption in ischemia stroke has not been studied. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.017DOI Listing
March 2019
2 Reads

Understanding the link between insulin resistance and Alzheimer's disease: Insights from animal models.

Exp Neurol 2019 Mar 28. Epub 2019 Mar 28.

Centre for Neuroscience Studies, Queen's University, Kingston, ON, Canada; Department of Psychiatry, Queen's University, Kingston, ON, Canada; Institute of Medical Biochemistry Leopoldo De Meis, Federal University of Rio de Janeiro, Brazil. Electronic address:

Alzheimer's disease (AD) is a devastating neurodegenerative disease affecting millions of people worldwide. AD is characterized by a profound impairment of higher cognitive functions and still lacks any effective disease-modifying treatment. Defective insulin signaling has been implicated in AD pathophysiology, but the mechanisms underlying this process are not fully understood. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.016DOI Listing

Translational approach towards determining the role of cerebral autoregulation in outcome after traumatic brain injury.

Exp Neurol 2019 Mar 27;317:291-297. Epub 2019 Mar 27.

Department of Anesthesiology, Pediatrics, and Neurological Surgery, Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA, United States of America.

Cerebral autoregulation is impaired after traumatic brain injury (TBI), contributing to poor outcome. In the context of the neurovascular unit, cerebral autoregulation contributes to neuronal cell integrity and clinically Glasgow Coma Scale is correlated to intactness of autoregulation after TBI. Cerebral Perfusion Pressure (CPP) is often normalized by use of vasoactive agents to increase mean arterial pressure (MAP) and thereby limit impairment of cerebral autoregulation and neurological deficits. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.015DOI Listing
March 2019
2 Reads

Impairment of pericyte-endothelium crosstalk leads to blood-brain barrier dysfunction following traumatic brain injury.

Exp Neurol 2019 Mar 26;317:260-270. Epub 2019 Mar 26.

Laboratory of CNS Injury and Molecular Therapy, JFK Neuroscience Institute, Hackensack Meridian Health JFK Medical Center, 65 James St, Edison, New Jersey 08820, United States. Electronic address:

The blood-brain barrier (BBB) constitutes a neurovascular unit formed by microvascular endothelial cells, pericytes, and astrocytes. Brain pericytes are important regulators of BBB integrity, permeability, and blood flow. Pericyte loss has been implicated in injury; however, how the crosstalk among pericytes, endothelial cells, and astrocytes ultimately leads to BBB dysfunction in traumatic brain injury (TBI) remains elusive. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.014DOI Listing

Neuroprotective effects of inter-alpha inhibitor proteins after hypoxic-ischemic brain injury in neonatal rats.

Exp Neurol 2019 Mar 23;317:244-259. Epub 2019 Mar 23.

Department of Pediatrics, Women & Infants Hospital of Rhode Island, USA; The Warren Alpert Medical School of Brown University, USA. Electronic address:

Hypoxic-ischemic (HI) brain injury is one of the most common neurological problems occurring in the perinatal period. Hypothermia is the only approved intervention for neonatal HI encephalopathy. However, this treatment is only partially protective, has a narrow therapeutic time window after birth and only can be used to treat full-term infants. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.013DOI Listing
March 2019
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HDAC5 promotes optic nerve regeneration by activating the mTOR pathway.

Exp Neurol 2019 Mar 22;317:271-283. Epub 2019 Mar 22.

Department of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, United States of America; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, MO 63110, United States of America; Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, United States of America. Electronic address:

Neurons in the central nervous system (CNS) regenerate poorly compared to their counterparts in the peripheral nervous system. We previously showed that, in peripheral sensory neurons, nuclear HDAC5 inhibits the expression of regenerative associated genes. After nerve injury, HDAC5 is exported to the cytoplasm to promote axon regeneration. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.011DOI Listing

Does pediatric traumatic brain injury cause adult alcohol misuse: Combining preclinical and epidemiological approaches.

Exp Neurol 2019 Mar 22;317:284-290. Epub 2019 Mar 22.

Department of Physical Medicine and Rehabilitation, Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.

Traumatic brain injury (TBI) is closely interrelated with alcohol use disorders. This is mediated, in part, by the large number of individuals who are intoxicated at the time of their injuries. However, there is also evidence, both preclinically and epidemiologically that TBI, particularly when it occurs early in life can increase the incidence of alcohol use disorders later on. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.012DOI Listing
March 2019
4.696 Impact Factor

Chronic spinal cord injury impairs primary CD8 T cell antiviral immunity but does not affect generation or function of memory CD8 T cells.

Exp Neurol 2019 Mar 20;317:298-307. Epub 2019 Mar 20.

Biology Department, Drexel University, Philadelphia, PA 19104, United States of America. Electronic address:

Antiviral immunity is severely compromised following trauma to the central nervous system. In mice with chronic spinal cord injury (SCI), primary infection with influenza virus leads to high mortality rates due to impaired expansion of virus-specific CD8 T cells. One strategy to increase resistance to viral infections is to generate memory immune cells that protect from recurrent infections. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.010DOI Listing
March 2019
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Muscle ciliary neurotrophic factor receptor α helps maintain choline acetyltransferase levels in denervated motor neurons following peripheral nerve lesion.

Exp Neurol 2019 Mar 19;317:202-205. Epub 2019 Mar 19.

Department of Pharmacology and Systems Physiology, University of Cincinnati, Cincinnati, OH 45267-0576, USA. Electronic address:

Systemic ciliary neurotrophic factor (CNTF) administration protects motor neurons from denervating diseases and lesions but produces non-neuromuscular side effects. Therefore, CNTF related therapeutics will need to specifically target motor neuron protective receptor mechanisms. Expression of the essential ligand binding subunit of the CNTF receptor, CNTF receptor α (CNTFRα), is induced in skeletal muscle by denervating lesion and in human denervating diseases. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.009DOI Listing

Deep brain stimulation of the ventroanterior and ventrolateral thalamus improves motor function in a rat model of Parkinson's disease.

Exp Neurol 2019 Mar 16;317:155-167. Epub 2019 Mar 16.

Department of Neuroscience & Experimental Therapeutics, Albany Medical College, Albany, NY, United States of America; Department of Neurology, Albany Medical Center, Albany, NY, United States of America. Electronic address:

Parkinson's disease (PD) is a neurodegenerative disease with affected individuals exhibiting motor symptoms of bradykinesia, muscle rigidity, tremor, postural instability and gait dysfunction. The current gold standard treatment is pharmacotherapy with levodopa, but long-term use is associated with motor response fluctuations and can cause abnormal movements called dyskinesias. An alternative treatment option is deep brain stimulation (DBS) with the two FDA-approved brain targets for PD situated in the basal ganglia; specifically, in the subthalamic nucleus (STN) and globus pallidus pars interna (GPi). Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.008DOI Listing
March 2019
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Outcomes and clinical implications of intranasal insulin administration to the central nervous system.

Exp Neurol 2019 Mar 15;317:180-190. Epub 2019 Mar 15.

Institute of Medical Psychology and Behavioral Neurobiology, University of Tübingen, 72076 Tübingen, Germany; German Center for Diabetes Research (DZD), 72076 Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, 72076 Tübingen, Germany. Electronic address:

Insulin signaling in the brain plays a critical role in metabolic control and cognitive function. Targeting insulinergic pathways in the central nervous system via peripheral insulin administration is feasible, but associated with systemic effects that necessitate tight supervision or countermeasures. The intranasal route of insulin administration, which largely bypasses the circulation and thereby greatly reduces these obstacles, has now been repeatedly tested in proof-of-concept studies in humans as well as animals. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00144886183059
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http://dx.doi.org/10.1016/j.expneurol.2019.03.007DOI Listing
March 2019
6 Reads

Nociceptor-dependent locomotor dysfunction after clinically-modeled hindlimb muscle stretching in adult rats with spinal cord injury.

Exp Neurol 2019 Mar 14. Epub 2019 Mar 14.

Kentucky Spinal Cord Injury Research Center, Department of Neurological Surgery, University of Louisville, 220 Abraham Flexner Way, Louisville, KY 40202, USA; Anatomical Sciences and Neurobiology, University of Louisville, School of Medicine, 511 South Floyd, Room 111, Louisville, KY 40202, USA; Department of Physiology, University of Louisville, School of Medicine, HSC A 1115, 500 South Preston Street, Louisville, KY 40292, USA. Electronic address:

In the course of investigating how common clinical treatments and adaptive technologies affect recovery after spinal cord injury (SCI), we discovered that a clinically-modeled hindlimb stretching protocol dramatically, but transiently, reduces locomotor function. Nociceptive sensory input is capable of altering motor output at the spinal level, and nociceptive neurons are sensitized after SCI. Here we tested the possibility that the stretch-induced motor deficits required the presence of nociceptors using neonatal capsaicin induced depletion of TRPV1+ nociceptive neurons. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.006DOI Listing
March 2019
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4.696 Impact Factor

The emerging role of neutrophils as modifiers of recovery after traumatic injury to the developing brain.

Exp Neurol 2019 Mar 12;317:144-154. Epub 2019 Mar 12.

Department of Neurology, Dell Medical School, The University of Texas at Austin, 1701 Trinity St., Austin, TX 78712, USA. Electronic address:

The innate immune response plays a critical role in traumatic brain injury (TBI), contributing to ongoing pathogenesis and worsening long-term outcomes. Here we focus on neutrophils, one of the "first responders" to TBI. These leukocytes are recruited to the injured brain where they release a host of toxic molecules including free radicals, proteases, and pro-inflammatory cytokines, all of which promote secondary tissue damage. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.004DOI Listing
March 2019
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Upregulation of interleukin-6 on Ca3.2 T-type calcium channels in dorsal root ganglion neurons contributes to neuropathic pain in rats with spinal nerve ligation.

Exp Neurol 2019 Mar 11;317:226-243. Epub 2019 Mar 11.

Neuroscience Research Institute, Peking University, Beijing 100083, China; Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing 100083, China; Key Laboratory for Neuroscience, Ministry of Education/National Health Commission, Peking University, Beijing 100083, China. Electronic address:

The T-type calcium channels Ca3.2, one of the low voltage-activated (LVA) calcium channels, have been found to play important roles in the neuronal excitability. Recently, we and others have demonstrated that accumulation of Ca3. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.005DOI Listing
March 2019
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Brain interrupted: Early life traumatic brain injury and addiction vulnerability.

Exp Neurol 2019 Mar 9;317:191-201. Epub 2019 Mar 9.

Department of Pathology and Laboratory Medicine, The Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA; Center for Substance Abuse Research, The Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA; Shriners Hospitals Pediatric Research Center, The Lewis Katz School of Medicine at Temple University, Philadelphia, PA 19140, USA. Electronic address:

Recent reports provide evidence for increased risk of substance use disorders (SUD) among patients with a history of early-life traumatic brain injury (TBI). Preclinical research utilizing animal models of TBI have identified injury-induced inflammation, blood-brain barrier permeability, and changes to synapses and neuronal networks within regions of the brain associated with the perception of reward. Importantly, these reward pathway networks are underdeveloped during childhood and adolescence, and early-life TBI pathology may interrupt ongoing maturation. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.003DOI Listing

Ethanol-induced DNA repair in neural stem cells is transforming growth factor β1-dependent.

Exp Neurol 2019 Mar 8;317:214-225. Epub 2019 Mar 8.

Department of Neuroscience and Physiology, State University of New York - Upstate Medical University, Syracuse, NY 13210, USA; Developmental Exposure Alcohol Research Center, Binghamton NY 13902, Cortland NY 13045, and Syracuse, NY 13210, USA; Department of Anatomy, Touro College of Osteopathic Medicine, Middletown, NY 10940, USA; Research Service, Veterans Affairs Medical Center, Syracuse, NY 13210, USA. Electronic address:

Following neurotoxic damage, cells repair their DNA, and survive or undergo apoptosis. This study tests the hypothesis that ethanol induces a DNA damage response (DDR) in neural stem cells (NSCs) that promotes excision repair (ER) and this repair is influenced by the growth factor environment. Non-immortalized NSCs treated with fibroblast growth factor 2 or transforming growth factor (TGF) β1 were exposed to ethanol. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00144886183059
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http://dx.doi.org/10.1016/j.expneurol.2019.02.003DOI Listing
March 2019
2 Reads

Mechanisms underlying vulnerabilities after repeat mild traumatic brain injuries.

Exp Neurol 2019 Mar 8;317:206-213. Epub 2019 Mar 8.

UCLA Department of Neurosurgery, 300 Stein Plaza, Los Angeles, CA 90095, United States. Electronic address:

Traumatic brain injury (TBI) has drawn national attention for its high incidence and mechanistic complexity. The majority of TBI cases are "mild" in nature including concussions and mild TBI (mTBI). Concussions are a distinct form of mTBI where diagnosis is difficult, quantification of the incidence is challenging and there is greater risk for subsequent injuries. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.01.012DOI Listing
March 2019
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Calcium imaging approaches in investigation of pain mechanism in the spinal cord.

Exp Neurol 2019 Mar 7;317:129-132. Epub 2019 Mar 7.

The Solomon H. Snyder Department of Neuroscience and the Center for Sensory Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address:

The continuous advancement of microscopic imaging techniques combined with the discovery and use of more powerful calcium indicators has made calcium imaging technology much more effective and has increased its use in the study of pain circuitry. Using calcium imaging to study spinal pain mechanisms causes less damage to animals compared to electrophysiological techniques and is also able to observe the firing pattern of spinal neurons and the connections between them on a large scale. These advantages allow any changes in spinal cord circuits caused by pain transmission to be observed more effectively. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.002DOI Listing

Efgartigimod improves muscle weakness in a mouse model for muscle-specific kinase myasthenia gravis.

Exp Neurol 2019 Mar 6;317:133-143. Epub 2019 Mar 6.

Department of Neurology, Leiden University Medical Centre, Leiden, the Netherlands.

Myasthenia gravis is hallmarked by fatigable muscle weakness resulting from neuromuscular synapse dysfunction caused by IgG autoantibodies. The variant with muscle-specific kinase (MuSK) autoantibodies is characterized by prominent cranial and bulbar weakness and a high frequency of respiratory crises. The majority of MuSK MG patients requires long-term immunosuppressive treatment, but the result of these treatments is considered less satisfactory than in MG with acetylcholine receptor antibodies. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.03.001DOI Listing
March 2019
1 Read

Sex differences in pediatric traumatic brain injury.

Exp Neurol 2019 Mar 2;317:168-179. Epub 2019 Mar 2.

Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA; Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. Electronic address:

The response of the developing brain to traumatic injury is different from the response of the mature, adult brain. There are critical developmental trajectories in the young brain, whereby injury can lead to long term functional abnormalities. Emerging preclinical and clinical literature supports the presence of significant sex differences in both the response to and the recovery from pediatric traumatic brain injury (TBI). Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.016DOI Listing

Central neuropeptide-S treatment improves neurofunctions of 6-OHDA-induced Parkinsonian rats.

Exp Neurol 2019 Feb 27;317:78-86. Epub 2019 Feb 27.

Faculty of Medicine, Department of Physiology, Akdeniz University, Antalya, Turkey. Electronic address:

Parkinson's disease (PD) is characterized by degeneration of the dopaminergic neurons in substantia nigra (SN). The motor symptoms of PD include tremor, rigidity, bradykinesia and postural impairment. In rodents, central administration of neuropeptide-S (NPS) has been shown to induce locomotor activity, dopamine release and neuronal survival by decreasing lipid peroxidation, additionally, the NPS receptor (NPSR) was detected in SN. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.015DOI Listing
February 2019
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Caffeine inhibits hypoxia-induced nuclear accumulation in HIF-1α and promotes neonatal neuronal survival.

Exp Neurol 2019 Feb 26;317:66-77. Epub 2019 Feb 26.

Department of Biology, Medgar Evers College, City University of New York, United States.

Apnea of prematurity (AOP) defined as cessation of breathing for 15-20 s, is commonly seen in preterm infants. Caffeine is widely used to treat AOP due to its safety and effectiveness. Caffeine releases respiratory arrest by competing with adenosine for binding to adenosine A and A receptors (AR and AR). Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.01.014DOI Listing
February 2019

Dim light at night impairs recovery from global cerebral ischemia.

Exp Neurol 2019 Feb 26;317:100-109. Epub 2019 Feb 26.

Department of Neuroscience, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA.

Nighttime lighting is one of the great conveniences of modernization; however, there is mounting evidence that inopportune light exposure can disrupt physiological and behavioral functions. Hospital patients may be particularly vulnerable to the consequences of light at night due to their compromised physiological state. Cardiac arrest/cardiopulmonary resuscitation (CA) was used to test the hypothesis in mice that exposure to dim light at night impairs central nervous system (CNS) recovery from a major pathological insult. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.008DOI Listing
February 2019
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Repetitive closed-head impact model of engineered rotational acceleration (CHIMERA) injury in rats increases impulsivity, decreases dopaminergic innervation in the olfactory tubercle and generates white matter inflammation, tau phosphorylation and degeneration.

Exp Neurol 2019 Feb 26;317:87-99. Epub 2019 Feb 26.

Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC V6T 1Z3, Canada. Electronic address:

Traumatic brain injury (TBI) affects at least 3 M people annually. In humans, repetitive mild TBI (rmTBI) can lead to increased impulsivity and may be associated with chronic traumatic encephalopathy. To better understand the relationship between repetitive TBI (rTBI), impulsivity and neuropathology, we used CHIMERA (Closed-Head Injury Model of Engineered Rotational Acceleration) to deliver five TBIs to rats, which were continuously assessed for trait impulsivity using the delay discounting task and for neuropathology at endpoint. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.012DOI Listing
February 2019
4.696 Impact Factor

Free d-aspartate triggers NMDA receptor-dependent cell death in primary cortical neurons and perturbs JNK activation, Tau phosphorylation, and protein SUMOylation in the cerebral cortex of mice lacking d-aspartate oxidase activity.

Exp Neurol 2019 Feb 26;317:51-65. Epub 2019 Feb 26.

Department of Environmental, Biological and Pharmaceutical Sciences and Technologies, University of Campania Luigi Vanvitelli, 81100, Caserta, Italy; Laboratory of Behavioural Neuroscience, Ceinge Biotecnologie Avanzate, 80145, Naples, Italy. Electronic address:

In mammals, free d-aspartate (D-Asp) is abundant in the embryonic brain, while levels remain very low during adulthood as a result of the postnatal expression and activity of the catabolizing enzyme d-aspartate oxidase (DDO). Previous studies have shown that long-lasting exposure to nonphysiological, higher D-Asp concentrations in Ddo knockout (Ddo) mice elicits a precocious decay of synaptic plasticity and cognitive functions, along with a dramatic age-dependent expression of active caspase 3, associated with increased cell death in different brain regions, including hippocampus, prefrontal cortex, and substantia nigra pars compacta. Here, we investigate the yet unclear molecular and cellular events associated with the exposure of abnormally high D-Asp concentrations in cortical primary neurons and in the brain of Ddo mice. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.014DOI Listing
February 2019
4.696 Impact Factor

FGF21 promotes functional recovery after hypoxic-ischemic brain injury in neonatal rats by activating the PI3K/Akt signaling pathway via FGFR1/β-klotho.

Exp Neurol 2019 Feb 23;317:34-50. Epub 2019 Feb 23.

Department of Neonatology, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, Zhejiang 325027, China. Electronic address:

Perinatal asphyxia often results in neonatal cerebral hypoxia-ischemia (HI), which is associated with high mortality and severe long-term neurological deficits in newborns. Currently, there are no effective drugs to mitigate the functional impairments post-HI. Previous studies have shown that fibroblast growth factor 21 (FGF21) has a potential neuroprotective effect against brain injury. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.013DOI Listing
February 2019
1 Read

Membrane transporters in traumatic brain injury: Pathological, pharmacotherapeutic, and developmental implications.

Exp Neurol 2019 Feb 21;317:10-21. Epub 2019 Feb 21.

Center for Clinical Pharmaceutical Sciences, School of Pharmacy, University of Pittsburgh, PA, United States of America; Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, PA, United States of America. Electronic address:

Membrane transporters regulate the trafficking of endogenous and exogenous molecules across biological barriers and within the neurovascular unit. In traumatic brain injury (TBI), they moderate the dynamic movement of therapeutic drugs and injury mediators among neurons, endothelial cells and glial cells, thereby becoming important determinants of pathogenesis and effective pharmacotherapy after TBI. There are three ways transporters may impact outcomes in TBI. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.011DOI Listing
February 2019

Imaging in vivo dynamics of sensory axon responses to CNS injury.

Exp Neurol 2019 Feb 20;317:110-118. Epub 2019 Feb 20.

German Center for Neurodegenerative Diseases, Bonn, Germany. Electronic address:

Axons in the adult mammalian brain and spinal cord fail to regenerate upon lesion. In vivo imaging serves as a tool to investigate the immediate response of axons to injury and how the same injured axons behave over time. Here, we describe the dynamic changes that injured sensory axons undergo and methods of imaging them in vivo. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.010DOI Listing
February 2019

Temporal and age-dependent effects of haptoglobin deletion on intracerebral hemorrhage-induced brain damage and neurobehavioral outcomes.

Exp Neurol 2019 Feb 19;317:22-33. Epub 2019 Feb 19.

Department of Anesthesiology, University of Florida, Gainesville, FL, United States of America; Department of Neuroscience, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida, Gainesville, FL, United States of America; Departments of Neurology, Psychiatry, and Pharmaceutics, University of Florida, Gainesville, FL, United States of America. Electronic address:

Intracerebral hemorrhage (ICH) is a devastating stroke subtype and the presence of extracorpuscular hemoglobin (Hb) exacerbates brain damage. Haptoglobin (Hp) binds Hb, which prevents its oxidation and participation in neurotoxic reactions. Multiple studies have investigated the role of Hp under conditions of intravascular hemolysis, but little is known about its role in the brain and following ICH where extravascular hemolysis is rampant. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.01.011DOI Listing
February 2019

Mitoquinone attenuates blood-brain barrier disruption through Nrf2/PHB2/OPA1 pathway after subarachnoid hemorrhage in rats.

Exp Neurol 2019 Feb 16;317:1-9. Epub 2019 Feb 16.

Department of Physiology and Pharmacology, Loma Linda University, 11041 Campus St, Risley Hall, Room 219, Loma Linda, CA 92354, USA. Electronic address:

Background And Purpose: Mitochondrial dysfunction is involved in the mechanism of early brain injury (EBI) following subarachnoid hemorrhage (SAH). Blood-brain barrier disruption is a devastating outcome in the early stage of SAH. In this study, we aimed to investigate the role of a mitochondria-related drug Mitoquinone (MitoQ) in blood-brain barrier disruption after SAH in rats. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.009DOI Listing
February 2019
2 Reads

Self-propagating, non-synaptic epileptiform activity recruits neurons by endogenous electric fields.

Exp Neurol 2019 Feb 15;317:119-128. Epub 2019 Feb 15.

Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH 44106, USA. Electronic address:

It is well documented that synapses play a significant role in the transmission of information between neurons. However, in the absence of synaptic transmission, neural activity has been observed to continue to propagate. Previous studies have shown that propagation of epileptiform activity takes place in the absence of synaptic transmission and gap junctions and is outside the range of ionic diffusion and axonal conduction. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.005DOI Listing
February 2019
1 Read

Endogenous multidien rhythm of epilepsy in rats.

Exp Neurol 2019 May 15;315:82-87. Epub 2019 Feb 15.

Aix Marseille Univ, INSERM, INS, Inst Neurosci Syst, Marseille, France.

Recent trials of chronic EEG in humans showed that epilepsy is a cyclical disorder of the brain with rhythms at multiple time-scales: circadian, multi-day (multidien) or even seasonal. Here, we analyzed chronic EEG data (>30 days) in male epileptic rats and unraveled not only circadian but also, slower, multidien rhythms of interictal epileptiform activity with periodicity of about 2-3 and 5-7 days. Importantly, seizures were not uniformly distributed over time, but rather clustered at preferential phases of these underlying rhythms, delineating critical circadian times and multidien phase of heightened seizure risk. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.006DOI Listing
May 2019
2 Reads

Parkinson's disease and pain: Modulation of nociceptive circuitry in a rat model of nigrostriatal lesion.

Exp Neurol 2019 May 14;315:72-81. Epub 2019 Feb 14.

Laboratory of Neuroscience, Hospital Sírio-Libanês, São Paulo, SP, Brazil. Electronic address:

Parkinson's disease (PD) is a neurodegenerative disorder that causes progressive dysfunction of dopaminergic and non-dopaminergic neurons, generating motor and nonmotor signs and symptoms. Pain is reported as the most bothersome nonmotor symptom in PD; however, pain remains overlooked and poorly understood. In this study, we evaluated the nociceptive behavior and the descending analgesia circuitry in a rat model of PD. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.007DOI Listing
May 2019
1 Read

Methylphenidate administration reverts attentional inflexibility in adolescent rats submitted to a model of neonatal hypoxia-ischemia: Predictive validity for ADHD study.

Exp Neurol 2019 May 13;315:88-99. Epub 2019 Feb 13.

Programa de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde (ICBS), Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil; Departamento de Ciências Morfológicas, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.

Perinatal complications such as birth asphyxia were associated with a higher risk for Attention-Deficit/Hyperactivity Disorder (ADHD) in humans. Data from a rat model of neonatal hypoxia-ischemia (HI) have revealed inattention, impulsive behavior and dopamine (DA) disturbances in the prefrontal cortex (PFC), confirming the face validity and construct validity for ADHD study. However, the predictive validity (similar therapeutic efficacy of the pharmacological treatment available in the clinic) should be considered. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.004DOI Listing
May 2019
1 Read

Treatment of myotonia congenita with retigabine in mice.

Exp Neurol 2019 May 7;315:52-59. Epub 2019 Feb 7.

Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, OH 45435, United States. Electronic address:

Patients with myotonia congenita suffer from muscle stiffness caused by muscle hyperexcitability. Although loss-of-function mutations in the ClC-1 muscle chloride channel have been known for 25 years to cause myotonia congenita, this discovery has led to little progress on development of therapy. Currently, treatment is primarily focused on reducing hyperexcitability by blocking Na current. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6431423PMC
May 2019
12 Reads

Conditioning electrical stimulation promotes functional nerve regeneration.

Exp Neurol 2019 May 5;315:60-71. Epub 2019 Feb 5.

Department of Surgery, University of Alberta, Edmonton, AB T6G 2H7, Canada. Electronic address:

Peripheral nerve regeneration following injury is often incomplete, resulting in significant personal and socioeconomic costs. Although a conditioning crush lesion prior to surgical nerve transection and repair greatly promotes nerve regeneration and functional recovery, feasibility and ethical considerations have hindered its clinical applicability. In a recent proof of principle study, we demonstrated that conditioning electrical stimulation (CES) had effects on early nerve regeneration, similar to that seen in conditioning crush lesions (CCL). Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.02.001DOI Listing

Chronic treatment with galantamine rescues reversal learning in an attentional set-shifting test after experimental brain trauma.

Exp Neurol 2019 May 31;315:32-41. Epub 2019 Jan 31.

Physical Medicine & Rehabilitation, University of Pittsburgh, Pittsburgh, PA 15213, United States; Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, PA 15213, United States; Neurobiology, University of Pittsburgh, Pittsburgh, PA 15213, United States; Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15213, United States. Electronic address:

Approximately 10 million new cases of traumatic brain injury (TBI) are reported each year worldwide with many of these injuries resulting in higher order cognitive impairments. Galantamine (GAL), an acetylcholine esterase inhibitor (AChEI) and positive allosteric modulator of nicotinic acetylcholine receptors (nAChRs), has been reported to ameliorate cognitive deficits after clinical TBI. Previously, we demonstrated that controlled cortical impact (CCI) injury to rats resulted in significant executive function impairments as measured by the attentional set-shifting test (AST), a complex cognitive task analogous to the Wisconsin Card Sorting Test (WCST). Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.01.019DOI Listing

Mild blast-related TBI in a mouse model alters amygdalar neurostructure and circuitry.

Exp Neurol 2019 May 31;315:9-14. Epub 2019 Jan 31.

Department of Anatomy and Anthropology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv 69978, Israel; Dr. Miriam and Sheldon G. Adelson Chair, Center for the Biology of Addictive Diseases, Tel Aviv University, Tel Aviv 69978, Israel.

Traumatic brain injury (TBI) continues to be a signature injury of our modern conflicts. Due in part to increased use of improvised explosive devices (IEDs), we have seen blast trauma make up a significant portion of TBIs sustained by deployed troops and civilians. In addition to the physical injury, TBI is also a common comorbidity with post-traumatic stress disorder (PTSD). Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.01.020DOI Listing

Experimental traumatic brain injury results in estrous cycle disruption, neurobehavioral deficits, and impaired GSK3β/β-catenin signaling in female rats.

Exp Neurol 2019 May 31;315:42-51. Epub 2019 Jan 31.

NeuroBehavioral Research Laboratory, Department of Veterans Affairs, New Jersey Health Care System, East Orange, NJ, USA; Graduate School of Biomedical Sciences, Rutgers Biomedical and Health Sciences, 65 Bergen Street, Newark, NJ 07103, USA; Department of Pharmacology, Physiology and Neuroscience, New Jersey Medical School, Rutgers Biomedical and Health Science, Newark, NJ, USA. Electronic address:

An estimated 2.8 million traumatic brain injuries (TBI) occur within the United States each year. Approximately 40% of new TBI cases are female, however few studies have investigated the effects of TBI on female subjects. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.01.017DOI Listing
May 2019
1 Read

GATA-4 regulates neuronal apoptosis after intracerebral hemorrhage via the NF-κB/Bax/Caspase-3 pathway both in vivo and in vitro.

Exp Neurol 2019 May 30;315:21-31. Epub 2019 Jan 30.

Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou 215006, Jiangsu Province, China.

GATA-binding protein 4 (GATA-4),a member of the GATA family of transcription factors, is expressed in the normal brain and participates in the neural inflammatory response and senescence. However, few studies have investigated whether GATA-4 is involved in the brain damage induced by intracerebral hemorrhage (ICH). The aim of this study was to investigate in vivo and in vitro the role of GATA-4 in ICH-induced secondary brain injury (SBI) and its potential underlying mechanisms. Read More

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http://dx.doi.org/10.1016/j.expneurol.2019.01.018DOI Listing
May 2019
2 Reads

Long non-coding RNA AK038897 aggravates cerebral ischemia/reperfusion injury via acting as a ceRNA for miR-26a-5p to target DAPK1.

Exp Neurol 2019 Apr 29;314:100-110. Epub 2019 Jan 29.

Department of Emergency Medicine, The First Affiliated Hospital of Kunming Medical University, No. 295 Xichang Road, Wu Hua District, Kunming 650032, Yunnan Province, China. Electronic address:

Emerging evidence has suggested a significant role of long non-coding RNAs (lncRNAs) in ischemic stroke by acting as competing endogenous RNAs (ceRNAs) for microRNAs (miRNAs) to regulate certain RNA transcripts. AK038897 is an lncRNA that was reported to be upregulated in rat brains in response to transient focal ischemia. We aimed to investigate the possible regulatory role of AK038897 in ischemic stroke. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00144886183039
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http://dx.doi.org/10.1016/j.expneurol.2019.01.009DOI Listing
April 2019
11 Reads
4.696 Impact Factor